SPECIATION
Variation, information and the created kind ……………………………………………………………………………... 4 Refuting Evolution—Chapter 2 …………………………………………………………………………………………… 7 Refuting Evolution 2—Chapter 4 …………………………………………………………………….…………………… 9 Ligers and wholphins? What next? ………………………………………………………………………………………14 Speedy species surprise
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Eat your Brussels sprouts! …………………………………………………………………………………………………18
WHAT DO CREATIONISTS MEAN BY ‘CREATED KINDS
‘Parade of Mutants’—Pedigree Dogs and Artificial Selection ………………………………………………………… 20 The Australian dingo—a wolf in dog’s clothing
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Zenkey, zonkey, zebra donkey! …………………………………………………………………………..………………24 Comparative cytogenetics and chromosomal rearrangements ……………………………………………………….25 ‘Fast mouse evolution’ claims ………………………………………………………………….…………………………26 Resurrecting a ‘prehistoric’ horse ……………………………………………………………………...…………………27
HAS CREATIONIST RESEARCH FOUND ANY SPECIFIC EXAMPLES OF ANIMALS THAT ARE IN THE SAME BARAMIN
A baraminology tutorial with examples from the grasses (Poaceae) …………………………………………………28 Identification of species within the sheep-goat kind (Tsoan monobaramin) ………………………………………….31 Identification of species within the cattle monobaramin (kind) …………………………………………………………34 Karyotypic and allelic diversity within the canid baramin (Canidae) …………………………………………………..35 Identification of a large sparrow-finch monobaramin in perching birds (Aves: Passeriformes) ……………………. 39
WHAT IS SPECIATION.DOES IT TAKE MILLIONS OF YEARS TO OCCUR
Brisk biters …………………………………………………………………………………………………………………… 41 Darwin’s finches ………………………………………………………………….…………………………………………42 Dogs breeding dogs? ………………………………………………………………………………….……………………42 Genetic engineers unwind species barrier ………………………………………………………………………………44 The Heliconius hybrid butterfly: speciation yes, evolution no ………………………………………….……….………45
DAILY ARTICLES
Comparative cytogenetics and chromosomal rearrangements ………………………………….…….………………45 Inheritance of biological information—part I: the nature of inheritance and of information ………………………….46 Inheritance of biological information—part II: redefining the ‘information challenge’ ………………………………... 51 Inheritance of biological information—part III: control of information transfer and change ………………………….. 54 The 3 Rs of Evolution: Rearrange, Remove, Ruin—in other words, no evolution!
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The Island rule—recipe for evolution or extinction? . ………………………………………………………………….… 60 Molecular limits to natural variation ………………………………………………………………..……………………… 61 Galápagos with David Attenborough: Evolution ……………………………………………………………….…………67 Galápagos with David Attenborough: Adaptation …………………………………………………………………...……70 Post-Flood mutation of the KIT gene and the rise of white coloration patterns ………………………………………..72 The paradoxical urinary concentrating mechanism ……………………………………………………………………...76 ‘Vampire moth’ discovered ………………………………………………………………………………………………… 79 Lizards moving from eggs to live birth: evolution in action? ………………………………………………………..……79 The evolution of the horse …………………………………………………………………………………….…………… 80 Karyotypic and allelic diversity within the canid baramin (Canidae) …………………………………...……………… 83 Climbing Mt Improbable “evo devo” style …………………………………………………………………………………86 Facilitated variation: a new paradigm emerges in biology ……………………………………………………………… 88 Creative frogamandering ……………………………………………………………………………………………………93 Colourful creature coats ……………………………………………………………………….…………………………… 93
MIGRATION Migration after the Flood ………………………………………………………………………….……………………… 95 ABiogeography* …………………………………………………………………………………………………………….99 How did animals get to places such as Australia? ……………………………………………………………………102 Natural rafts carried animals around the globe …………………………………………………………………………104
Plants and animals around the world ……………………………………………………………………………………105 Genetics and geographical distribution ……………………………………………………………….…………………106 How did unique fish appear in particular areas? ……………………………………………………………..…………109 Birds of a feather don’t breed together …………………………………………………………………………...………111 No evidence of evolution and ‘deep time’ ……………………………………………………………………..…………112
NATURAL SELECTION
Refuting Evolution -Variation and natural selection versus evolution …………………………………………………114 Refuting Evolution 2 Argument: Natural selection leads to speciation ……………………………………………….116 Muddy Waters …………………………………………………………………………………………….…………………120 Refutation of New Scientist’s Evolution: 24 myths and misconceptions …………………………………………….. 122
DOES NATURAL SELECTION SUPPORT EVOLUTION Too dry for a fly …………………………………………………………………………….………………………………129 Bighorn horns not so big ……………………………………………………………………………...……………………129 Defining terms …………………………………………………………………………………….…………………………130 The evolution train’s a-comin’ ……………………………………………………………………………………………..131 A review of Genetic Entropy & The Mystery of the Genome by John C. Sanford …………………………………...133 Islands’ weeds don’t support evolution ………………………………………………………………………………….136 Well-armed water fleas and radishes ……………………………………………………………………………………. 137 What! … no potatoes? …………………………………………………………………………………………………….137 Dawkins playing bait and switch with guppy selection ………………………………………………………………….139 Molecular limits to natural variation ………………………………………………………………………………………. 140 DO MUTATIONS THAT CONFER RESISTANCE TO ANTIBIOTICS,POISONS, ETC PROVE EVOLUTION Anthrax and antibiotics: Is evolution relevant? ………………………………………………………………..……….. 145 Poison-resistant tomcods and the meaning of ‘evolution’ ………………………………………………………….….146 Superbugs not super after all 148 Patterns of change over time: organophosphorus resistance in the Australian sheep blowfly, Lucilia cuprina ....150 Creationist article ‘saved my favourite cow’ …………………………………………………………………………… 152 Has AIDS evolved? ………………………………………………………………………………………………………..154 HOW DOES NATURAL SELECTION FIT INTO A CREATIONISTS PARADIGM
Natural selection ≠ evolution …………………………………………………………………………………………….155 Darwin’s finches 156
DOES IT TAKE LONG PERIODS OF TIME FOR NATURAL SELECTION TO OCCURE Brisk biters …………………………………………………………………………………………………………………157 Book review: The Beak of the Finch ……………………………………………………………………………………157 Do toads goad snake evolution? ………………………………………………………………………………………..159 Rapid tomcod ‘evolution by pollution’? Yeah, right … and wrong …………………………………………………... 160 DOES SEXUAL SELECTION EXPLAIN HOW FEATUERS LIKE PEACOCK`S TAIL DEVELOPED The beauty of the peacock tail and the problems with the theory of sexual selection ……………………………..161 WHAT ABOUT PEPPERED MOTHS?WHY ARE THEY FREQUENTLY USED TO SUPPORT EVOLUTION. Goodbye, peppered moths ………………………………………………………………………………………………..167 The Moth Files …………………………………………………………………………………………………………….. 167 More about moths ………………………………………………………………………………………………………….167 WHAT ABOUT COMPTER SIMULATIONS ALLEGEDLY PROVING EVOLUTION BY CUMULATIVE SELECTION
Weasel, a flexible program for investigating deterministic computer ‘demonstrations’ of evolution ………………170
HOMOLOGY AND EMBRYOLOGY
Homology made simple …………………………………………………………………………………………………... 173 Refuting Evolution 2—Chapter 6 Argument: Common design points to common ancestry ……………………….176 Does homology provide evidence of evolutionary naturalism? ………………………………………………………..177 Fraud rediscovered ………………………………………………………………………………………………………...181
ARE THERE SIMILARITIES BETWEEN LIVING THINGS EVIDENCE FOR COMMON ANSESTRY OR COMMON DESIGN Saddle up the horse, it’s off to the bat cave ……………………………………………………………………………. 182 Are look-alikes related? ……………………………………………………………………………………………...…….183 A serious problem for homology ………………………………………………………………………………………….185 Could the mammalian middle ear have evolved … twice? ……………………………………………………………..189 Did eyes evolve by Darwinian mechanisms? ……………………………………………………………………………190 Problems with the evolutionary interpretation of limb design …………………………………………………………. 195 Morphology and molecules in conflict yet again ………………………………………………………………………..195 Tiktaalik roseae—a fishy ‘missing link’ …………………………………………………………………………………..196
Mammal-like reptiles: major trait reversals and discontinuities ………………………………………………………. 198 Walking whales, nested hierarchies, and chimeras: do they exist? …………………………………………………..204
ARE EARLY EMBRYOS VERY SIMILAR?DO THEY RECAPITATULATE EVOLUTIONARY HISTORY?
The ‘fish gills’ girl …………………………………………………………………………………………………………...209 Evangelist for evolution and apostle of deceit …………………………………………………………………………...209 A fishy story ………………………………………………………………………………….………………………………211 The human umbilical vesicle (‘yolk sac’) and pronephros—Are they vestigial? …………………………………….212
Variation, information and the created kind by Dr Carl Wieland Summary All observed biological changes involve only conservation or decay of the underlying genetic information. Thus we do not observe any sort of evolution in the sense in which the word is generally understood. For reasons of logic, practicality and strategy, it is suggested that we: Avoid the use of the term ‘microevolution’. Rethink our use of the whole concept of ‘variation within kind’. Avoid taxonomic definitions of the created kind in favour of one which is overtly axiomatic. Most popular literature on evolution more or less implies that since we see small changes going on today in successive generations of living things, we only have to extend this in time and we will see the types of changes which have caused single-cell-to-man evolution. Creationists are thus seen as drawing some sort of imaginary ‘Maginot line’, and saying in effect ‘this much variation we will allow but no more—call it microevolution or variation within kind.’ When a creationist says that, after all, mosquitoes are not seen turning into elephants or moths, this is regarded as a simplistic retreat. Such a criticism is not without some justification, because the neo-Darwinist can rightly say that he would not expect to see that sort of change in his lifetime either. The post-neo-Darwinist may say that our sample of geologic time is too small to be sure of seeing a ‘hopeful monster’ or any sort of significant saltational change.Another reason why the creationist position often appears as one of weakness is that we are perceived as admitting variation only because of being forced to do so by observation, then simply escaping the implications of variation by saying it does not go far enough. And we appear to redraw our ‘Maginot line’ depending on how much variation is demonstrated. It will be shown shortly, though, that this is a caricature of the creationist position, and that the limits to variation arise from basic informational considerations at the genetic level. The created kinds Observed variation does appear to have limits. It is tempting to use this fact to show that there are created kinds, and that variation is only within the limits of such kinds.However, the argument is circular and thus vulnerable. Since creationists by definition regard all variation as ‘within the limits of the created kind’ (see for example the statement of belief of the Creation Research Society of the USA), how can we then use observations to prove that variation is within the limits of the kind? To put it another way—of course we have never observed variation ‘across the kind’, since whatever two varieties descend from a common source, they are regarded as the same kind. It is no wonder that evolutionists are keen to press us for an exact definition of the created kind, since only then does our claim of ‘variation is only within the kind’ become nontautologous and scientifically falsifiable.Circular reasoning does not invalidate the concept of created kinds, however. In the same way, natural selection is also only capable of a circular definition (those who survive are the fittest, and the fittest are the ones who survive), but it is nevertheless a logical, easily observable concept. All we are saying is that arguments which are inherently circular cannot be invoked as independent proof of the kinds.When I claim that such independent proof may not be possible by the very nature of things, this statement is in no way a ‘cop out’. For instance, let us say we happened upon the remnants of an island which had exploded, leaving behind the debris of rocks, trees, sand, etc. It may be impossible in principle to reconstruct the original positions of the pieces in relation to each other before the explosion. This does not, however, mean that it is not possible to deduce with a great degree of confidence that the current state of the debris is consistent with that sort of an explosion which was recorded for us by eyewitness testimony, rather than arising by some other mechanism.In like manner, we can show that the observations of the living world are highly consistent with the described concept of original created kinds, and inconsistent with the idea of evolution. This is best done by focusing on the underlying genetic/informational basis of all biological change. This is more realistic and more revealing than focusing on the degree or extent of morphological change.The issue is qualitative, not quantitative. It is not that the train has had insufficient time to go far enough—it is heading in the wrong direction. The limits to variation—observed or unobserved—will come about inevitably because gene pools run out of ‘functionally efficient’ genetic information (or ‘teleonomic’ information). A full understanding of this eliminates the image of the desperately backpedalling creationist, redrawing his line of last resistance depending on what new observations are made on the appearance of new varieties.It also defuses the whole issue of ‘micro’ and ‘macro’ evolution. I believe it is better for creationists to avoid these confusing and misleading terms altogether. The word ‘evolution’ generally conveys the meaning of the sort of change which will ultimately be able to convert a protozoon into a man or a reptile into a bird, and so on. I hope to show that in terms of that sort of meaning, we do not see
any evolution at all. By saying ‘we accept micro but not macroevolution’ we risk reinforcing the perception that the issue is about the amount of change, which it is not. It is about the type of change.This is not merely petty semantics, but of real psychological and tactical significance. Of course one can say that ‘microevolution’ occurs when this word is defined in a certain fashion, but the impact of the word, the meaning it conveys, is such as to make it unwise to persevere with this unnecessary concessional statement. Microevolution, that is, a change, no matter how small, which is unequivocally the right sort of change to ultimately cause real, informationally ‘uphill’ change, has never been observed.In any case, leading biologists are themselves now coming to the conclusion that ‘macroevolution’ is not just ‘microevolution’ [using their terminology] extended over time. In November 1980 a conference of some of the world’s leading evolutionary biologists, billed as ‘historic’, was held at the Chicago Field Museum of Natural History on the topic of ‘macroevolution’. Reporting on the conference in the journal Science, Roger Lewin wrote:The central question of the Chicago conference was whether the mechanisms underlying microevolution can be extrapolated to explain the phenomena of macroevolution. At the risk of doing violence to the positions of some of the people at the meeting, the answer can be given as a clear, No. 1Francisco Ayala (Associate Professor of Genetics, University of California), was quoted as saying:… but I am now convinced from what the paleontologists say that small changes do not accumulate.2The fact that this article reaches essentially the same conclusion in the following pages can thus hardly cause it to be regarded as radical. Nevertheless, the vast majority of even well-educated people still persist in ignorance of this. That is, they believe that ‘Big Change = Small Change x Millions of Years.’ The concept of information The letters on this [printed] page—that is, the matter making up the ink and paper—all obey the laws of physics and chemistry, but these laws are not responsible for the information they carry. Information may depend on matter for its storage, transmission and retrieval, but is not a property of it. The ideas expressed in this article, for instance, originated in mind and were imposed on the matter. Living things also carry tremendous volumes of information on their biological molecules—again, this information is not a property of their chemistry, not a part of matter and the physical laws per se. It results from the order—from the way in which the letters of the cell’s genetic ‘alphabet’ are arranged. This order has to be imposed on these molecules from outside their own properties. Living things pass this information on from generation to generation. The base sequences of the DNA molecule effectively spell out a genetic ‘blue-print’ which determines the ultimate properties of the organism. In the final analysis, inherited biological variations are expressions of the variations in this information. Genes can be regarded as ‘sentences’ of hereditary information written in the DNA ‘language’.Imagine now the first population of living things on the evolutionist’s ‘primitive earth’. This so-called ‘simple cell’ would, of course, have a lot of genetic information, but vastly less than the information in only one of its present-day descendant gene pools, e.g., man. The evolutionist proposes that this ‘telegram’ has given rise to ‘encyclopedias’ of meaningful, useful genetic sentences. (See later for discussion of ‘meaning’ and ‘usefulness’ in a biological sense.) Thus he must account for the origin with time of these new and meaningful sentences. His only ultimate source for these is mutation.3Going back to the analogy of the printed page, the information in a living creature’s genes is copied during reproduction, analogous to the way in which an automatic typewriter reproduces information over and over. A mutation is an accident, a mistake, a ‘typing error’. Although most such changes are acknowledged to be harmful or meaningless, evolutionists propose that occasionally one is useful in a particular environmental context and hence its possessor has a better chance of survival/reproduction. By looking now at the informational basis for other mechanisms of biological variation, it will be seen why these are not the source of new sentences and therefore why the evolutionist generally relies on mutation of one sort or another in his scheme of things. 1. Mendelian variation This is the mechanism responsible for most of the new varieties which we see from breeding experiments and from reasonable inferences in nature. Sexual reproduction allows packets of information to be combined in many different ways, but will not produce any new packets or sentences. For example, when the many varieties of dog were bred from a ‘mongrel’ stock, this was achieved by selecting desired traits in successive generations, such that the genes or sentences for these traits became isolated into certain lines. Although some of these sentences may have been ‘hidden from view’ in the original stock, they were already present in that population. (We are disregarding mutation for the moment, since such new varieties may arise independently of any new mutations in the gene pool. Some dogs undoubtedly have mutant characteristics.)This sort of variation can only occur if there is a storehouse of such sentences available to choose from. Natural (or artificial) selection can explain the survival of the fittest but not the arrival of the fittest, which is the real question. These Mendelian variations tell us nothing about how the genetic information in the present stock arose. Hence, it is not the sort of change required to demonstrate ‘upward’ evolution—there has been no addition of new and useful ‘sentences’. And this is in spite of the fact that it is possible to observe many new varieties in this way—even new species. If you define a species as a freely interbreeding natural unit, it is easy to see how new species could arise without any ‘uphill’ change. That is, without the addition of any new information coding for any new functional complexity. For example, mutation could introduce a defect which served as a genetic barrier, or simple physical differences, such as the sizes of Great Dane and Chihuahua, could make interbreeding impossible in nature.It is a little surprising to still see the occasional creationist literature clinging to the concept that no new species have ever been observed. Even if this were true, and there is some suggestion that it has actually been observed, there are instances of ‘clines’ in field observations which make it virtually certain that two now-isolated (reproductively) species have arisen from the same ancestral gene pool. Yet the very same creationists who seem reluctant to make that sort of admission would be quite happy to agree with the rest of us that the various species within what may be regarded as the ‘dog’ kind, including perhaps wolves, foxes, jackals, coyotes and the domestic dog, have arisen from a single ancestral kind. So why may this no longer be permitted to be happening under present-day observations? It sets up a ‘straw man’ in the sense that any definite observation of a new species arising is used as a further lever with which to criticize creationists.What we see in the process of artificial selection or breeding giving rise to new varieties, is a thinning-out of the information in the parent stock, a reduction in the genetic potential for further variation. If you try and breed a Chihuahua from a Great Dane population or vice versa, you will find that your population lacks the necessary ‘sentences’. This is because, as each variety was selected out, the genes it carried were not representative of the entire gene pool.What appeared to be a dramatic example of change with the appearance of apparently new traits thus turns out, when its genetic basis is understood, to be an overall downward movement in informational terms. The number of sentences carried by each subgroup is reduced thus making it less likely to survive future environmental changes. Extrapolating that sort of process forward in time does not lead to upwards evolution, but ultimately to extinction with the appearance of evermore-informationally-depleted populations. 2. Polyploidy Again, no sentences appear which did not previously exist. This is the multiplication (‘photocopying’) of information already present. 3. Hybridizatlon Again, no new sentences. This is the mingling of two sets of information already present.
4. Mutation Since mutations are basically accidents, it is not surprising that they are observed to be largely harmful, lethal or meaningless to the function or survival of an organism. Random changes in a highly ordered code introduce ‘noise’ and chaos, not meaning, function and complexity, which tend to be lost. However, it is conceivable that in a complex world, occasionally a ‘destructive’ change will have a limited usefulness. For example, if we knock out a sentence such that there is a decrease in leg length in sheep (and there is such a mutation), this is useful to stop them jumping over the farmer’s fence. A beetle on a lonely, wind-swept island may have a mutation which causes it to lose or corrupt the information coding for wing manufacture; hence its wingless successors will not be so easily blown out to sea and will thus have a selective advantage. Eyeless fish in caves, some cases of antibiotic resistance—the handful of cases of mutations which are quite ‘beneficial’—do notinvolve the sort of increase in functional complexity which evolutionary theory demands. Nor would one expect this to be possible from a random change.At this point some will argue that the terms ‘useful’, ‘meaningful’, ‘functional’, etc. are misused. They claim that if some change gives survival value then by definition it has biological ‘meaning’ and usefulness. But this assumes that living systems do nothing but survive—when in fact they and their subsystems carry out projects and have specific functions. That is, they carry teleonomic information. This is one of the essential differences between living objects and non-living ones (apart from machines). These projects do not always give rise to survival/reproductive advantages—in fact, they may have very little to do with survival, but are carried out very efficiently. The Darwinian assumption is always made, of course, that at some time in the organism’s evolutionary history, the project had survival/reproductive value. (For example, the archer-fish with its highly-skilled ‘hobby’ of shooting down bugs which it does not require for survival at the present time.) However, since these are nontestable assumptions, it is legitimate to talk about genetic information in a teleonomic sense, in isolation from any possible survival value.The gene pools of today carry vast quantities of information coding for the performance of projects and functions which do not exist in the theoretical ‘primeval cell’. Hence, in order to support protozoon-to-man evolution, one must be able to point to instances where mutation has added a new ‘sentence’ or gene coding for a new project or function. This is so regardless of one’s assumptions on the survival value of any project or function.We do not know of a single mutation giving such an increase in functional complexity. Probabilistic considerations would seem to preclude this in any case, or at least make it an exceedingly rare event, far too rare to salvage evolution even over the assumed multibillion year time span.To illustrate further—the molecule haemoglobin in man carries out its project of transporting and delivering oxygen in red cells in a functionally efficient manner. A gene or ‘sentence’ exists which codes for the production of haemoglobin. There is a known mutation (actually three separate ones, giving the same result) in which only one letter in the sentence has been accidentally replaced by another. If you inherit this change from both parents, you will be seriously ill with a disease called sickle cell anaemia and will not survive for very long. Yet evolutionists frequently use this as an example of a ‘beneficial mutation’. This is because if you inherit it from only one parent, your red cells will be affected, but not seriously enough to affect your survival—just enough to prevent the malaria parasite from using them as an effective host. Hence, you will be more immune to malaria and better able to survive in malaria-infested areas. This shows us how a functionally efficienthaemoglobin molecule became a functionally crippled haemoglobin molecule. The mutation-caused gene for this disease is maintained at high levels in malaria-endemic regions by this incidental phenomenon of heterozygote superiority. Its damaging effect in a proportion of offspring is balanced by the protection it gives against malaria. It is decidedly not an ‘upward’ change. We have not seen a new, efficient oxygen transport mechanism or its beginnings evolve. We have not seen the haemoglobin transport mechanism improved.One more loose but possibly useful analogy. Let us say an undercover agent is engaged in sending a daily reassuring telegram from enemy territory. The text says ‘the enemy is not attacking today’. One day an accident occurs in transmission and the word ‘not’ is lost. This is very likely going to be a harmful change, perhaps even triggering a nuclear war by mistake. But perhaps, in a freak situation, it could turn out to be useful (for example, by testing the fail-safe mechanisms involved). But this does not mean that it is the sort of change required to begin to convert the telegram into an encyclopedia.The very small number of ‘beneficial’ mutations actually observed are simply the wrong kind of change for evolution—we do not see the addition of new sentences which carry meaning and information. Again surprisingly, one often reads creationist works which insist that there is no such thing as a beneficial mutation. If benefit is defined purely in survival terms, then we would not expect this to be true in all instances, and in fact it is not—that is, there are indeed ‘beneficial’ mutations in that sense only.Information depends on order, and since all of our observations and our understanding of entropy tells us that in a natural, spontaneous, unguided and unprogrammed process order will decrease, the same will be true of information. The physicist and communications engineer should not be surprised at the realisation that biological processes involve no increases in useful or functional (teleonomic) information and complexity. In fact, the net result of any biological process involving transmission of information (i.e., all hereditary variation) is conservation or loss of that genetic information.This is the reason why there are inevitable limits to variation, why the creationist does not have to worry about how many new ‘species’ the future may bring—because there is a limit to the amount of functionally efficient genetic information present, and natural processes such as mutation cannot add to this original storehouse.Notice that since organisms were created to migrate out from a central point at least once and fill empty ecological niches, as well as having to cope with a decaying and changing environment, they would require considerable variation potential. Without this built-in genetic flexibility, most populations would not be present today. Hence the concept of biological change is in a sense predicted by the young age model, not something forced upon it only because such change has occurred. The created kind The originally created information was not in the form of one ‘super species’ from which all of today’s populations have split off by this ‘thinning out’ process, but was created as a number of distinct gene pools. Each group of sexually reproducing organisms had at least two members. Thus, Each original group began with a built-in amount of genetic information which is the raw material for virtually all subsequent useful variation. Each original group was presumably genetically and reproductively isolated from other such groups, yet was able to interbreed within its own group. Hence the original kinds would truly have earned the modern biological definition of ‘species’.4 We saw in our dog example that such ‘species’ can split into two or more distinct subgroups which can then diverge (without adding anything new) and can end up with the characteristics of ‘species’ themselves—that is, reproductively isolated from each other but freely interbreeding among themselves. The more variability in the original gene pool, the more easily can such new groups arise. However, each ‘splitting’ reduces the potential for further change and hence even this is limited. All the descendants of such an original kind which was once a species, may then end up being classified together in a much higher taxonomic category—e.g., family.
Take a hypothetical created kind A—truly a biological ‘species’ with perhaps a tremendous genetic potential. See Figure 1. (For the sake of simplicity, the diagram avoids the issue of what is meant by two of each kind—however, the basic point is not affected.) Note that A may even continue as an unchanged group, as may any of the subgroups. Splitting off of daughter populations does not necessarily mean extinction of the parent population. In the case of man, the original group has not diverged sufficiently to produce new species.Hence, D1, D2, D3, E1, E2, E3, P1, P2, Q1, Q2, Q3 and Q4 are all different species, reproductively isolated. But all the functionally efficient genetic information they contain was present in A. (They presumably carry some mutational defects as well).Let us assume that the original kind A has become extinct, and also the populations X, B, C, D, E, P and Q. (But not D1, Figure 1. The ‘splitting off’ of daughter populations from D2, etc.) If X carried some of the original information in A, an original created kind. which is not represented in B or C, then that information is Click here for larger image. lost forever. Hence, in spite of the fact that there are many ‘new species’ which were not originally present, we would have witnessed conservation of most of the information, loss of some, and nothing new added apart from mutations (harmful defects or just meaningless ‘noise’ in the genetic information). All of which is the wrong sort of informational change if one is trying to demonstrate protozoon-to-man evolution.Classifications above species are more or less arbitrary groupings of convenience, based generally on similarities and differences of structure. It is conceivable that today, D1, D2 and D3 could be classified as species belonging to one genus, and E1, E2 and E3 as species in another genus, for example. It could also be that the groups B and C were sufficiently different such that their descendants would today be in different families. We begin to see some of the problems facing a creationist who tries to delineate today’s representatives of the created kinds.Creatures may be classified in the same family, for example, on the basis of similarities due to common design while in fact they belong to two totally different created kinds. This should sound a note of caution against using morphology alone, as well as pointing out the potential folly of saying ‘in this case, the baramin is the family; in this case, it is the genus, etc.’ (Baramin is an accepted creationist term for ‘created kind’.) There is no easy solution as yet to the problem of establishing each of these genetic relationships—in fact, we will probably never be able to know them all with certainty. Interbreeding, in vitro fertilization experiments, etc. may suggest membership of the same baramin but lack of such genetic compatibility does not prove that two groups are not in the same kind. (See earlier discussion—genetic barriers could arise via mutational deterioration.) However, newer insights, enabling us to make direct comparisons between species via DNA sequencing, open up an entirely new research horizon. (Although the question of where the funding for such extensive research will come from in an evolution-dominated society remains enigmatic.) What then do we say to an evolutionist who understandably presses us for a definition of a created kind or identification of same today? I suggest the following for consideration:Groups of living organisms belong in the same created kind if they have descended from the same ancestral gene pool.To talk of ‘fixity of kinds’ in relation to any present-day variants thus also becomes redundant—no new kinds can appear by definition.Besides being a simple and obvious definition, it is axiomatic. Thus it is as unashamedly circular as a rolled-up armadillo and just as impregnable, deflecting attention, quite properly, to the real issue of genetic change.The question is not—what is a baramin, is it a species, a family or a genus? Rather, the question is—which of today’s populations are related to each other by this form of common descent, and are thus of the same created kind? Notice that this is vastly removed from the evolutionist’s notion of common descent. As the creationist looks back in time along a line of descent, he sees an expansion of the gene pool. As the evolutionist does likewise, he sees a contraction.As with all taxonomic questions, common sense will probably continue to play the greatest part. The yong model, the fossil record and common sense unite to prevent creationists doing too much ‘lumping together’ as we go back in time. For instance, it is conceivable (though not necessarily so) that crocodiles and alligators both descended from the same ancestral gene pool which contained all their functionally efficient genes, but not really conceivable that crocodiles, alligators and ostriches had a common ancestral pool which carried the genes for all three! Refuting Evolution—Chapter 2 A handbook for students, parents, and teachers countering the latest arguments for evolution by Jonathan Sarfati, Ph.D., F.M. First published in Refuting Evolution, Chapter 2 Variation and natural selection versus evolution This chapter contrasts the evolution and creation models, and refutes faulty understandings of both. A major point is the common practice of Teaching about Evolution and the Nature of Science to call all change in organisms ‘evolution.’ This enables Teaching about Evolution to claim that evolution is happening today. However, creationists have never disputed that organisms change; the difference is the type of change. A key difference between the two models is whether observed changes are the type to turn particles into people. Evolution Evolution, of the fish-to-philosopher type, requires that non-living chemicals organize themselves into a self-reproducing organism. All types of life are alleged to have descended, by natural, ongoing processes, from this ‘simple’ life form. For this to have worked, there must be some process which can generate the genetic information in living things today. Chapter 9 on ‘Design’ shows how encyclopedic this information is.So how do evolutionists propose that this information arose? The first self-reproducing organism would have made copies of itself. Evolution also requires that the copying is not always completely accurate—errors (mutations) occur. Any mutations which enable an organism to leave more self-reproducing offspring will be passed on through the generations. This ‘differential reproduction’ is called natural selection. In summary, evolutionists believe that the source of new genetic information is mutations sorted by natural selection—the neo-Darwinian theory. Young age model The different kinds of organisms, reproduced ‘after their kinds’ . Each of these kinds was created with a vast amount of information. There was enough variety in the information in the original creatures so their descendants could adapt to a wide variety of environments.All (sexually reproducing) organisms contain their genetic information in paired form. Each offspring
inherits half its genetic information from its mother, and half from its father. So there are two genes at a given position (locus, plural loci) coding for a particular characteristic. An organism can be heterozygous at a given locus, meaning it carries different forms (alleles) of this gene. For example, one allele can code for blue eyes, while the other one can code for brown eyes; or one can code for the A blood type and the other for the B type. Sometimes two alleles have a combined effect, while at other times only one allele (called dominant) has any effect on the organism, while the other does not (recessive). With humans, both the mother’s and father’s halves have 20,687 protein-coding genes, while 97% of the rest of the DNA has an important role in coding for RNA, for control of gene expression. Overall, the information equivalent to a thousand 500-page books (3 billion base pairs, asTeaching about Evolution correctly states on page 42). The ardent neoDarwinist Francisco Ayala points out that humans today have an ‘average heterozygosity of 6.7 percent.’ 1 This means that for every thousand gene pairs coding for any trait, 67 of the pairs have different alleles. If we consider only the proteincoding genes, this would mean 1,340 heterozygous loci overall. Thus, any single human could produce a vast number of different possible sperm or egg cells 2 1,340 or 2.4 × 10403. The number of atoms in the whole known universe is ‘only’ 10 80, extremely tiny by comparison. So there is no problem for creationists explaining that the original created kinds could each give rise to many different varieties. In fact, the original created kinds would have had much more heterozygosity than their modern, more specialized descendants. No wonder Ayala pointed out that most of the variation in populations arises from reshuffling of previously existing genes, not from mutations. Many varieties can arise simply by two previously hidden recessive alleles coming together. However, Ayala believes the genetic information came ultimately from mutations, not creation. His belief is contrary to information theory, as shown in chapter 9 on ‘Design’. Deterioration from perfection As the previous chapter showed, all scientists interpret facts according to their assumptions. From this premise of perfection followed by deterioration, it follows that mutations, as would be expected from copying errors, destroyed some of the original genetic information. Many evolutionists point to allegedly imperfect structures as ‘proof’ of evolution, although this is really an argument against perfect design rather than for evolution. But many allegedly imperfect structures can also be interpreted as a deterioration of once-perfect structures, for example, eyes of blind creatures in caves. However, this fails to explain how sight could have arisen in the first place.2 Adaptation and natural selection Also, the once-perfect environments have deteriorated into harsher ones. Creatures adapted to these new environments, and this adaptation took the form of weeding out some genetic information. This is certainly natural selection—evolutionists don’t have a monopoly on this. In fact, a creationist, Edward Blyth, thought of the concept 25 years before Darwin’s Origin of Species was published. But unlike evolutionists, Blyth regarded it as a conservative process that would remove defective organisms, thus conserving the health of the population as a whole. Only when coupled with hypothetical informationgaining mutations could natural selection be creative.For example, the original dog/wolf kind probably had the information for a wide variety of fur lengths. The first animals probably had medium-length fur. In the simplified example illustrated below,3 a single gene pair is shown under each dog as coming in two possible forms. One form of the gene (L) carries instructions for long fur, the other (S) for short fur.In row 1, we start with medium-furred animals (LS) interbreeding. Each of the offspring of these dogs can get one of either gene from each parent to make up their two genes. In row 2, we see that the resultant offspring can have either short (SS), medium (LS) or long (LL) fur. Now imagine the climate cooling drastically (as in the Ice Age). Only those with long fur survive to give rise to the next generation (line 3). So from then on, all the dogs will be a new, long-furred variety. Note that: They are now adapted to their environment. They are now more specialized than their ancestors on row 1. Figure 1: The evolutionary ‘tree’ which postulates that all today’s species are This has occurred through natural descended from the one common ancestor (which itself evolved from nonselection. living chemicals). This is what evolution is really all about. There have been no new genes added. In fact, genes have been lost from the population—i.e., there has been a loss of genetic information, the opposite of what microbe-to-man evolution needs in order to be credible.Now the population is less able to adapt to future environmental changes— were the climate to become hot, there is no genetic information for short fur, so the dogs would probably overheat.Another Figure 2: The alleged creationist ‘lawn’ this represents the caricature of information-losing process occurs in creationism presented by Teaching about Evolution —the ‘kinds’ were the sexually reproducing organisms— same as today’s species. remember, each organism inherits only half the information carried by each parent. For example, consider a human couple with only one child, where the mother had the AB blood group (meaning that she has both A and B alleles) and the father had the O blood group (both alleles are O and recessive). So the child would have either AO or BO alleles, so either the A or the B Figure 3: The true creationist ‘orchard’ diversity has occurred with time allele must be missing from the child’s within the original ‘kinds’ (creationists often call them baramin, from genetic information. Thus, the child could Hebrewbara = create, and min = kind). Much of the evidence of variation not have the AB blood group, but would presented by Teaching about Evolutionrefutes only the straw-man version of have either the A or the B blood group creationism in Figure 2, but fits the true creationist ‘orchard’ model perfectly well.
respectively.4A large population as a whole is less likely to lose established genes because there are usually many copies of the genes of both parents (for example, in their siblings and cousins). But in a small, isolated population, there is a good chance that information can be lost by random sampling. This is called genetic drift. Since new mutant genes would start off in small numbers, they are quite likely to be eliminated by genetic drift, even if they were beneficial. 5In an extreme case, where a single pregnant animal or a single pair is isolated, e.g., by being blown or washed onto a desert island, it may lack a number of genes of the original population. So when its descendants fill the island, this new population would be different from the old one, with less information. This is called the founder effect.Loss of information through mutations, natural selection, and genetic drift can sometimes result in different small populations losing such different information that they will no longer interbreed. For example, changes in song or color might result in birds no longer recognizing a mate, so they no longer interbreed. Thus a new ‘species’ is formed. The Flood Another aspect of the young age model is that the whole world was flooded. Creationists scientists conclude that these kinds multiplied and their descendants spread out over the earth. ‘Founder effects’ would have been common, so many ‘kinds’ would each have given rise to several of today’s ‘species.’ Contrasting the Models Once the young age is properly understood, it is possible to analyze the ‘evidence’ for ‘evolution as a contemporary process’ presented byTeaching about Evolution on pages 16–19. The three diagrams below should help:
The alleged evidence for evolution in action This section will deal with some of the examples used by Teaching about Evolution, and show that they fit the creationist model better. Antibiotic and pesticide resistance Teaching about Evolution claims on pages 16–17: The continual evolution of human pathogens has come to pose one of the most serious health problems facing human societies. Many strains of bacteria have become increasingly resistant to antibiotics as natural selection has amplified resistant strains that arose through naturally occurring genetic variation.Similar episodes of rapid evolution are occurring in many different organisms. Rats have developed resistance to the poison warfarin. Many hundreds of insect species and other agricultural pests have evolved resistance to the pesticides used to combat them—even to chemical defenses genetically engineered into plants.However, what has this to do with the evolution of new kinds with new genetic information? Precisely nothing. What has happened in many cases is that some bacteria already had the genes for resistance to the antibiotics. In fact, some bacteria obtained by thawing sources which had been frozen before man developed antibiotics have shown to be antibiotic-resistant. When antibiotics are applied to a population of bacteria, those lacking resistance are killed, and any genetic information they carry is eliminated. The survivors carry less information, but they are all resistant. The same principle applies to rats and insects ‘evolving’ resistance to pesticides. Again, the resistance was already there, and creatures without resistance are eliminated.In other cases, antibiotic resistance is the result of a mutation, but in all known cases, this mutation has destroyed information. It may seem surprising that destruction of information can sometimes help. But one example is resistance to the antibiotic penicillin. Bacteria normally produce an enzyme, penicillinase, which destroys penicillin. The amount of penicillinase is controlled by a gene. There is normally enough produced to handle any penicillin encountered in the wild, but the bacterium is overwhelmed by the amount given to patients. A mutation disabling this controlling gene results in much more penicillinase being produced. This enables the bacterium to resist the antibiotic. But normally, this mutant would be less fit, as it wastes resources by producing unnecessary penicillinase.Another example of acquired antibiotic resistance is the transfer of pieces of genetic material (called plasmids) between bacteria, even between those of different species. But this is still using pre-existing information, and doesn’t explain its origin. More information on antibiotic resistance can be found in the article Superbugs Not Super after All.6 Lacewing species Another example of ‘evolution’ is given on page 17, where Teaching about Evolution states: The North American lacewing species Chrysoperla carnea and Chrysoperla downesi separated from a common ancestor species recently in evolutionary time and are very similar. But they are different in color, reflecting their different habitats, and they breed at different times of year.This statement is basically correct, but an evolutionary interpretation of this statement is not the only one possible. A creationist interpretation is that an original Chrysoperla kind was created with genes for a wide variety of colors and mating behavior. This has given rise to more specialized descendants. The specialization means that each has lost the information for certain colors and behaviors. The formation of new species (speciation) without information gain is no problem for creationists.7 Adaptation/variation within Chrysoperla, which involves no addition of complex new genetic information, says nothing about the origin of lacewings themselves, which is what evolution is supposed to explain. Darwin’s finches On page 19, Teaching about Evolution claims: A particularly interesting example of contemporary evolution involves the 13 species of finches studied by Darwin on the Galápagos Islands, now known as Darwin’s finches … . Drought diminishes supplies of easily cracked nuts but permits the survival of plants that produce larger, tougher nuts. Drought thus favors birds with strong, wide beaks that can break these tougher seeds, producing populations of birds with these traits. [Peter and Rosemary Grant of Princeton University] have estimated that if droughts occur about every 10 years on the islands, then a new species of finch might arise in only about 200 years.However, again, an original population of finches had a wide variety of beak sizes. When a drought occurs, the birds with insufficiently strong and wide beaks can’t crack the nuts, so they are eliminated, along with their genetic information. Again, no new information has arisen, so this does not support molecules-to-man evolution. Also, the rapid speciation (200 years) is good evidence for the young age model. Darwin’s finches show that it need not take very long for new species to arise.9 Breeding versus evolution On pages 37–38, Teaching about Evolution compares the artificial breeding of pigeons and dogs with evolution. However, all the breeders do is select from the information already present. For example, Chihuahuas were bred by selecting the smallest dogs to breed from over many generations. But this process eliminates the genes for large size.The opposite process would have bred Great Danes from the same ancestral dog population, by eliminating the genes for small size. So the breeding has sorted out the information mixture into separate lines. All the breeds have less information than the original
dog/wolf kind.Many breeds are also the victims of hereditary conditions due to mutations, for example the ‘squashed’ snout of the bulldog and pug. But their loss of genetic information and their inherited defects mean that purebred dogs are less ‘fit’ in the wild than mongrels, and veterinarians can confirm that purebreds suffer from more diseases.Actually, breeds of dogs are interfertile, even Great Danes and Chihuahuas, so they are still the same species. Not that speciation is a problem for creationists—see the section on lacewings above. But if Great Danes and Chihuahuas were only known from the fossil record, they would probably have been classified as different species or even different genera. Indeed, without human intervention, Great Danes and Chihuahuas could probably not breed together (hybridize), so they could be considered different species in the wild. Refuting Evolution 2—Chapter 4 A sequel to Refuting Evolution that refutes the latest arguments to support evolution (as presented by PBS and Scientific American). by Jonathan Sarfati, Ph.D. with Michael Matthews Argument: Natural selection leads to speciation Galápagos finches—evolution in action? The opening episode of the PBS Evolution series makes much of the Galápagos finches—considered one of the classic evidences of ‘evolution in action.’ But PBS admits that Darwin didn’t even realize that the birds were finches and he failed to label which island they came from. All the same, he managed to acquire this information, and he eventually concluded that they had descended from mainland finches with modification just as the young model would predict! He correctly realized that finch beak size was the result of adaptation to different food sources. The problem is that Darwin and the PBS series taught that this adaptation could explain the general theory of evolution (GTE). But the finch beak variation is merely the result of selection of existing genetic information, while the GTE requires new information. Also, an 18-year study by zoologist Peter Grant showed that a new species could arise in only 200 years,1 which is inadvertent support for the young age model of rapid speciation.2 However, another problem with using these finches is that the variation seems to be cyclic—while a drought resulted in a slight increase in beak size, the change was reversed when the rains returned. So it looks more like builtin adaptability to various climatic conditions than anything to do with the GTE.PBS also discusses the change in beak length of hummingbirds, to adapt to changes in the lengths of flowers where they obtain nectar. But the same points apply—no evidence was produced that any new information is required for these changes, as opposed to selection of already-existing information. What is the young age model? Perhaps the most frequently repeated mistake that evolutionists make in their attacks on creation is to assert that ‘natural selection’ and ‘speciation’ prove evolution and disprove the young age account of origins. Their bait-and-switch arguments imply that creationists believe in ‘fixity of species.’ The glossary for the PBS Evolution series Online Course for Teachers: Teaching Evolution explicitly makes this empty allegation:In creationism, species are described as ‘fixed’ in the sense that they are believed not to change their form, or appearance, through time.But no reputable creationist denies speciation—in fact, it is an important part of creationist biology. In the previous chapter, I showed that the real issue is whether evolution can explain the increase of genetic information content—enough changes to turn microbes into men, not simple change through time. Before laying to rest the evolutionists’ pointless arguments on this issue, it might be helpful to review the creationist model in detail. Pre-flood ‘kinds’ are not modern species The different kinds of organisms reproduced ‘after their kinds’.Thus the “kinds” would have originallybeen distinct biological species, i.e., a population of organisms that can interbreed to produce fertile offspring but that cannot so breed with a different biological species.But creationists point out that the ‘kind’ is larger than one of today’s ‘species.’ Each of the original kinds was created with a vast amount of information. The original creatures had enough variety in their genetic information so that their descendants could adapt to a wide variety of environments.Based on the young age criterion for kinds, creationists have made several deductions about the modern descendants of the original living organisms. They deduce, for example, that as long as two modern creatures can hybridize with true fertilization, the two creatures are descended from the same kind.3Also, if two creatures can hybridize with the same third creature, they are all members of the same kind.4 The hybridization criterion is a valid operational definition, which could in principle enable researchers to list all the kinds. The implication is one-way—hybridization is evidence that two creatures are the same kind, but it does not necessarily follow that if hybridization cannot occur then they are not members of the same kind (failure to hybridize could be due to degenerative mutations). After all, there are couples who can’t have children, and we don’t classify them as a different species, let alone a different kind.The boundaries of the ‘kind’ do not always correspond to any given man-made classification such as ‘species,’ genus, family, etc. But this is not the fault of the term ‘kind’; it is actually due to inconsistencies in the man-made classification system. That is, several organisms classified as different ‘species,’ and even different genera or higher groupings, can produce fertile offspring. This means that they are really the same species that has several varieties, hence a polytypic (many type) species. A good example is Kekaimalu the wholphin, a fertile hybrid between a male false killer whale (Pseudorca crassidens) and a female bottlenose dolphin (Tursiops truncatus), i.e., between two different so-calledgenera.5 There are more examples in reference 3.Biologists have identified several ways that a loss of genetic information through mutations (copying mistakes) can lead to new species—e.g., the loss of a protein’s ability to recognize ‘imprinting’ marks, ‘jumping genes,’ natural selection, and genetic drift. When these mutations take place in small populations, they can sometimes result in sterile or nonviable offspring. Or changes in song or color might result in birds that no longer recognize a mate, so they no longer interbreed. Either way, a new ‘species’ is formed. Thus, each created kind may have been the ancestor of several present-day species.But again, it’s important to stress that speciation has nothing to do with real evolution (GTE), because it involves sorting and loss of genetic information, rather than new information. The young age model predicts rapid speciation The young age model would also predict rapid formation of new varieties and even species. This is because all the modern varieties of land vertebrates must have descended from comparatively few animals that surivived the flood only around 4,500 years ago. In contrast, Darwin thought that this process would normally take eons. It turns out that the very evidence claimed by evolutionists to support their theory supports the young age model.Biologists have identified several instances of rapid adaptation, including guppies on Trinidad, lizards in the Bahamas, daisies on the islands of British Columbia, and
house mice on Madeira.6 Another good example is a new ‘species’ of mosquito that can’t interbreed with the parent population, arising in the London Underground train system (the ‘Tube’) in only 100 years. The rapid change has ‘astonished’ evolutionists, but should delight creationists.7 Scientific American admits as much.These days even most creationists acknowledge that microevolution has been upheld by tests in the laboratory (as in studies of cells, plants and fruit flies) and in the field (as in Grant’s studies of evolving beak shapes among Galápagos finches). [SA 80]And why should creationists deny such things? All of this so-called microevolution has never been observed to add new genetic information. In fact, the sorts of changes which are observed are the wrong type to drive the evolutionary story. 8 Scientific American is forced to make a pointless claim about evidence of ‘profound’ changes:Natural selection and other mechanisms —such as chromosomal changes, symbiosis, and hybridization—can drive profound changes in populations over time. [SA 80]Again, do these profound changes increase information? No populations are seen losing information, and adapting within the constraints of the information they already have. In contrast, goo-to-you evolution requires something quite different—the progressive addition of massive amounts of genetic information that is novel not only to that population, but to the entire biosphere. Straw man 1: Natural selection can’t explain new species Scientific American falls for the same straw-man argument as PBS, failing to recognize that creationists accept new species arising within the kind. Creationists recognize how reproductive isolation can result from information loss. (See discussion above.) 11. Natural selection might explain micro-evolution, but it cannot explain the origin of new species and higher orders of life. Evolutionary biologists have written extensively about how natural selection could produce new species. For instance, in the model called allopatry, developed by Ernst Mayr of Harvard University, if a population of organisms were isolated from the rest of its species by geographical boundaries, it might be subjected to different selective pressures. Changes would accumulate in the isolated population. If those changes became so significant that the splinter group could not or routinely would not breed with the original stock, then the splinter group would be reproductively isolated and on its way toward becoming a new species. [SA 82]Indeed, creationists point out that Mayr’s allopatric model would explain the origin of the different people groups (‘races’) after the confusion of languages at Babel induced small population groups to spread out all over the earth.9 Of course, the modern people groups are notreproductively isolated and are still a single biological species. Note that the reproductive isolation is an informationally negative change, even if beneficial, because it blocks the interchange of genetic information between populations.Evolutionists brag that natural selection is the best studied of the evolutionary mechanisms, but these studies show that it has nothing to do with evolution of more complex life forms! All we observe it doing is removing information, not adding it. Scientific American suggests that there are other feasible mechanisms to explain evolution, but they do not hold up, either.Natural selection is the best studied of the evolutionary mechanisms, but biologists are open to other possibilities as well. Biologists are constantly assessing the potential of unusual genetic mechanisms for causing speciation or for producing complex features in organisms. Lynn Margulis of the University of Massachusetts at Amherst and others have persuasively argued that some cellular organelles, such as the energy-generating mitochondria, evolved through the symbiotic merger of ancient organisms. [SA 82]The endosymbiosis theory has many problems, such as the lack of evidence that prokaryotes are capable of ingesting another cell and keeping it alive, and the large differences in genes between mitochondria and prokaryotes.10 Scientific American admits that it’s open to any other mechanism to explain nature—as long as it excludes a designer!Thus, science welcomes the possibility of evolution resulting from forces beyond natural selection. Yet those forces must be natural; they cannot be attributed to the actions of mysterious creative intelligences whose existence, in scientific terms, is unproved. [SA 82]We have already cited more honest admissions by evolutionists Lewontin and Todd about their a priori rejection of a Designer before even examining the evidence. But evolutionary propaganda for public consumption persists in claiming that evolution is accepted purely on scientific grounds. Straw man 2: Evolutionists have seen species evolve Scientific American tries to make hay with this straw man, devoting two points to ‘proving’ natural selection and speciation. Informed creationists don’t teach against these biological processes—even though some ‘day-age’ advocates, like Hugh Ross, do.11 12. Nobody has ever seen a new species evolve. Speciation is probably fairly rare and in many cases might take centuries. [SA 82]It might take centuries, but it need not. In fact, speciation can happen much faster than most evolutionists (and ‘day-age’ advocates) realize. Furthermore, recognizing a new species during a formative stage can be difficult, because biologists sometimes disagree about how best to define a species. The most widely used definition, Mayr’s Biological Species Concept, recognizes a species as a distinct community of reproductively isolated populations—sets of organisms that normally do not or cannot breed outside their community. In practice, this standard can be difficult to apply to organisms isolated by distance or terrain or to plants (and, of course, fossils do not breed). Biologists therefore usually use organisms’ physical and behavioral traits as clues to their species membership. [SA 82]We agree. It’s important to note this difficulty in defining ‘species’ whenever evolutionists claim that creationists don’t have a consistent definition of ‘kinds’ (which we do, as discussed before). We also agree with Scientific American’s recognition of recent experiments that have caused artificial speciation.Nevertheless, the scientific literature does contain reports of apparent speciation events in plants, insects, and worms. In most of these experiments, researchers subjected organisms to various types of selection for anatomical differences, mating behaviors, habitat preferences, and other traits and found that they had created populations of organisms that did not breed with outsiders. For example, William R. Rice of the University of New Mexico and George W. Salt of the University of California at Davis demonstrated that if they sorted a group of fruit flies by their preference for certain environments and bred those flies separately over 35 generations, the resulting flies would refuse to breed with those from a very different environment. [ SA 82–83]None of this is news to informed creationists. Once again, there is no new information, but sorting and loss of already existing information. Ecology proves evolution? While evolutionists claim that natural selection is the best-studied mechanism for evolution, they also must explain the reallife processes behind natural selection. Their discussion of ecology is very interesting (and factual), but it tells us nothing about GTE. Changing populations within healthy forest ecosystems For example, PBS 3 devotes a whole segment to show how a healthy forest ecosystem has a large carnivore at the top of the food chain, which can cause drastic changes in the population of the forest. It takes 100 pounds of plant to feed 10 pounds of herbivore, which in turn feed 1 pound of carnivore. So the existence of carnivores indicates the health of the supporting animals and plants. Later on in the program, Wildlife Conservation Society biologist Alan Rabinowitz claims that this healthy forest exhibits ‘evolution going on around us,’ but all he means is the replacement of one species with another. Of course, already-existing species replacing other already-existing species has nothing to do with the origin of new species
with new genetic information. Once again, ‘evolution’ is a vacuous catch-all term, with any change in population numbers tossed out to the unwary listener as evidence of the goo-to-you theory. Founder effect Then the PBS program moves on to isolated habitats and the ‘founder effect.’ This is where a single breeding pair or pregnant female colonizes a new niche, and carries only a fraction of the gene pool. Therefore its descendants also contain a small fraction of the original gene pool, so the new population can be very different from the old. This also offers no comfort or support to the notion of evolution because the new population has less information than the old. Invasion—the leafy spurge Another ecological topic is biological invaders, the bane of all countries that depend on agriculture and livestock to feed their people and earn export dollars. The invaders are often more mobile and adaptive, so they out-compete native species. Modern technology has vastly increased the rate of hostile invasions, as animals stow away on ships and in the undercarriage of airplanes, although some species have been introduced deliberately. Fordham University paleoecologist David Burney investigated what happened in Hawaii when Polynesians and then Europeans introduced new species. He claimed:Evolution has now entered a new mode. Something altogether new is happening, and it has to do with what humans do to the evolutionary process. [PBS 3]Ho hum, this is just another example of replacement of one species with another, which again has nothing to do with showing how particles could have turned into people.Pioneers introduced a weed called leafy spurge into North Dakota from Russia, and it ‘threatens to kill off all native grasses.’ A cattle rancher claimed on PBS that ‘it is a cancer to the land … it makes the land just totally useless.’ Actually, the first claim is an exaggeration, and the second is a matter of perspective—sheep and goat farmers would have no problems. But the rancher said that herbicides were very expensive, so the narrator asks:… what’s left? … The solution may be another invader—discovered when scientists learned what kept leafy spurge in check in its native Russia. It’s the flea beetle —a case of fighting evolutionary fire with fire. [PBS 3] Canisters of flea beetles are dropped from airplanes, then the narrator says: So now we’re in a race most of us don’t even know we’re running—to learn as much as possible about evolution before it’s too late. [PBS 3]Huh? Using already-existing enemies of the leafy spurge requires ‘evolution’? This must be the nadir of the contentless nature of this word, even by the pathetic standards of the PBS series. Farmers have used such common-sense biological controls for centuries, well before Darwin. Interestingly, one of the classic cases of successful biological control was the defeat of Australia’s cactus invader, the prickly pear, through the introduction of the Cactoblastis organism. John Mann, the scientist responsible for saving Australia from ecological and economic ruin in this way, was heaped with accolades and honors for his feat. Mann was a convinced creationist, who was interviewed byCreation before his death.12 Symbiosis PBS 3 also describes the leaf-cutting ants of Brazil. They form colonies containing eight million insects, and they cut leaves into pieces and bring them to the nest, but they don’t eat them. Rather, other leafcutter ants mulch them and use the mulch to grow a fungus ‘garden.’ This fungus is used as food for the young leafcutters, which thus depend on the fungus for survival, but the fungus depends on the ants to provide the mulch.But this fungus garden has a ‘weed,’ a virulent mold that badly hinders the fungal growth. To combat this, some ants have a white waxy coating that is now known to be tangled mats of bacteria that produce antibiotics that kill the mold.Presumably, by this stage in the series, the producers hope that viewers are so indoctrinated in evolution that they don’t even need to try to produce evidence. To the diehard evolutionist, any phenomenon at all can be adduced as ‘evidence’ for evolution. In this case, they don’t bother to explain how such a complex symbiosis could have evolved, but merely assert that the bacteria and mold are products of an arms race lasting 50 million years. Predator–prey, driving force of evolution? While evolutionists discuss natural selection and speciation, they like to emphasize the bloodshed and violence that drives these biological changes. They see ‘Nature, red in tooth and claw,’ in the memorable phrase from the very long 1850 poem In Memoriam, A.H.H. by Alfred Lord Tennyson (1809–1892). In debates they love to pull out this as ‘knock-down’ evidence against people, believing it disproves the possibility of intelligent designer—following Darwin. The fact that Tennyson’s poem predated Darwin’s Origin indicates that Darwin was greatly influenced by philosophical ideas of his day. Episode 4 of the PBS Evolution series aims to show that these violent biological forces, rather than the environmental ones, drive evolution most strongly, based largely on extensive interviews with the atheistic sociobiologist Edward O. Wilson. The title of PBS 4, ‘The Evolutionary Arms Race!’ reflects the struggle between predator and prey: as a prey evolves stronger defense mechanisms, an attacker must evolve stronger mechanisms to survive, and vice versa. Of course, evolutionary biologists think there is no design behind this: the only prey that survive have chance copying mistakes in their genes that confer a strong defense, and they pass on these genes to their offspring. Faced with these stronger defense mechanisms, only those predators that happen to have mutations conferring better attacking power will be able to eat the prey, while the others starve and fail to pass on their genes.But as explained earlier, real evolution requires changes that increase genetic information, while non-information-increasing changes are part of the young age model. None of the examples presented in episode 4 prove that information has increased, so they provide no support for evolution or against the young age model . Poison newt PBS takes viewers to Oregon, where there were mysterious deaths of campers, but it turned out that newts were found boiled in the coffee pot. These rough-skinned newts (Taricha granulosa) secrete a deadly toxin from their skin glands so powerful that even a pinhead-sized amount can kill an adult human. They are the deadliest salamanders on earth. So scientists investigated why this newt should have such a deadly toxin.They theorized that a predator was driving this ‘evolution,’ and they found that the common garter snake (Thamnophis sirtalis) was the newt’s only predator. Most snakes will be killed by the newt’s toxin, but the common garter snake just loses muscle control for a few hours, which could of course have serious consequences. But the newts were also driving the ‘evolution’ of the snakes—they also had various degrees of resistance to the newt toxin.Are these conclusions correct? Yes, it is probably correct that the predators and prey are driving each other’s changes, and that they are the result of mutations and natural selection. Although it might surprise the ill-informed anti-creationist that creationists accept mutations and selection, it shouldn’t be so surprising to anyone who understands the young age model .So is this proof of particles-to-people evolution? Not at all. There is no proof that the changes increase genetic information. In fact, the reverse seems to be true.The snakes with greater resistance have a cost —they move more slowly. Since PBS provided no explanation of the poison’s activity, it’s fair to propose possible scenarios to explain the phenomenon under a young age framework (it would be hypocritical for evolutionists to object, since they often produce hypothetical ‘just-so’ stories to explain what they cannot see).Suppose the newt’s poison normally reacts with a particular neurotransmitter in its victims to produce something that halts all nerve impulses, resulting in death. But if the snake had a mutation which reduced the production of this neurotransmitter, then the newt’s poison would have fewer targets to act upon. Another possibility is a mutation in the snake altering the neurotransmitter’s precise structure so that its shape no longer matches the protein. Either way, the poison would be less effective. But at the same time, either mutation
would slow nerve impulses, making the snake’s muscle movement slower.So either of these would be an information loss in the snake that happens to confer an advantage. This is far from the only example. The best known is sickle-cell anemia, a common blood disorder in which a mutation causes the sufferer’s hemoglobin to form the wrong shape and fail to carry oxygen. People who carry two copies of the sickle-cell gene (homozygous) often develop fatal anemia. But this misshapen hemoglobin also resists the malaria parasite (Plasmodium). So humans who are heterozygous (have both a normal and abnormal gene) have some advantage in areas where malaria is prevalent, even though half their hemoglobin is less effective at its job of carrying oxygen. Another example is wingless beetles, which survive on windy islands because they won’t fly and be blown into the sea. 14As for the newt, likewise, increased secretion of poison can result without any new information. One possibility is an information-losingmutation that disables a gene controlling the production of the poison. Then it would be over-produced, which would be an advantage in defending against the snake, but a wasteful use of resources otherwise.There are other related examples, e.g., one way that the Staphylococcus bacteria becomes resistant to penicillin is via a mutation that disables a control gene for production of penicillinase, an enzyme that destroys penicillin. When it has this mutation, the bacterium over-produces this enzyme, which means it is resistant to huge amounts of penicillin. But in the wild, this mutant bacterium is less fit, because it squanders resources by producing unnecessary penicillinase.Another example is a cattle breed called the Belgian Blue. This is very valuable to beef farmers because it has 20–30% more muscle than average cattle, and its meat is lower in fat and very tender. Normally, muscle growth is regulated by a number of proteins, such as myostatin.However, Belgian Blues have a mutation that deactivates the myostatin gene, so the muscles grow uncontrolled and become very large. This mutation has a cost, in reduced fertility.15 A different mutation of the same gene is also responsible for the very muscular Piedmontese cattle. Genetic engineers have bred muscular mice by the same principle.In all these cases, a mutation causes information loss, even though it might be considered ‘beneficial.’ Therefore it is in the opposite direction required for particles-to-people evolution, which requires the generation of new information. Evolution of pathogens If evolutionists hope to find evidence of modern-day evolution, they have a perfect opportunity with pathogens. In just a few months, bacteria can go through hundreds of thousands of generations, equivalent to ‘millions of years’ in vertebrates. Yet in spite of this rapid change, the bacteria that we see today are essentially the same as the bacteria retrieved from the tombs of the pharaohs, and even with those discovered in salt crystals ‘dated’ millions of years old.21 HIV resistance to drugs PBS 1 claims that Darwin didn’t really see evolution in action, but now we do. Supposedly HIV, the cause of AIDS, evolves resistance to drugs faster than we can make them. Because the virus can produce billions of copies per day, it can ‘evolve’ in minutes to hours. One researcher said that this rapid change would be a ‘surprise’ if we didn’t have the concept of evolution. PBS also attempted to tug heartstrings, by portraying AIDS patients as ‘victims of evolution.’First, we see the equivocation—HIV producing HIV is supposed to show that particles could turn into people; but they’re still HIV—they haven’t changed into something else.Second, in PBS 4, it’s made clear that the related phenomenon of antibiotic resistance in bacteria took the medical community by surprise—this means that it wasn’t a prediction of evolution, except after the fact. Third, they fail to demonstrate that new information is involved, and in fact the next segment of the program showed that the opposite is true. Veronica Miller of Goethe University in Germany experimented by ceasing all antiviral drug treatments to a patient. Without the drugs, the few surviving original (‘wild’) types that had infected the patient could grow more easily. It turned out that they easily out-competed the vast numbers of resistant forms that had developed in the hospital. She said this was a risk because the wild types were also more dangerous—more efficient than the new strains that had survived the earlier drug treatments. The superior efficiency and reproductive success of the wild type implies that the other ‘evolved’ strains acquired resistance due to a loss of information somewhere.This should not be surprising, because the same is true of many examples of antibiotic resistance in bacteria. For example, some bacteria (seePoison newt, above) have an enzyme that usually has a useful purpose, but it also turns an antibiotic into a poison. That is, it’s not the antibiotic per se that’s damaging, but its chemical byproduct from the bacterium’s metabolism. So a mutation disabling this enzyme would render the antibiotic harmless. But this bacterium is still disabled, because the enzyme is now hindered, so the bacterium would be unable to compete in the wild with non-resistant ones. The information loss in both HIV and the bacterium is the opposite of what evolution requires.22 Tuberculosis and antibiotic resistance PBS describes the microbe as a ‘predator’ of humans, although ‘parasite’ would be more accurate. Mummies show that the tuberculosis bacillus (TB) affected Egyptians 4,000 years ago. The Black Death wiped out one-third of Europe’s population in 1347–1351, and the influenza pandemic of 1918–1919 killed 20 million people—more than World War 1 that had just ended.After the world wars, antibiotics were considered the ‘magic bullet,’ and there were optimistic claims even as late as 1969 that ‘infectious diseases were a thing of the past.’ But they failed to anticipate the development of resistance. This shows that bacterial resistance was hardly a ‘prediction’ of evolution, but is really a phenomenon they try to explain ‘after the fact’ as due to evolution. As will be shown, there is nothing to support molecules-to-man evolution; rather, a properly understood creation model makes good sense of the evidence.PBS 4 discussed a new strain of TB that had arisen in the overcrowded Russian prison system, containing malnourished prisoners with weakened immune systems. One inmate, ‘Sasha’ (Alexandr), had failed to complete his course of antibiotics. This meant that a few bacteria survived because they had some resistance to the antibiotic, and then proliferated once the treatment stopped. But the program itself makes it clear that the resistance was already present, so this is not evolution, although it is natural selection.These resistant bacteria are not confined to the prison, but have spread because of travel. One 19-year-old Russian student, ‘Anna,’ has a strain resistant to five antibiotics. Immunologists predict that TB could soon claim 2–3 million lives per year.But as shown, there is no proof that any antibiotic resistance is due to increased genetic information. The above example shows that the information was already present, and I previously explained how a loss of information could confer resistance. Sometimes bacteria can pass genes to each other by exchanging plasmids, and sometimes these genes confer resistance. But of course, these examples involve no new information produced in the biosphere. Evolution of less harmful bacteria? Paul Ewald of Amherst College claimed on PBS 4 that ‘evolution’ may not only be a problem, but could also be harnessed to ‘evolve’ less harmful bacteria. If a pathogen spreads by close contact between people, then it’s in its best interest not to make people so sick that they can’t move around. But those pathogens spread by water and insects tend to be deadly.In the 1991 cholera epidemic in South America, a million people were infected, and 10,000 died. The bacterium (Vibrio cholerae) was spread by contaminated water, so ‘evolved’ high levels of toxicity. The solution was to clean the water supply, so that only healthier people could spread the germ. So the germ ‘evolved’ mildness, and many infected people didn’t even develop symptoms.But here again, there is indeed natural selection, but the result is that Vibrio cholerae turn into Vibrio cholerae! There is no proof that any new information was produced, but rather, selection of existing genetic variation. PBS 4 compared this phenomenon to breeding domestic dogs from wolves, but again this involved loss of information.
Pathogens and young age model The phenomenon described in the previous section can provide some insights. It clearly shows that even something usually known as a deadly germ can have a mild variant that causes no illness. Presumably something like this was created—even today, Vibrio cholerae has a role in the ecosystems of brackish waters and estuaries, and the original may have had a role living symbiotically with some people. Even its toxin probably has a beneficial function in small amounts, like most poisons. The virulence arose, by natural selection of varieties producing more and more toxin as contaminated water became more plentiful. No new information would be needed for this process. Recent evidence shows that the loss of chemotaxis—the ability to move in response to changes in chemical concentrations—will markedly increase infectivity in an infant mouse model of cholera.23Another likely example of virulence arising by information loss is the mycoplasmas, the smallest known self-reproducing organisms (parasitic bacteria with no cell walls and fewer than 1,000 genes, found in the respiratory system and urogenital tracts of humans). Loss of genetic information, e.g., for amino acid synthesis, could have resulted in the mycoplasmas becoming increasingly dependent on their hosts for survival. 24 Some clues to possible benign roles for viruses can be gleaned from functions they have even today. Viruses are non-living entities, which function like seeds and spores, transporting genes among plants and animals. They also help keep soil fertile, keep water clean, and regulate gases in the atmosphere.25 So once again, some alleged evidence for evolution actually provides support for the young age model. Has immunity evolved? In PBS 4, Stephen O’Brien of the National Cancer Institute wondered why the big cats have ‘evolved’ resistance to a disease deadly to humans. There is a Feline Immunodeficiency Virus (FIV) that should cause AIDS-like symptoms. Supposedly the cats’ ancestors were almost wiped out by the virus, but some had resistant genes. Supposedly, the FIV evolved to mildness.More interesting was the claim that about 10 percent of humans have a ‘whopping mutation’ that confers resistance to HIV. This turns out to be the loss of certain receptors on the immune cells preventing the HIV from docking on them. Again, this change is in the opposite directionrequired to change particles into people.From mycoplasmas to big cats, from TB to poison newts, there’s not a shred of evidence that might explain the evolution of new genetic information, but the loss that we see fits nicely with the young model. Ligers and wholphins? What next? by Don Batten If we can cross-breed a zebra and a horse (to produce a ‘zorse’), a lion and a tiger (a liger or tigon), or a false killer whale and a dolphin (a wholphin), what does this tell us about the original kinds of animals that created? When we plant a tomato seed, we don’t expect to see a geranium pop up out of the ground. Nor do we expect that our dog will give birth to kittens or that Aunt Betty, who is expecting, will bring home a chimpanzee baby from the hospital! Our everyday experience that things produce offspring true to their kind.But what is a created ‘kind’? The creationist scientist, Carolus Linnaeus (1707–1778), the founder of the science of taxonomy,1 tried to determine the created kinds. He defined a ‘species’ as a group of organisms that could interbreed among themselves, but not with another group, akin to the young age concept. (See aside below.) Finding the created kinds The ability to produce offspring, i.e. to breed with one another, defines the original created kinds. Linnaeus recognised this, but named many species2 without any breeding experiments, on the basis of such things as flower characteristics. In his mature years he did extensive hybridization (cross-breeding) experiments and realised that his ‘species’ concept was too narrow for the species to be considered as created kinds; he thought that the genus perhaps corresponded better with the created kind.3,4 The Cat Kind Speciation (based on pre-existing created genetic information) probably occurred faster after the Flood due to greater environmental pressures, isolation due to migration of small populations, and many unoccupied ecological niches.Even today, creationists are often misrepresented as believing that all the species we have today were created , just like they are today, in the beginning. This is called ‘fixity of species’. Nevertheless, university professors often show students that a new ‘species’ has arisen in ferment flies, for example, and then claim that this disproves the young age account. Darwin made this very mistake when he studied the finches and tortoises on the Galapagos islands. (He also erred in assuming that creation implied that each organism was made where it is now found; but from the young model it is clear that today’s landdwelling vertebrates migrated to their present locations after the Flood.)If two animals or two plants can hybridize (at least enough to produce a truly fertilized egg), then they must belong to (i.e. have descended from) the same original created kind. If the hybridizing species are from different genera in a family, it suggests that the whole family might have come from the one created kind. If the genera are in different families within an order, it suggests that maybe the whole order may have derived from the original created kind.On the other hand, if two species will not hybridize, it does not necessarily prove that they are not originally from the same kind. We all know of couples who cannot have children, but this does not mean they are separate species!In the case of three species, A, B and C, if A and B can each hybridize with C, then it suggests that all three are of the same created kind—whether or not A and B can hybridize with each other. Breeding barriers can arise through such things as mutations. For example, two forms of ferment flies (Drosophila) produced offspring that could not breed with the parent species.5 That is, they were a new biological ‘species’. This was due to a slight chromosomal rearrangement, not any new genetic information. The new ‘species’ was indistinguishable from the parents and obviously the same kind as the parents, since it came from them.Following are some examples of hybrids that show that the created kind is often at a higher level than the species, or even the genus, named by taxonomists. Images courtesy Camilla Maluotoga
Zonkeys result from a cross between a zebra and a donkey (left). ‘Tigger’ (right), belongs to Camilla Maluotoga, from New Mexico in the USA, and is the name she gave to this cross between a horse and a zebra, known as a zorse. Mules, zeedonks and zorses Crossing a male ass (donkey— Equus asinus) and a horse (Equus caballus) produces a mule (the reverse is called a hinny). Hybrids between zebras and horses (zorse) and zebras and donkeys (zedonk, zonkey, zebrass) also readily occur. Some creationists have reasoned that because these hybrids are sterile, the horse, ass and zebra must be separate created kinds. However It is overwhelmingly likely that horses, asses and zebras (six species ofEquus) are the descendants of the one kind. Hybridization itself suggests this, not whether the offspring are fertile or not. Infertility in offspring can be due to rearrangements of chromosomes in the different species— changes such that the various species have the same DNA information but the chromosomes of the different species no longer match up properly to allow the offspring to be fertile. Such (non-evolutionary) changes within a kind can cause sterility in hybrids. Ligers A male African lion (Panthera leo) and a female tiger (Panthera tigris) can mate to produce a liger. The reverse cross produces a tigon. Such crossing does not normally happen in the wild because most lions live in Africa and most tigers live in Asia. Also, lions and tigers just don’t mix; they are enemies in the wild. However, the Institute of Greatly Endangered and Rare Species, Myrtle Beach, South Carolina (USA), raised a lion and a tigress together. Arthur, the lion, and Ayla, the tigress, became good friends and bred to produce Samson and Sudan, two huge male ligers. Samson stands 3.7 m (12 feet) tall on his hind legs, weighs 500 kg (1,100 lbs) and can run at 80 km/hr (50 mph). Lions and tigers belong to the same genus, Panthera, along with the jaguar, leopard and snow leopard, in the subfamily Felinae. This subfamily also contains the genus Felis, which includes the mountain lion and numerous species of smaller cats, including the domestic cat. The cheetah, genus Acinonyx, belongs to a different subfamily.6 Thus the genera Panthera, Felis and Acinonyx may represent descendants of three original created cat kinds, or maybe two: Panthera-Felis andAcinonyx, or even one cat kind. The extinct sabre-tooth tiger may have been a different created kind (see diagram above).The Panthera cats lack a hyoid bone at the back of the tongue, compared to Felis. Acinonyx has the hyoid, but lacks the ability to retract its claws. So the differences between the cats could have arisen through loss of genetic information due to mutations (loss of the bone; loss of claw retraction). Note that this has nothing to do with molecules-to-man evolution, which requires the addition of new information, not loss of information (which is to be expected as things tend to ‘fall apart’). Kekaimalu the wholphin In 1985, Hawaii’s Sea Life Park reported the birth of a baby from the mating of a male false killer whale (Pseudorca crassidens) and a female bottlenose dolphin (Tursiops truncatus).7 The birth surprised the park staff, as the parents are rather different in appearance. Here we have a hybrid between different genera in the same family, Delphinidae (dolphins and killer whales).8 Since the offspring in this case are fertile (Kekaimalu has since given birth to a baby wholphin), these two genera are really, by definition, a single polytypic biological species. 2 Other genera in the group are much more alike than the two that produced the offspring in Hawaii, which suggests that the 12 living genera might have all descended from the original created kind. Rama the cama Veterinarians in the United Arab Emirates successfully cross-bred a camel and a llama. The ‘cama’, named ‘Rama’, has the cloven hooves of a llama and the short ears and tail of a camel. The scientists hope to combine the best qualities of both into the one animal—the superior fleece and calmer temperament of the llama with the larger size of the camel. Photo by Dave and Lynn Jolly ‘Genae’ the snake—the live, healthy offspring of snakes from two different genera (see main text). Genae the hybrid snake ‘Genae’ (pictured right) resulted from a cross between an albino corn snake (Elaphe guttata) and an albino king snake (Lampropeltis triangulum) in a reptile park in California.9Apparently, this particular intergeneric hybrid is fertile. Genae is almost four years old and already 1.4 m (4½ ft) long. The parent snakes belong to the same snake family,
Colubridae; the success of this hybrid suggests that the many species and genera of snakes in this family today could have all originally come from the same created kind. Other hybrids With the cattle kind, seven species of the genus Bos hybridize, but so also does the North American buffalo, Bison bison, with Bos, to produce a ‘cattalo’. Here the whole family of cattle-type creatures, Bovidae, probably came from an original created cattle kind.10Plant breeders have bred some agriculturally important plants by hybridizing different species and even genera. For example, triticale, a grain crop, came from a cross of wheat (Triticum) and rye (Secale), another fertile hybrid between genera. During my years as a research scientist for the government in Australia, I helped create a hybrid of the delicious fruit species lychee (Litchi chinensis) and longan (Dimocarpus longana), which both belong to 11 The delicious fruit species, lychee (left) and longan (right) hybridize, despite being different genera. the same family. I also studied the hybrids of six species of the custard apple family, Annonaceae. Each of these two family groupings, recognised by botanists today, probably represents the original created kinds.All kinds, or basic types of creatures and plants were creatded with the ability to produce variety in their offspring. These varieties come from recombinations of the existing genetic information created in the beginning. The variations allow for the descendants of the created kinds to adapt to different environments and fill the earth. If genera represent the created kinds,after the flood,the”kinds” occasionally gave rise to families. From these kinds came many ‘daughter species’, which generally each have less information (and are thus more specialized) than the parent population from the pre-flood period. Properly understood, adaptation by natural selection (which gets rid of information) does not involve the addition of new complex DNA information. Thus, students should not be taught that it demonstrates ‘evolution happening’, as if it showed the process by which fish could eventually turn into people. A ‘geep’? No—a ‘chimera’ Despite the fact that the ‘geep’ has both sheep and goat in its parentage, and shares the characteristics of both species, it is not a hybrid. It is a ‘chimera’, formed by mixing the (fertilized) embryo cells of two different species.The DNA in each adult cell (including sex cells) is thus either fully sheep or fully goat—hence there are patches of either thin white goat fur or thick sheep’s wool. Thus also, any offspring will be either all sheep or all goat. This artificial manipulation is very different from the situation where two animals of the same kind (but different species) mate producing live offspring. Linnaeus and the classification system Linnaeus established the two-part naming system of genus and species. For example, he called wheat Triticum aestivum, which means in Latin, ‘summer wheat’. Such ‘scientific’ names are normally italicised, with the genus beginning with a capital. When used in scientific works, the names are followed by the abbreviated name of the scientist responsible for the name. When ‘L.’ follows a name, this shows that Linnaeus first applied the name. For example, the name for maize or ‘corn’ is Zea mays L. Linnaeus named many plants and animals.There can be one or many species in a genus, so genus is a higher level of classification. Linnaeus also developed the idea of grouping genera (plural of genus) within higher groupings he called orders, and the orders within classes. Linnaeus opposed the pre-Darwin evolutionary ideas of his day, pointing out that life was not a continuum, or a ‘great chain of being’, an ancient pagan Greek idea. He could classify things, usually into neat groups, because of the lack of transitional forms.Later, other levels of classification were added so that today we have species, genus, family, order, class, phylum and kingdom. Sometimes other levels are added, such as subfamily and subphylum.
Kekaimalu the wholphin, a 19-year-old offspring of a false killer whale and an Atlantic bottlenose dolphinwhale-dolphin, mated with a dolphin to produce a girl, Kawili Kai (above). The world’s only Wholphin … false killer whale/dolphin cross False killer whales (pseudorcas) and bottlenose dolphins are each from a different genus. Man-made classification systems were thrown into confusion when these two creatures mated and produced a live offspring (see main text). This suggests that all killer whales and dolphins, which are all in the same family, are the one created kind. This wholphin’s size, shape and colour are right in between those of her parents. She has 66 teeth—an ‘average’ between pseudorcas (44 teeth) and bottlenose dolphins (88). Kekaimalu has since mated with a dolphin to produce a live baby. Speedy species surprise
by David Catchpoole and Carl Wieland Researchers in Trinidad relocated guppies (Poecilia reticulata) from a waterfall pool teeming with predators to previously guppy-free pools above the falls where there was only one known possible predator (of small guppies only, therefore large guppies would be safe).1 The descendants of the transplanted guppies adjusted to their new circumstances by growing bigger, maturing later, and having fewer and bigger offspring.The speed of these changes bewildered evolutionists, because their standard millionsof-years view is that the guppies would require long periods of time to adapt. One evolutionist said, ‘The guppies adapted to their new environment in a mere four years—a rate of change some 10,000 to 10 million times faster than the average rates determined from the fossil record.’2 Leggy lizards ‘The guppies adapted to their new environment in a mere four years—a rate of change some 10,000 to 10 million times faster than the average rates determined from the fossil record.’—Morell, V.,Science, 275:1880, 1997.And it’s not just guppies. In the Bahamas, small numbers of anole lizards (Anolis sagrei) were transplanted from an island with tall trees to nearby islands where there were previously no lizards and only smaller bushy vegetation. Body form rapidly changed in succeeding generations. 3 In particular, the relative length of hindlimbs was greatly decreased—thought to be an adaptation for life amongst the twigs of the scrubby vegetation in the lizards’ new habitat. (Lizards that live on tree trunks have longer legs than those that live on twigs—an apparent trade-off between the agility necessary for twig-to-twig jumping and the speed that longer limbs provide on the broad surface of tree trunks.)4,5 But again it was the speed of adaptation, many thousands of times higher than (their interpretation of) the ‘fossil record’ that surprised evolutionists.6 Daisy diaspora On small islands off British Columbia, the seeds of wind-dispersed weedy plants in the daisy family (Asteraceae) are rapidly losing their ability to ‘fly’. Specifically, the embryo part of the seed is becoming fatter while the parachute-like ‘pappus’ that keeps each seed aloft is becoming smaller. These changes are advantageous because they reduce dispersal—otherwise, on such tiny islands, lightweight windblown seeds would be lost in the ocean (which is why they have left fewer descendants). Note that these changes involve the loss of the capacity for long-range airborne dispersal.7 Flies, fish and finches Other examples of rapid adaptation, even to the extent of producing ‘new species’—speciation—abound. (If a population arises from another which cannot interbreed anymore with its parent population, it is generally defined as a new species.) Creation magazine recently reported how evolutionists described as ‘alarming’ the rate of change in the wingspan of European fruit flies introduced accidentally to America.8,9,10 Similarly, rapid changes have been reported recently for Drosophila fruit flies and sockeye salmon—within just nine and thirteen generations respectively.11In the case of Darwin’s famous finches, it had been estimated that from one million to five million years would have been necessary for today’s Galapagos Island species to radiate from their parent populations. But actual observations of rapid finch adaptation have forced evolutionists to scale that back to a timeframe of just a few centuries.12 Mosquitoes and mice Not long ago, evolutionists were astonished to find that bird-biting mosquitoes, which moved into the London Underground train network (and are now biting humans and rats instead), have already become a separate species.13 And now a study of house mice in Madeira (thought to have been introduced to the island following 15th century Portuguese settlement) has found that ‘several reproductively isolated chromosomal races’ (in effect, new ‘species’) have appeared in less than 500 years.14In all of these instances, the speedy changes have nothing to do with the production of any new genes by mutation (the imagined mechanism of molecules-to-man evolution), but result mostly from selection of genes that already exist. Here we have real, observed evidence that (downhill) adaptive formation of new forms and species from the one created kind can take place rapidly. It doesn’t need millions of years.Shouldn’t evolutionists rejoice, and creationists despair, at all this observed change? Hardly. Informed creationists have long stressed that natural selection can easily cause major variation in short time periods, by acting on the created genetic information already present. But this does not support the idea of evolution in the molecules-to-man sense, because no new information has been added.Anole lizards have been observed to change rapidly under the right conditions … observable evidence in favour of the young history.Selection by itself gets rid of information, and of all observed mutations which have some effect on survival or function,15 so far even the rare ‘beneficial’ ones are also losses of information. The late-maturing, larger guppies resulted simply from a re-shuffling of existing genetic material. 16 Such variation can even be sufficient to prevent two groups from interbreeding with each other any more, thus forming new ‘species’ by definition, without involving any new information.The young account of history is not only accommodates such rapid changes in body form, but actually requires that it would have happened much faster than evolutionists would expect. As the animals multiplying to fill the Earth and all those empty ecological niches, natural selection could easily have caused an original ‘dog kind’ (e.g.) to ‘split’ into wolves, coyotes, dingoes, etc. Because there are historical records showing some of
these subtypes in existence only a few hundred years after the Flood, this means that there had to have been some very rapid (non-evolutionary) speciation. So it is encouragingly supportive of the young history when some such rapid changes are seen still occurring today.17 And this is being repeatedly confirmed.But since evolutionists mistakenly interpret all such adaptation/speciation as ‘evolution happening’, they are left stunned when it happensmuch faster than their traditional interpretations of the fossil record would allow. (This is, of course, easy to understand when it is realized that the standard idea about the fossil record—that it is a ‘tape-recording’ of millions of years—is in fact a misinterpretation. The record reflects the way in which a global Flood and some of its after-effects buried a world of plants and animals, in a time sequence which did not involve millions of years.)Because such fast changes challenge traditional evolutionary ideas, the findings are often disputed, but with little success.2 Rapid ‘evolution’ (a misnomer, as we have seen) is welcomed by some fossil experts who support the idea of ‘punctuated equilibrium’. 18 This is the notion that the evolutionary history of life is one of mostly no change, ‘punctuated’ by short, sharp bursts of evolution (which, conveniently, happen too briefly to be recorded in the fossils). However, not only is this still a minority view among evolutionists, it begs the question of why, if fast change is everywhere, has not a vastly greater number of new species been generated over ‘geologic time’? I.e. the observed changes are still too fast for comfort.Not only is this rapid change not adding information, even some evolutionists point out that evolution in the molecules-to-man sense was not observed in any of these studies. The finches are still finches, the mosquitoes stay mosquitoes, and the mice remain mice. One evolutionary geneticist, referring to the guppy data, said, ‘As far as I know, these are still guppies.’2 Setting the record straight If we start with the Word of the One who knows all, the evidence of today’s world makes a great deal of sense. Creatures were to reproduce ‘after their kind’, so mice come from mice, lizards from lizards, daisies from daisies. Evolution has never occurred, nor does it occur today. But organisms have a wonderful ‘built-in’ genetic capacity for rapid change in response to environmental pressures—most easily observed today in isolated island environments.Such examples of rapid adaptation give us an insight into how the Earth’s many vacant ecological niches were recolonized after the Flood—a global event in real history. Eat your Brussels sprouts! by Don Batten Many parents have had trouble convincing their children to eat one of the members of the cabbage group of vegetables. This group includes cabbage, broccoli, Brussels sprouts, cauliflower, kohlrabi and kale. Most children do not rate these vegetables as their favourite flavour!But these vegetables, some of the most nutritious of all, contain lots of minerals and vitamins, and antioxidants that greatly surpass the power of vitamins A, C and E—the antioxidants commonly available in vitamin pills. They also have substances that inhibit cancer cells.1Clearly, vitamin pills cannot make up for the benefits of eating the real food. Furthermore, you can eat ‘boatloads’ of these vegetables without getting fat—it sounds like many of us should be eating a lot more of them.Sauerkraut, a German delicacy, is produced by alternating layers of cabbage and salt; acid fermentation quickly sets in, preserving the cabbage along with the vitamin C. Koreans have a similar food called kimchi. In the past, with the lack of fresh fruit and vegetables during the long European winters, sauerkraut helped people avoid scurvy.Captain James Cook, who mapped the east coast of Australia in 1770, carried sauerkraut on his voyages to prevent scurvy in his crew.2 Were Brussels sprouts created? Interestingly, the extreme variety of types has arisen in the last two thousand years or so, by people selecting the various forms. They all belong to one species, Brassica oleracea. The original created type of cabbage was probably similar to kale or collards. Records of its use go back to the Greeks about 600 BC. Undoubtedly, its use goes back earlier; the first people may well have eaten it.We cannot know for sure how the various forms arose (see table below). They probably arose spontaneously, either by recombination of existing genetic information or with mutations giving rise to the various forms.Diagram shows how three species (red/brown boxes) naturally hybridize (’cross’) to produce three other named ‘species’ (green boxes). Thus, cabbage X black mustard gives Ethiopian mustard. The number of chromosome pairs is in parentheses for each species.For example, in the common heading cabbage, only one bud at the top of the stem—the terminal bud—produces leaves. There are other buds, one at the base of each leaf, but they do not develop unless the terminal bud suffers damage—say, by an insect eating it. Then one or more of these axillary buds develops.In Brussels sprouts, the plant fails to suppress the growth of the other buds, and so each one becomes a little cabbage. It also has an elongated stem compared to the cabbage. It is easy to see how a mutation that damaged the mechanism in the cabbage that suppresses extra bud development could produce a Brussels sprouts plant. 3Such mutations would not increase the complexity of an organism; rather they mess up some part of its functionality. Other mutations could have created the deformed flowers of the cauliflower or broccoli. Such downhill mutations occur in plant and animals, but these will not change a cabbage into a banana plant—that requires the sorts of gross information-adding changes that evolutionists need to find to justify their claim that microbes changed into mangoes. It’s all in the family
These plants belong to the family Brassicaceae. This family is also still widely known as Cruciferae, due to the crucifix appearance of the flower petals when viewed from above. The creationist founder of the science of classifying organ isms, Carolus Linnaeus, gave names to many members of the cabbage family in the 1700s. Other well-known members include turnip and Chinese cabbages (forms of Brassica rapa), brown mustard (Brassica juncea) and radish (Raphanus sativus).We get canola oil from the seeds of one form of Brassica napus. Unlike most plant oils, canola oil has a useful amount of a type of oil similar to that found in fish such as salmon and sardines. Eating fish-oil has healthy effects, reducing the risk of heart disease and symptoms of arthritis, for example. 4 However, the health value of the canola form of the oil is unclear at this stage.5 We know another form of B. napus as swede, or rutabaga, which has an edible globe-shaped fleshy root.Thale cress (Arabidopsis thaliana) is a favourite plant for laboratory experiments. It was the first plant to have its DNA decoded.Farmers regard a number of this family as weeds. A weed is a plant growing where you do not want it to; like black mustard growing in a wheat crop. However, people around the world used this plant to produce mustard before the modern use of brown mustard for this purpose—the latter suits mechanical harvesting better.The presence of black mustard seeds as contaminants in wheat, for example, probably contributed to its distribution around the world in the dispersion following the Tower of Babel.Since today’s mustard is an annual herb, some have proposed that the mustard must have been a different plant. However, the Greek word used in the Gospels issinapi, from which we get Sinapsis, one of the genera in Brassicaceae, and known as white mustard. It germinates rapidly and grows very quickly into ‘the largest of garden plants’— to the extent that birds can ‘perch in its branches’.6 Table. Various forms of Brassica oleracea; their origins and characteristics.1 Name
Origin
Characteristics
Kale, collards
5th C BC, likely earlier
Closest to the original, or ‘wild’, cabbage. Open leaves, no head. Collards is similar, but has broader, non-frilly leaves cf. kale.
Cabbage
By the 1st C BC
Single large terminal head
Kohlrabi
In the area of Germany about Edible thickened stem the time of the cabbage.
Brussels sprouts
As the name implies, Belgium; by the 13th C.
Cauliflower
Southern France 15thCentury.
Broccoli
In Italy, as the name implies, Enlarged flower heads of deformed flowers, without covering soon after the cauliflower. leaves so that sunlight turns the flowers green due to chlorophyll production.
Tronchuda or Portuguese cabbage
Portugal?
Smaller, cabbage-like plants, loose (not compact) heads.
Savoy cabbage
Not known?
Hardy green, loose heads, very crinkly leaves.
by
in Elongated main stem with each axillary leaf bud developing into a mini-cabbage. the Enlarged clusters of deformed flowers, covered by leaves such that flowers do not turn green.
1. Grouping from Gómez-Campo, C. (Editor), Biology of Brassica Coenospecies, Elsevier Science B.V., p. 316, 1999, with the addition of kohlrabi. Other plant scientists divide B. oleracea into up to 12 varieties or subspecies, by splitting kale and collards, for example. One created kind? Certainly, the vegetables listed in the table have all come from an original cabbage type. The scientific name reflects this, all belonging to the same genus and species, Brassica oleracea. That cabbage type itself may have been part of an original broader kind, encompassing all members of the Brassica family.The degree of variation within this family could be partly due to a tendency to undergo spontaneous chromosomal rearrangements. Such rearrangements in animals usually result in death, but many plants can tolerate them. Many of the different Brassica species readily form natural hybrids when planted together, the pollen being transferred by insects or wind. Plant breeders have recreated some of the ‘species’ of Brassica by hybridizing other species (see diagram above).For example, planting cabbage together with turnip produces some seeds of rutabaga. Planting cabbage and black mustard together gives some seeds of Ethiopian mustard. Planting turnip and black mustard together produces some seeds of brown mustard. These examples show that we should not view modern day ‘species’ as the ‘kinds’. At the very least, these three species of (the genus) Brassica arose by hybridizing existing species. These hybrids involve the crossing of plants with different chromosome numbers (see Chromosome gymnastics below for details of how this happens).Now many plants can do this, but it is rare among animals. Animals seem to be a lot less tolerant of having extra chromosomes—in humans an extra chromosome 21 results in Down’s syndrome.Different numbers of chromosomes is a major barrier to hybridizing different kinds, especially animals. This is one way that the created kinds reproduced ‘after their kind’ .We can also see the unity of the brassicas in the way that people have used different species to produce mustard (B. nigra, B. juncea or B. carinata, B. rapa) or oil (B. rapa, B. napus) or various forms of cabbage (B. oleracea: cabbage, kale, etc.; B. rapa: Chinese cabbage and pak choi, etc.).
Dangers for farmers The ability of brassicas to hybridize means that scientists have to take great care to prevent genetically modified plants from pollinating weedy species of the family. If black mustard gained genes for herbicide resistance, from genetically modified canola, farmers would have greater problems controlling the weed.Even different genera within the family often produce a small number of hybrid seeds. Plant breeders crossed a radish (Raphanus) with a cabbage (Brassica), hoping to get a plant that produced an edible radish-like root with a cabbage top. They did create this hybrid, dubbedRaphanobrassica,7 but unfortunately it had a cabbage-like root and a radish-like top! Research often results in disappointments—a good scientist needs patience. Brassicas to brassicas—not evolution! Plant breeders have hybridized many other members of the Brassicaceae—different genera to Brassica.8(See box below.) This suggests that the whole family might derive from an original created brassica-kind. Note this is not evolution as it is not an uphill ‘bog slime to Brussels sprouts’ process, but a downhill ‘brassica to broccoli and Brussels sprouts’ process. For example Brussels sprouts, being much more selected and specialized than black mustard, is more prone to disease and is less ‘fit to survive’ (black mustard is a common weed). Note that all the brassicas are still brassicas—reproducing ‘after their kind’, just as they were programmed to do . Chromosome gymnastics Interestingly, many of these hybrids involve the addition of whole sets of chromosomes.1 Normally when plants reproduce, the pairs of chromosomes split to form the pollen and egg with half the full number of chromosomes each. Joining them together at fertilization restores the chromosome pairs. When chromosome numbers differ, the hybrids do not end up with proper pairs of chromosomes; one or more chromosomes do not have a pair. Such hybrids cannot then produce viable pollen or eggs because the unpaired chromosomes cannot split into two and so the hybrid cannot produce any seed. For example, cabbage has nine pairs of chromosomes and black mustard has eight pairs. The joining of a pollen grain from cabbage (9 single chromosomes) with an ovum from black mustard (8 chromosomes) results in 9+8, which means that we have one cabbage chromosome without a pair. However, occasionally plants produce a few pollen grains and eggs with the full set of chromosome pairs. Now when nine cabbagepairs join with eight black mustard pairs, we have 17 complete pairs, 34 in total. This hybrid can produce viable pollen and eggs, with 17 single chromosomes each, and we have Ethiopian mustard (diagram above). WHAT DO CREATIONISTS MEAN BY ‘CREATED KINDS ‘Parade of Mutants’—Pedigree Dogs and Artificial Selection by Lita Cosner When choosing a pet, many people opt for purebred pedigree dogs. Though they come at a price, it is easier to predict the eventual size, temperament, and needs of a purebred dog breed than for a ‘mutt’. But as a new BBC documentary, “Pedigree Dogs Exposed”,1 shows, the cost of breeding purebred dogs is genetic as well as economic.All dogs are descendants of a wolf-like ancestor. This ancestor had the genetic diversity that allowed people to breed dogs as different in size as the Chihuahua and the Great Dane. Other traits such as colour, temperament, and exercise needs are just as diverse among the breeds. This great variability is an example of just how much genetic variation is built into the various created animal kinds.2 Other breeds, as will be shown, are the result of downhill mutations. Genetic specialization Over many hundreds of years, humans have produced the various breeds by specifically selecting different traits to breed for; there are currently over 200 distinct varieties of dog, but all belong to the same species, and could theoretically breed with each other, though size difference between larger and smaller breeds renders some combinations unlikely.3Over time, breeding only for certain traits allows great predictability in what a dog’s offspring will look like—a Dalmatian mated with a Dalmatian will produce Dalmatian puppies, and so on. When this occurs regularly, the type of dog becomes an official breed. But this predictability comes at a genetic cost. The breeders have drastically reduced the amount of genetic information in the population of dogs—such as for other coat colours and lengths, or different sizes or temperaments. This sort of selection is done on purpose, but there are other traits that are inadvertently selected for as well.The bigger dog breeds become susceptible to hip dysplasia, others are plagued by heart problems. The King Charles Spaniel is prone to an extremely nasty condition, syringomyelia (SM), in which the skull is too small to house the brain. In the documentary, veterinary neurologist Clare Rusbridge described the condition: “A burning pain, a piston-type headache, abnormal sensations to even light touch, even items of clothing, a collar, for example, can induce discomfort for these animals.” She believes up to one-third of the breed could be affected by this condition.Overall, there are 500 genetic diseases which are known to occur in dogs. This is fewer than those documented in humans, but in dogs they occur at a much higher rate. The problem is that when the gene pool has been so depleted, it is not possible to avoid breeding diseased dogs, because that would be impoverishing the gene pool even more, and could lead to new diseases and disorders in a breed. Rusbridge acknowledged this to be true.4“Mutts”, or even crossbred dogs, have a much lower chance of having these diseases, because many are genetically recessive—a healthy copy of the gene will override a diseased gene. Because the diseases are also often breed-specific, even breeding two purebred dogs of different breeds will normally produce much healthier offspring than a purebred mating. The mutts will have lower instances of disease as well as being slightly longer-lived on average. A ‘Perfect’ Animal—Dog Shows
Early dog breeding mimicked natural selection, in that dogs were bred to work—the dogs that could herd sheep or cattle, or that could defend against intruders, etc., were the ones that were bred to produce the next generation. This process over time produced the modern breeds. However, with the advent of dog showing in the middle of the nineteenth century, the focus shifted away from function to aesthetics.Competitive dog-showing, in its pursuit of perfection, has driven the various breeds to ever more drastic extremes in body proportion and shape. The Dachshund’s legs have become much shorter over the last century, but their long back often gives them spinal problems, and they often suffer epilepsy and eye problems as well. The Bull Terrier’s head has been deformed, as has that of the Pit Bull—the documentary’s computer rendering of how breeders have contorted the skull shapes showed how drastically these breeds have changed in less than a century. Bulldogs have slower relative growth of the nasal bones, and this causes breathing difficulties and the need to be born by Caesarian section.The German Shepherd shows that these changes are carried out for purely cosmetic reasons. There are actually two varieties of German Shepherd: the working variety, which is often used in police forces and as guard dogs, and the show variety. The former looks very much like the original German Shepherd, but the show variety has a very different shape, with their back ends slouching. Orthopedic surgeon Graham Oliver described the gait of the show dogs as ataxic, lacking full coordination and control. This is the case for most of the show German Shepherds in the dog shows that were covered in the documentary. Extreme artificial selection In Britain, an already bad situation has been compounded in many ways by the Kennel Club’s breeding and show dog practices. First, the gene pool of the breeds is artificially restricted to the descendants of the originally-registered dogs from the mid-nineteenth century—in some cases, only a handful of dogs. This means that genetic diversity cannot be reintroduced into a breed, even if this means making the population healthier.Second, there is extreme selection for absolute perfection in appearance—breeders seek to produce dogs which adhere to the breed standard as closely as possible. This causes them to remove dogs that fall short of that standard, such as Dalmatians with non-standard markings, albino dogs, or Rhodesian Ridgebacks with no ridge, from the gene pool of the species, either by simply not mating them, or by culling them as puppies. This renders the overall population even more genetically impoverished.Third, extreme inbreeding has been the norm—it is common to mate littermates, or to mate a female dog with her “grandfather”, or “mother” to “son”. Evolutionary geneticist Steve Jones criticized the practice: “People are carrying out breeding which would be, first of all, it’s illegal in humans, and second of all, it’s absolutely insane from the point of view of the health of the animals.” Such close interbreeding is done to ‘fix’ certain desirable traits in the line, but it also makes the dogs more disease-prone. The Kennel Club website, www.thekennelclub.org.uk, currently states that “the Kennel Club will not accept an application to register … offspring of any mating between father and daughter, mother and son, and or brother and sister, save in exceptional circumstances, for scientifically-proven welfare reasons.” Even so, the average dog is much more inbred than any human is likely to be.Because there is no regulation against breeding dogs which are known to carry a genetic disease like syringomyelia, dogs with conditions like this, if they are popular studs, can go on to sire dozens of litters. This spreads the genetic disease throughout the breed. The Eugenics connection The Eugenics movement, founded by Darwin’s cousin Francis Galton, 5 held that the key to human improvement was in controlling who could reproduce with whom—the idea was to improve the race by eliminating undesirable traits, and in disallowing mixing between ‘races’. While we know today that the eugenicists’ ideas about purity make no scientific sense, the documentary argues that The Kennel Club is one of the few organizations that still operate under the fundamental assumptions of eugenics. Every dog registered with the Kennel Club has an ancestry that goes back to the original registered dogs—no new registrations are allowed, and any litters resulting from breeding with non-registered dogs or breeding between two registered dogs of different breeds cannot be registered.Because of the eugenicist principles in breeding, puppies that do not conform to the strict requirements of the breed standards are sometimes culled. This is particularly the case with Rhodesian Ridgebacks that lack ridges. While the Kennel Club, both through its spokespeople in the documentary and in the Ethics Code on its site, condemns the practice, the documentary contains statements from breeders saying that they routinely cull puppies without ridges. One even lamented the young veterinarians who refused to cull the healthy puppies! (It should be noted that although the Rhodesian Ridgeback Club code of ethics 6 prescribed the culling of ridgeless puppies before the documentary aired, the page has since been modified to prohibit such acts.) The ridge is actually a mild form of spina bifida, so a slightly diseased dog is actually preferred to the healthy animal in this breed. Genetic impoverishment All these factors together have made modern breeds very genetically impoverished—in some breeds, only 10% of the genetic variety that was in the breed 40 years ago has been passed down to the current descendants of the breed. For instance, the Pug breed in the UK, although it has 10,000 dogs, has the genetic information equivalent to that of 50 distinct individuals. In 2004, Dr Jeff Sampson wrote:“Unfortunately, the restrictive breeding patterns that have been developed as part and parcel of the purebred dog scene have not been without collateral damage to all breeds … Increasingly, inherited diseases are imposing a serious disease burden on many, if not all, breeds of dog.”The Kennel Club, to its credit, has responded to the issues raised by the documentary. It has banned close inbreeding, along with banning the practice of culling healthy puppies for breed points. They have also revised the breed standards to discourage the extreme exaggeration of features to the point that it affects the dog’s health. It also encourages its accredited breeders to make use of any health tests to screen for genetic diseases.
The dangers of inbreeding: These dogs inherited one stretch of DNA from each parent. We see the good genes and mutations. The dog on the left is the offspring of two distantly related parents, so the mother’s DNA has different defects from the fathers. Every one of her defective genes is masked by the backup copy from the father, and vice versa. But the unfortunate dog on the right is the offspring of close relatives; here, the father and mother have many of the same mutations. So in a number of spots, the dog inherited a pair of mutant genes.
How artificial selection depletes information. In the example on the right (simplified for illustration), a single gene pair is shown under each dog as coming in two possible forms. One form of the gene (S) carries instructions for large size, the other (s) for small size. In row 1, we start with medium-sized animals (Ss) interbreeding. Each of the offspring of these dogs can get one of either gene from each parent to make up their two genes. In row 2, we see that the resultant offspring can have either large (SS), medium (Ss) or small (ss) size. But let’s suppose that breeders want large dogs. They would select the largest dogs in the next generation to breed. Thus only the big dogs pass on genes to the next generation (line 3). So from then on, all the dogs will be a new, large variety. This is artificial selection, but natural selection would work on the same principle, if large dogs would do better in their environment. Note that: They are now adapted to their environment, in this case breeders who want big dogs. They are now more specialized than their ancestors on row 1. This has occurred through artificial selection, and could have occurred through natural selection. There have been no new genes added In fact, genes have been lost from the population—i.e. there has been a loss of genetic information, the opposite of what microbe-to-man evolution needs in order to be credible. Not only genes for smallness were lost, but any other genes these small dogs carried. They may have had genes for endurance, strong sense of smell, and other things, but they are lost from the population. Genes on their own are not selected; it’s the whole creature and all the genes they carried. Now the population is less able to adapt to future environmental changes—if small dogs became fashionable, or would perform better in some environment, they could not be bred from this population. They are also genetically impoverished since they lack the good genes that happened to be carried by the small dogs. Conclusion The current state of many of the dog breeds shows what happens when selection is taken too far. These dogs, far from being more perfect, ‘evolved’, animals, were described as “a parade of mutants” by one critic in the documentary. Because they are over-specialized, they are more prone to disease and shorter-lived than their ‘mongrel’ relatives. It is clear that both artificial and natural selection work by decreasingthe amount of genetic information in a population, which is the exact opposite of what evolution would require. The Australian dingo—a wolf in dog’s clothing
by David Catchpoole Here’s an animal that sure could use an ‘image make-over’ and public relations campaign.For many years, the dingo was best known as the wild dog of Australia—the largest carnivore on the Australian mainland—and for being the scourge of the sheep industry. A single dingo can maul up to 50 sheep in one night, killing far more than it needs for food. 1 (See box ‘Dingoes and sheep don’t mix’)No wonder many pastoralists would often mutter, ‘The only good dingo is a dead dingo.’Then, as if the dingo’s reputation was not already bad enough, in 1980, a baby named Azaria Chamberlain disappeared from a tent at Uluru (Ayers Rock) in Australia’s Northern Territory, amid cries that a wild dingo had taken the infant. (This was famously portrayed in the 1988 movie A Cry In the Dark, a.k.a. Evil Angels,starring Meryl Streep and Sam Neill). Then, in 2001, the dingo again made headlines when a nine-year-old boy was tragically attacked and killed by two dingoes on Queensland’s Fraser Island. His seven-year-old brother was also attacked, but survived.2,3 (See box ‘Would you trust a dingo?’.) Many pastoralists mutter, ‘The only good dingo is a dead dingo’ Yet, when European settlers first arrived in Australia, 4 they found that many of these ‘wild dogs’ were not truly ‘wild’, but instead lived, ate and hunted with their human keepers. Aboriginal people highly prized the dingo, also known as the ‘warrigal’, as a domestic animal. Dingoes were bed warmers, camp cleaners, hunting companions and guard dogs.5 Originally wild or domestic? The dingo is unmistakably canine—as was evident to the early European settlers, who eagerly crossed their imported herding dogs with the dingo in order to obtain breeds better adapted to the harsh Australian climate. The Australian cattle dog—a.k.a. the Queensland (blue) heeler—and the Australian kelpie are recognized dingo hybrid breeds. 6 Like all other canines (jackals, coyotes, and all domestic dogs), the dingo is closely related to the wolf—DNA studies point to all dogs being descended from some wolf-like ancestor.7–9 Aboriginal people highly prized the dingo, also known as the ‘warrigal’ But are dingoes domestic dogs gone wild, or wild animals of which, like wolves, some were domesticated? The dingo’s close resemblance to domestic dogs in Asia, its association with Aboriginal people and the fact that it was the only large placental mammal (except humans) on the continent led many to say its ancestors were domestic dogs. But others disagreed—hence the lack of agreement on a scientific name for the animal. For years the dingo was categorized as a subspecies of the domestic dog: Canis familiaris dingo. But in 1982, some taxonomists recommended it instead be classified as a subspecies of the wolf: Canis lupus dingo.10 Others decreed it a species in its own right: Canis dingo.11 Gone feral However, genetics seems to have resolved the debate, with a convincing demonstration that dingoes are descended from only a few domestic dogs introduced to Australia from South-east Asia, ‘as few as a single pregnant female’, and only turning feral later.12-14 But when? And who brought the dingo to Australia? Here’s where it gets hazy. According to evolutionary ‘dating’, the dingo would have arrived some time between 3,500 and 12,000 years ago. This is because evolutionists date the oldest dingo fossil to about 3,500 years ago—and dingoes never reached Tasmania, which is supposed to have become separated from the Australian mainland 12,000 years ago.So, given the widespread view that Aboriginal people have been in Australia for at least 40,000 years,15 the dingo could not have arrived with them.16 Therefore, the researchers conclude that the first dingo(es) must instead have been brought from the islands of South-east Asia by people of the Austronesian culture. 17 Later, Aboriginal people adopted the dingo as a companion animal. The young age timeframe A key event is the Flood around 4,500 years ago. Australia’s human and fauna population all arrived after that time. And when was Tasmania isolated from mainland Australia by rising sea levels? Most creation scientists researchers believe that the Ice Age (generated by warm seas and cold land masses in the aftermath of the Flood) ended roughly 3,800 years ago.18 That’s when water from melting ice poured into the oceans, inundating the ‘land bridges’ which had allowed animals such as the kangaroo to spread out beyond Asia all the way to Tasmania.With Tasmania isolated from mainland Australia, and the mainland itself cut off from Asia, the scene was set for the arrival of people by boat, raft or canoe. Dingo data Both male and female dingoes take part in raising their pups (litters average five). When the youngsters are 14 days old, the mother regurgitates food for them. By the time they are three weeks old, they will leave the den for short periods and are able to eat rabbit.A purebred dingo stands about 60 cm high and weighs about 15 kg—making it slightly smaller than a German shepherd. Although their coats are mainly sandy-yellow, they can also be black and tan in colour, depending on their habitat (golden yellow dingoes are found in sandy areas, while the darker ones are found in forests).The Australian Government was so concerned that dingoes might crossbreed with German shepherds that it banned the importation of that breed from 1920 until 1970.In the wild, dingoes often hunt for food alone, although they can hunt together with others when seeking large prey (e.g. kangaroos).They are different from most dogs in that they don’t bark, only howl; breed only once a year; and have no dew claws1 on their hind legs. Note In dogs, the ‘dew claw’ is the ‘toe’ hanging loosely attached to the skin, on the rear of the leg. (While the other toes touch the ground, the dew claw merely ‘brushes the dew’ from long grass.)Dingoes were then brought by either the first or subsequent waves of human immigrants. Tribal stories of the Larrakia people of the Northern Territory speak of their ancestors arriving by canoe and of bringing their canine companion with them.Dingoes are represented in rock-art sites,19 and feature
prominently in Aboriginal stories—e.g. the Pleiades constellation (or Seven Sisters) is depicted as a flock of kangaroos being chased by Orion’s two dingoes.1 The big picture We see: That ‘a single pregnant female’ could have populated an entire continent—a nice demonstration that from a limited number of animals, a healthy population can be sustained,. So, next time you hear someone claim that the world’s land animals and birds couldn’t possibly have come from male/female pairs, tell them about the Australian dingo!That the ready interbreeding of dingoes with other dogs (which continues apace today), 20 along with the uncertainty in assigning species names, points to the a single original dog ‘kind’. Rapid ‘speciation’ is not evolution, but just what we would expect from the young age account.21That a ‘wild’ animal can be tamed by man, reflecting the original created order—man to ‘rule over’ the animals.22 That the movement of dingoes and humans to this continent fits with the expected pattern of post-Flood during the last 4,500 years. Interestingly, lice that live on kangaroos have also been found on Indonesian dogs. Some researchers suggest, therefore, that the Australian dingo must have been taken back to Indonesia (carrying the kangaroo lice north from Australia).12 But this evidence could also be interpreted to mean that kangaroos once lived in Indonesia (en route to Australia), later becoming locally extinct as the large carnivores (e.g. Asian tigers) arrived there after the end of the Ice Age, when the land bridge to Australia was severed.That an animal classed as a ‘carnivore’ can actually survive without meat (see box ‘Dingoes and sheep don’t mix’) ! Would you trust a dingo? When Lindy Chamberlain, the wife of a pastor, told authorities in 1980 that a dingo had taken her baby Azaria from their tent at Ayers Rock (Uluru) in central Australia, the tragedy quickly became the focus of national attention. A young dingo, like this one seen here, is typical of those found around four wheel drive camping areas on Australia’s Fraser island. Media warnings suggest they should not be trusted.Sadly, the Australian public was more inclined to place faith in the (imagined good) character of a wild dog than in the word of a pastor’s wife. People wore T-shirts emblazoned with the slogan, The dingo is innocent.’Many were not surprised when Mrs Chamberlain was convicted of murder, on the basis of scientific experts’ seemingly irrefutable assessment of forensic evidence. This was despite eyewitness testimony that the baby was alive after the time at which the Crown Prosecutor claimed her mother had murdered her.Some years later —while Mrs Chamberlain was serving a life sentence in prison—the discovery of further evidence confirmed an aspect of her account. She was released from prison, and subsequently officially exonerated.Yet many Australians remained unconvinced, obviously unaware of (or deliberately ignoring) the counsel that ‘Every matter should be established on the testimony of two or more witnesses’ (2 Corinthians 13:1, Deuteronomy 19:15). In the minds of many, the original forensic findings held sway— despite official recognition that forensic scientists had misinterpreted the evidence. For example, the ‘bloodstains’ reported to have been identified inside the Chamberlains’ car were later found to be various chemicals sprayed during vehicle manufacture.It was not until the gruesome death in 2001 of a nine-year-old boy holidaying with his family on Fraser Island, just off Australia’s east coast, that many Australians finally began to consider it possible that a dingo did take the life of Azaria Chamberlain two decades earlier.Graphic eyewitness testimony from horrified family members of the young lad being chewed upon by the feeding canines shocked a nation. Consequently, government agencies now warn tourists that dingoes ‘are capable of killing people.’1 (Which is just as well, as a family recently scared away a dingo that had walked into their hotel room and was only 60 cm (2 ft) away from their baby lying on the bed. 2)Notice that these warnings are made on the basis of eyewitness testimony, not ‘forensic evidence’. There’s a moral there somewhere for when it comes to knowing how the world began. ‘Dingoes and sheep don’t mix’ As the First Fleet’s cargo of sheep, along with other livestock and goods necessary for establishing the colony, was offloaded onto the ‘Great South Land’ in 1788, could anyone have known that this fledgling nation’s economy would largely be built ‘on the sheep’s back’ (i.e. wool), and that an epic war against the dingo lay ahead?It didn’t take long for dingoes to learn that sheep were ‘easy pickings’ compared to their prey of native animals. When sheep farmers saw that dingoes would harass, bite and kill sheep in large numbers without actually eating them,1 they realized something had to be done. On stations (the Australian equivalent of ‘ranches’) that used to shear 100,000 sheep, dingoes inflicted such heavy losses that owners switched to cattle instead.Others mounted massive shooting, trapping and poisoning campaigns to try to control the problem of dingoes, which apparently multiplied substantially after sheep were introduced.2 Realizing that ‘dingoes and sheep don’t mix’,3 many woolgrowers constructed wire mesh fences to try to protect their sheep.Ultimately, the longest exclusion fence in the world—at 5,321 km (3,307 miles), longer even than the Great Wall of China—was built to try to protect the sheep industry in the entire south-east part of Australia. South of the Dog Fence, dingoes are declared vermin, attracting bounties of up to A$500 (US$380) per scalp.4–5 North of the fence, the dingo is regarded as a legitimate wildlife species and roams freely.South of this 1.8-metre-high (6 ft) protective fence, sheep can now graze in relative safety—alongside kangaroos, whose populations have exploded in the absence of a predator large enough to keep their numbers in check.6 But how could this be—don’t dingoes and wolves need to eat meat to live? Not so—today we see echoes that the dingo is able to not only eat fruit,8but also survive (for generation after generation) on a diet virtually devoid of meat.
In meat-poor south-east Asia, village dingoes predominantly make do with food scraps of cooked rice and vegetables, and fruit. A vegetarian wolf in our midst!9 Zenkey, zonkey, zebra donkey! by David Catchpoole For copyright reasons we are unable to display here the original images published in Creation magazine. Click on the image to enlarge.A zoo in Japan has proudly announced the birth of a zebra-donkey hybrid, describing it as a ‘zenkey’—a story excitedly picked up and relayed around the world by news media.1Actually, the offspring of a zebra stallion and donkey mare (jenny) is more usually defined as a ‘zonkey’ or ‘zedonk’, or even ‘zebrass’. But whether zenkey, zonkey or zedonk, the appearance of this little foal sure caused a stir at Nasu Safari Park (near Tokyo).‘As we keep herbivorous animals without separating them, the unbelievable can happen’, said Osamu Ishikawa, deputy head of the safari park. ‘A donkey was pregnant and everybody was expecting a donkey foal.’But the keepers were surprised when, in August 2003, a striped foal was born! Was it a donkey, or … ? It had a donkey’s ears, and the black cross mark on its withers2 is characteristic of donkey foals, but oh … those stripes! [Photo available in Creation magazine.]This is not the first time the arrival of a half-zebra foal from a non-zebra mare has surprised observers. A Shetland pony astonished its UK owners by giving birth to a half-zebra, half-horse foal—a ‘zorse’ or ‘zony’.3 The owners had earlier purchased the pony from a wildlife park, where, like the donkey mare at Nasu Safari Park, it had shared a field with a male zebra.This ability of donkeys, horses and zebras to breed with one another indicates they all descended from the same original created ‘kind’. Some people might argue that because hybrid offspring are often sterile, the horse, ass and zebra must therefore be separate created kinds. No-one would say that a human male/female couple unable to have children must therefore be separate species!Infertility in hybrid offspring can be due to rearrangements of chromosomes. Such (non-evolutionary) changes within the horse kind sees zebras today with 44 chromosomes, donkeys 62, and horses 64—so mules, the offspring of donkeys and horses, are often sterile as they end up with 63 chromosomes, which theoretically cannot divide into chromosome pairs.However, accounts of mules giving birth6 show they are not always infertile, and also demonstrate that the genetics in such cases is not yet fully understood. Occasional fertile hybrids such as these strengthen the case that all Equusspecies and their offspring (mules, hinnies, zorses, zonies, zedonks/zonkeys and whatever other inventive names we give them) are the same created kind— descendants of the ‘horses’ after the Flood around 4,500 years ago. Comparative cytogenetics and chromosomal rearrangements by Jean K. Lightner Figure 1. Chromosomal rearrangements involve the repair of double stranded breaks. They may be followed by changes in heterochromatin or centromeres, which suggest designed mechanisms are involved in the modifications. A better understanding of chromosomal rearrangements is necessary to developing both a more robust creation model and better reasoned apologetic arguments. Creationists accept that creatures can change over time, but a clearer understanding of the types of changes involved is necessary for a robust creation model. In creation apologetic arguments, many genetic changes are assumed to be “accidents” and the degenerative nature of these changes are commonly pointed out.Degenerative changes are expected.1 However, there is no reason why all genetic changes must be “accidents” or even degenerative. Related to this issue is a critical need for a reasonable estimate of genetic similarity between various kinds in the begining. For example, evolutionists often point to human-chimp similarities to support their model’s assumption of common ancestry. Creationists commonly respond that similarity can be from a common designer and then list genetic differences between humans and chimps. Which of these differences are because humans and chimps differently and which are from changes that have been acquired since then? If we point to differences that can reasonably be attributed to changes since Creation, our arguments will be weak and misleading. A proper use of evidential arguments depends on a robust young age model which requires a more detailed understanding of genetic changes that have occurred during history. Chromosomal rearrangements Comparative cytogentics has been important in establishing that many mammals have undergone significant chromosomal rearrangements during their history. A diversity of karyotypes may occur within a genus 3-5 or even a species.6-8 Given the considerable karyotypic diversity within some animal baramins (kinds), many of which were represented by only two animals on the Ark at the Flood, accounting for relatively rapid karyotype changes is a necessary part of the creation model. 9 All rearrangements involve the repair of double stranded breaks. Additionally, many rearrangements are associated with alteration of heterochromatin, silencing of a centromere, and/or the formation of a new centromere. 10 Because of the precision necessary to accomplish such changes while maintaining viability of the animal, it appears there are designed mechanisms in place to accomplish such rearrangements. Creating comparative genome maps
Comparative genome maps based on chromosome painting are useful and have been performed using more than eighty eutherian species. Yet chromosome painting has some significant limitations when comparing divergent species. There can be reduced hybridization efficiency of the probes from increased sequence divergence between these species (e.g. eutherians and marsupials). Comparative genome sequence analysis based on direct genome alignments has been used to overcome this problem. However, when evolutionists attempt to construct maps of a putative eutherian ancestor, the results are quite different between the two methods.A new in silico method of comparison, called electronic chromosome painting (E-painting), has been developed to overcome limitations of the previously mentioned techniques and reduce the complexity of whole genome sequence alignments. First, orthologous (corresponding) genes are identified using various means such as reciprocal BLAST best-hit searches.11 Comparative mapping of these orthologous genes allows for identification of regions with conserved gene order (syntenic segments). These can be used to infer details about past chromosomal rearrangements. E-painting makes comparisons easier because it ignores intergenic regions. This also means the method cannot be applied to telomeric, centromeric, or non-genic portions of the genome.A recent study using E-painting has revealed some interesting results.12 The genomes of six different mammalian species (human, mouse, rat, dog, cow, opossum) and the chicken were compared. The mammalian genomes have been sequenced with a 7-fold or greater coverage. The chicken genome was included because previous studies had shown it remarkably similar to eutherians in genome organization. Altogether 526 evolutionary breakpoints (EBs) were identified and mapped with a resolution around 120 kb. There was a positive correlation between EB frequency and gene density. Unlike some previous studies, these EBs did not significantly correspond to well known breakpoints in cancer and other disease related rearrangements. Primatespecific rearrangements occurred preferentially in regions containing segmental duplications and copy number variants. The authors concluded that EBs were not random and show evidence of reuse. Their reconstruction of a putative ancestral eutherian genome based on this technique showed remarkable similarity to previous ones based on comparative chromosome painting. Usefulness of comparisons across baramins At this point some readers may be questioning the relevance of the above study. After all, the results are interpreted within an evolutionary framework where all life is considered to be related. Further, these results may make some people feel uncomfortable. If rearrangements do occur, and evolutionists can show how a chimp genome can be rearranged to fit the order found in a human, doesn’t that lend credence to evolution?First, chromosomal rearrangements themselves do not change one type of animal into another. Carriers of balanced chromosomal rearrangements generally have a normal phenotype, although they may have reduced fertility.13 Additionally, intergenic regions, genes without orthologs, and the specific sequence of orthologous genes are not considered in these comparisons. One cannot turn a mouse into a man by simply aligning its genes in the same order as ours. Second, genomic comparisons, whether within or between baramins, can provide useful information on genomic structure. This information is essential for further building the creation model.The identification of syntenic segments shows that genes commonly appear in a specific order. If there is an advantage to a specific order of genes, then chromosomal rearrangements may provide a mechanism for new gene associations that are advantageous in a different environment. Intrabaraminic E-painting investigations would be useful in investigating this idea further. It would also be interesting to note any overlap between EBs and breakpoints required by the creation model.This study should also force creationists to address the issue of genome organization similarity between baramins at creation. Decades ago it was thought that karyotypes were fixed, at least at the species level. Understanding interbaraminic similarity at Creation will add robustness to the young age model and aid in interpreting interbaraminic investigations that exist in the literature. Baranomes, VIGEs and chromosomal rearrangements Peter Borger has suggested that baranomes, pluripotent uncommitted genomes, were created within the kinds.14 These genomes were designed to adapt rapidly, facilitated by the presence of variation inducing genetic elements (VIGEs). VIGEs include repetitive sequences and various mobile elements. 15 Interestingly, another recent study identified a significant enrichment of certain endogenous retrovirus (ERV) and long interspersed nucleotide (LINE1) elements in EBs in humans and marsupials.16 Studies of phylogenetic trajectory of orthologous chromosomes have shown many EBs are coincident with ancient centromere activity or the appearance of new centromeres.16 Thus the identified ERVs and LINE1s may be acting as VIGEs which play an important role in chromosomal rearrangements. Conclusion Creationists need a more complete understanding of the types of genomic changes that have occurred throughout history. This includes a more detailed understanding of chromosomal rearrangements. Identification of patterns of intrabaraminic chromosomal diversity should help clarify what types of rearrangements are consistent with the creation model. It may also help uncover underlying mechanisms for rearrangements and allow for reasonable inferences about the designed purpose of such rearrangements. This improved understanding of genomic structure and function may inform conjecture about interbaraminic similarities at Creation and aid in interpreting interbaraminic comparison that appear in secular literature. Epainting is a recently developed tool that can aid creation research in this area as genomic data continues to accumulate. ‘Fast mouse evolution’ claims Creationists should get excited. by Carl Wieland, CMI–Australia 26 May 2003 Researchers at Chicago’s University of Illinois were able to compare DNA from present-day mice with that of museum specimens (also captured around that city) dating as far back as 1855. 1 They focused on the DNA from the little powerhouses found in cells (mitochondria) that is easier to find in ancient specimens.They concluded that there had been a dramatic genetic shift, which they labelled ‘evolution,’ in that time. One of them, Oliver Pergams, was reported as saying that ‘mitochondrial DNA does evolve much more quickly than nuclear DNA, but the timeframe was thought to be over thousands of years.’ This was the first time anything like this speed had been observed in mammals, they said.So why do we say that creationists should get excited, not concerned? For one thing, as we’ve pointed out before, genetic changes as such are no big deal. Information reshuffling, shifts in gene frequency within populations, natural selection thinning out gene pools causing adaptation—all of these merely move around information that’s already there (see Muddy Waters).In fact, within a given population, selection removes information. That is, creatures that are not ‘fit’ for their environment are eliminated, thus their genetic information is not passed on to the next generation.The other main plank in neo-Darwinism, mutations (accidental hereditary copying mistakes in DNA), also do not cause an increase in genetic information. This applies even in those rare cases where the defect confers a survival advantage, so is ‘beneficial’ (see Beetle Bloopers and New eyes for blind fish?). So the changes we observe today, even though labeled ‘evolution,’ do not give even a whiff of a hint of how amebae could have blossomed progressively into aardvarks, avocado trees, and atomic physicists.It may surprise uninformed evolutionists, but rapid diversification is an implicit prediction of the young age model. This is because the kinds
had to diversify, even speciate, fairly quickly afterwards (dog kind into wolves, dingoes, coyotes, etc.; another kind into horses, zebras, asses, and so forth—see Speedy Species Surprise). Therefore, the faster such ‘downhill rearrangements’ can be seen to take place, the more neatly it fits the young age model.The reports of the Chicago mouse observations involve no suggestion that there has been any addition of new genetic information to the biosphere, such as ‘real’ evolution would have to involve (e.g., feather genes where previously there was no information for feathers anywhere in the world). Instead, we read of shifts in populations, mutations brought into the area, and so on.When it comes to mitochondrial DNA (mtDNA) there is an extra bonus. Changes in mtDNA are the basis for calculations concerning ‘mitochondrial Eve’ (or ‘African Eve’). This is a hypothetical woman (not meant by the labelers to be equated with the biblical Eve) who was living with other women at the time, but is the only one of those whose mtDNA (inherited mostly via one’s mother) was passed down to all humans living today. The calculations leading to the ‘dates’ she supposedly lived are based on assumptions about how fast mtDNA changes. These dates have ranged up to 250,000 years ago, although recent recalculations based on actual observed mutation rates in human mtDNA bring it down to around 6,000, interestingly—see A shrinking date for ‘Eve’.This observation of ‘astonishingly’ rapid mtDNA change in mice once more brings into serious question the assumptions on which all such ‘mitochondrial dates’ are based.The scientific community and the media insist on labeling all genetic change as ‘evolution,’ without taking into account the nature/direction of the change [see The evolution train’s acomin’]. This is why we have to make these same sorts of basic points again and again. The average citizen, bombarded in the media by talk of ‘observed evolution,’ can hardly be blamed for thinking that it is foolish to deny the idea of goo-to-you evolution—‘Why, look, they’re saying we can see it everywhere.’ But this is, as we have shown repeatedly, purely due to a dangerously careless equivocation on the meaning of the word ‘evolution.’ In fact, the changes we see not only have nothing to do with uphill evolution, they are readily and beautifully consistent with the notion of the young age model. Resurrecting a ‘prehistoric’ horse by Philip Bell Previous articles in Creation have dealt with depictions of so-called ‘prehistoric’ animals in cave paintings around the world.1 While we recognize many of these creatures because they are still alive today, others are apparently extinct. The ‘prehistoric’ label reinforces the idea that many types of creatures lived and died before mankind came on the scene. But starting with the real history , we can be sure that the beginning of earth history was also the beginning of human history, 2 so there has never been an era of prehistory in that sense! Breeding a Tarpan What would it be like to see a ‘prehistoric animal’ from a cave painting alive? Well a couple from central Oregon, USA, do that every day! Back in 1990, Lenette and Gordon Stroebel bought a herd of 20 Tarpan-style horses with a view to breeding horses that we typically associate with cave paintings. Other cave paintings of horses resemble Przewalski’s horses (see Przewalski’s horses below). The Stroebels call their ranch Genesis Equines and their herd of horses consists of genuine ‘look-alikes’ of wild Tarpans, which became extinct in the late 1800s. 3They carry on a breeding project begun in the 1960s by horse lover Harry Hegardt. His efforts to recreate a ‘prehistoric’ horse from wild American mustangs eventually resulted in something closely resembling the original Tarpan. The Stroebels have continued where he left off. Others have attempted to revive Tarpans, but their approach is rather different, and not without its critics. 4 Believing that Tarpan genes were in American wild mustangs,5 they captured mustangs that exhibited true Tarpan characteristics—including a more upright mane (seeTarpans and Tarpan-style horses below)—to breed from. So the Stroebels (like Hegardt before them) succeeded in ‘recreating’ Tarpan look-alikes without resorting to crossbreeding with Przewalski’s horses, as had been done previously.6 Artificial selection has limits The Stroebels are careful to point out that their Tarpan-style horses are very unlikely to be true genetic re-creations of the extinct Tarpan.7 They may have a very similar phenotype (physical appearance), but the information present in the original Tarpan genotype (genetic makeup) was lost due to extinction. By recombining genetic information that exists in other species of the horse kind, the breeders have apparently restored information for an upright mane, among other character traits. But, there are limits to our ability to ‘resurrect’ the genetic code of now extinct creatures. Notice that the Stroebels had to carefully select breeding mares and stallions that theyjudged were likely to possess the genetic information for desirable (Tarpan) characteristics. This selection process was nonrandom (obviously requiring the application of their knowledge of horse traits) and goal-orientated (offspring with the best mix of Tarpan traits were chosen for breeding the next generation). Although this has resulted in significant changes in features, it is quite unlike evolution. Evolution on the grand scale depends on the generation of totally new genetic information. However, no examples of this are known in living things, so it is a bankrupt theory.8 Not only that, evolution is meant to be a blind, purposeless process. This is quite unlike the intelligent, purposeful Tarpan-breeding program of the Stroebels! Artificial selection results in recombination of genetic information already present in various horses. Evolution must account for where all this information came from in the first place, but cannot do so. Rather, the biological and fossil evidence is fatal to all such theories.9 Cave art—more recent than you might think! Cave paintings of horses and other animals would have been created after the Babel dispersion. As small populations of human beings migrated from Babel across the continents, some sheltered/lived in caves and daubed the cave walls with images of horses and other animals they saw. Many of these creatures (including the classic ‘prehistoric’-looking horse) subsequently became extinct. In one way, the work of people like the Stroebels has served to bring this ‘cave painting era’ psychologically closer to the present.17 It also raises the question of whether these creatures and the paintings really date to many tens of thousands of years ago, as is popularly claimed.18 Przewalski’s horses The Russian explorer and naturalist Nikolai Przewalski (pronounced ‘shuh-vahl-skee1’) discovered these horses on the China/Mongolia border in 1879, although recent reports suggest other explorers had seen them many years earlier. 2,3 These are thought to be the only truly wild horses—that have not come from feral domestic horses. Now an endangered species, they are smaller than most domestic horses, with a stocky body, short legs, large head and a stiff, upright mane. They are dun-coloured (golden red) with a dark stripe along their backs but pale white undersides and muzzles—the coat grows lighter in winter.4Przewalski’s horse has 66 chromosomes, compared to 64 for the domestic horse, Equus caballus, seemingly supporting its separate species name, Equus przewalski.5 Nevertheless, recent DNA sequencing studies show that they are very similar to both modern horses and ancient ones (i.e. horses preserved in permafrost). 6Once thought to have covered the steppe (plains) regions of Europe and Asia, their numbers plummeted in the decades following their discovery. So a captive breeding program began at the turn of the last century. Thirteen of the horses from that conservation effort are the ancestors of about 1,200 Przewalski’s horses alive today, in zoos, private reserves and protected areas of Mongolia.3 Return to top.
Tarpans and Tarpan-style horses True Tarpans are extinct wild horses that seem to have lived principally in Eastern Europe, some on the steppes, some in scrubland and forested areas. Based on cave paintings, their range extended as far as Spain. 1 S.G. Gmelin, an 18th century explorer, first described the Tarpan. Its status as a distinct wild species was controversial until a University of Vienna paleontologist (O. Antonius) argued that it was a separate type and gave it the name Equus gmelini (sometimes called Equus przewalskii gmelini, that is, a subspecies of Przewalski’s horse).2As expanding agriculture destroyed their habitat, they began to die out, the last wild Tarpan dying in the Ukraine in 1879. 3,4 In the early 1900s, zoologist brothers Heinz and Lutz Heck, at the Munich Zoo (Tierpak Hellabrunn) in Germany, began a conservation effort to ‘re-create’ Tarpans. The Hecks selected representatives of several European pony breeds believed to be descendants of the original Tarpans for breeding. They bred mares from these breeds with Przewalski’s stallions and established a new ‘Tarpan’ breed at Munich in 1933. 1Modern Tarpantype horses are small, with a short back, thick neck, large head and a semi-erect mane. The coat is a mousy-grey colour (called ‘grulla’) with a dark stripe along the back.5 With the exception of the few dozen Tarpan-style horses bred at Genesis Equines, Oregon (see main article), there are about one hundred modern Tarpans worldwide, descended from a handful of horses from the Hecks’ breeding stock.1 Return to top.
HAS CREATIONIST RESEARCH FOUND ANY SPECIFIC EXAMPLES OF ANIMALS THAT ARE IN THE SAME BARAMIN A baraminology tutorial with examples from the grasses (Poaceae) by Todd Charles Wood Creationist biosystematics has existed since Frank Marsh coined the term baramin in 1941. Unfortunately, actual research into identifying baramins has been sparse. In the past decade, creation biologists have worked to develop a systematic methodology called baraminology. This paper presents a short tutorial on some of the techniques now in use to identify and study baramins. Readers are encouraged to use the information in this paper as a starting point for baraminology research of their own. The biological discipline of systematics was developed to discover natural groupings of organisms, such as species. A new systematic method, baraminology, specifically pertains to creationists. 1 Baraminology seeks not the species but the baramins, ‘created kinds’. In the broadest sense, baraminology has its roots in the writings of Frank Marsh. In 1941, Marsh coined the term baramin.2 However, Marsh’s ideas have begun to flourish in creationist research only in the past two decades. The German creationist group Wort und Wissen has produced a book of systematics papers, Typen des Lebens, in which they apply Marsh’s ideas to groups of plants and animals. 3 Fortunately for English-speaking creationists, Georg Huber is currently translating the book into English. Also during the 1990s, Kurt Wise applied baraminology to turtles, 4 and Ashley Robinson and David Cavanaugh produced a series of papers on baraminology in turtles, 5 primates6 and cats.7 I have been very active ‘behind the scenes’ in promoting baraminology to my fellow biologists. As part of the Baraminology Study Group (BSG), I helped organize two baraminology conferences at Liberty University and Cedarville University. 8,9Science in general and baraminology specifically require an appropriate philosophical basis in order to be successful in describing the world. At the baraminology conferences, so much emphasis has been placed on philosophy that researchers have not gained a practical understanding of the basic methodology and relevance of baraminology. Consequently, I find that many researchers do not know how to proceed. In this short work, I intend to demonstrate as clearly as possible how to undertake a baraminology study, using the grass family Poaceae as an example. It is my hope that once others see how straightforward it can be, they will be encouraged to try it themselves. What to look for Many creationists share the problematic desire to have a definition of baramin that makes it easy to recognize. Marsh’s heavy emphasis on hybridization as the defining feature of a baramin has certainly contributed to this bias. 10 An unambiguous criterion makes research easy, but even the hybridization criterion has serious limitations (e.g. it is inapplicable to asexual or fossil organisms). Because of these problems, baraminologists of today focus on approximating the limits of the baramin using a suite of characteristics. To assist in the approximation, we employ three terms that are derived from Marsh’s baramin:11The monobaramin is a group of organisms that share continuity, either genetic or phenetic. The apobaramin is a group of organisms that is discontinuous with everything else. Creationists have long used bats as an example of animals that are unrelated to any other mammals. 12,13 Since we don’t know how many kinds (baramins) of bats were created, baraminologists refer to the bats as an apobaramin.The holobaramin is roughly what we call the ‘created kind’. Technically, it simply combines the definitions of monobaramin andapobaramin. A holobaramin contains a complete set of organisms that share continuity among themselves but are discontinuous with all other organisms.Because these definitions are not mutually exclusive, they form the basis of the baraminological method of successive approximation. If you divide groups of organisms into smaller and smaller apobaramins by subtractive evidence, you will eventually come to a point when you can legitimately divide the group no longer. Similarly, if you add more and more species to a monobaramin by additive evidence, you will eventually come to a point when you cannot legitimately add any more species. Hopefully, the point at which the apobaramin can no longer be divided and the point at which the monobaramin can no longer be expanded is the same point: the holobaramin. At this point, the ‘membership list’ of the monobaramin and the apobaramin are exactly the same; therefore, this group probably represents the holobaramin.To do baraminology then, we evaluate two kinds of evidence: Additive and subtractive. Hybridization works well as additive evidence. The ability of members of two different species to produce offspring strongly indicates that they share basic genetic machinery and a common developmental path; however, failure to hybridize is not subtractive evidence. There are too many factors that can cause reproductive isolation that have nothing to do with baraminic status. Unfortunately, subtractive evidence proves difficult to identify in many cases. If subtractive evidence cannot be found, you should not consider your baraminology study a failure:You might be looking at only part of the holobaramin; that is, your focus is too narrow. Prior studies have shown that the holobaramin is larger than most genera.Baraminology constantly advances and refines its methodology. Discontinuity that is undetectable today may be detected tomorrow.Practically speaking, establishing a monobaramin is useful information. For example, in a baraminology study of a group of species in the sunflower family, I found good evidence for continuity (hybridization) but no discontinuity with other species of the same family.14 At the very least, my results indicated that the holobaramin is broader than this group. The grasses: choosing a subject Biologists reading this article probably have a research subject in mind, but for those who do not, guidance on choosing a group may be in order: First, realize that you will likely choose a group that no creationist has studied before. Because
precious little baraminological research has been published, you will probably not choose one of the few groups that have already been studied. Studying a group that has been the subject of previous baraminological analysis is also good. The essence of the baraminology method is approximation, so follow-up studies are always welcome.Also consider how your baraminology study might relate to others already published. Will you study a group similar to one already studied, or will you choose something completely new? For example, since the dogs, 15 bears16 and cats7 have all been the subjects of baraminology studies, another carnivore group, such as the weasels or raccoons, would complement the previous work well. On the other hand, studying a new group (e.g. invertebrates, microbes, or fungi) will blaze new trails in baraminology and expand our understanding of the general features of the baramin.Practical issues involved in gathering appropriate data for your group of interest should be considered as well. Will there be enough published data to do a good baraminology study, or are you willing and able to gather your own data? Re-interpreting published data is less laborious than gathering new data, but published datasets can be sparse. For example, I was surprised to find almost no published, family-level cladistic (tabulations of shared / non-shared characters) datasets on dinosaurs. On the other hand, baraminologists need to begin generating our own data rather than simply re-interpreting what someone else has already published. If you are able, I would strongly encourage collecting your own data.To illustrate the baraminological method, I have chosen the grasses. The grass family Poaceae is one of the most important families on the planet. People associate the word ‘grass’ with the stuff in their lawns, but grasses also include important cereal crops such as rice, maize, oats, wheat, barley, rye, and sugarcane. Half of the world’s population subsists on members of the grass family. The family itself consists of approximately 10,000 species in 5–6 subfamilies and 46 tribes.17In addition to its utilitarian importance, Poaceae makes an excellent baraminology subject for a number of other reasons. Because of the importance of the grasses, many botanists actively research Poaceae systematics. Scientists have formed a collaborative group to study the phylogeny of the grasses, and several genomics projects are underway for the more important cereal crops, mainly rice 18 and maize.19 A great deal of data from these research projects is publicly available. Third, a creationist study of the wheat tribe has been published in Typen des Lebens,20 allowing a comparison of results and conclusions. Finally, my own research work has focused on rice, so grass baraminology will help me understand other areas of my research interests.18,21 The baraminology method There really is no single ‘baraminology method’ but rather a collection of methods used in successive approximation. In the following sections, I present a few techniques that can be used by nearly any biologist. I begin with Scriptural considerations, then move to additive and subtractive evidences, and conclude with an interpretation of my results. At each step, I present general methods that can be applied to any group and illustrate their application in my study of the grasses. This paper is necessarily short, so some methods in baraminology have been omitted. Consult the literature for discussions of phylogenetic discontinuity detection,4 the use of mitochondrial DNA,5 and Analysis of Pattern.14,22 Additive evidence: hybridization Due to its popularity, I will present hybridization as the first scientific method. If you are working with a group that is not amenable to hybridization experiments, you might want to skip to the next section on Robinson and Cavanaugh’s baraminic distance method, which can be used on any group. 6 Space does not permit a full discussion of the theory of the hybridization criterion, so I recommend consulting other references 1,30 for more information.Unfortunately, good compilations of hybridization records are difficult to obtain. The Center for Origins Research and Education at Bryan College is developing a computerized database of hybrids to assist in baraminology studies. 31 Though the HybriDatabase (HDB) (www.bryancore.org/hdb) currently contains 2,711 hybrid records, I have gained valuable experience during the development of the HDB. I formulated an effective method of locating hybrid records.First, consult the HDB. Although incomplete, it contains valuable information. For each hybrid, a complete literature citation is available at the click of a mouse. Second, try computerized search engines. PubMed (www.ncbi.nlm.nih.gov) offers free searching of mostly biomedical and molecular biology journals. Ovid (www.ovid.com) and Biosis (www.biosis.org) offer database searching of a wider array of biology literature for a subscription fee. Many public university libraries provide Ovid or Biosis searching to their patrons. Third, consult published hybrid compilations. Excellent sources include Gray’s Bird Hybrids32 and Mammalian Hybrids,33 the periodicals Plant Breeding Abstracts and Animal Breeding Abstracts, and numerous specialty compilations (e.g. Orchid Hybrids34). You may consult online university library catalogues or Bookfinder (www.bookfinder.com) to locate hybridization compilations. I recommend the two Breeding Abstract periodicals as comprehensive sources of papers on hybrids. Creationists often recommend Gray’s books,30 but some of the hybrids listed are not accepted as valid.35 In all cases, try to locate the original paper to confirm the hybrid success. Finally, if you find a research article on a hybrid of interest, scan the references for other hybrid records.I found a plethora of grass hybridization information in Knobloch’s A Check List of Crosses in the Gramineae,29 Омдаленная Гибридиза Растений (Omdalennaya Gibridiza Rasteniĭ, The Remote Hybridization of Plants, a Russian book on distant plant hybridization),36 Watson and Dallwitz’s Grass Genera of the World17 and several papers in Plant Breeding Abstracts. I also used the AltaVista search engine (www.altavista.com) to locate other records of newer hybrids.37-40 Figure 1. Inter-tribal hybridizations in the grass family. Black squares indicate reports of inter-tribal hybrids. Grey squares indicate two tribes known to hybridize to the same third tribe. Open squares indicate no reported hybrids. Click here for larger viewTo display hybridization information, baraminologists frequently use a graphical tool called ahybridogram. To create a hybridogram, begin with graph paper or a computer spreadsheet. Next, list your species down the left side and across the top, forming a square matrix where each cell represents a potential interspecific hybrid (Figure 1). Record successful hybridizations by filling in the appropriate cells. The Wort und Wissen creationist group uses the hybridogram extensively in their book Typen des Lebens.3The 10,000 grass species make a challenging subject for a hybridogram. Because I cannot put all species on one hybridogram, I made several approximations for the hybridogram in Figure 1. I listed only the 46 grass tribes recognized by Watson and Dallwitz. 17 Next, I filled in cells indicating successful intergeneric hybridization within and between tribes. I also used Scherer’s secondary membership criterion, ‘Two individuals belong to the same basic type if they have hybridized with the same third organism.’ 30 By extension, I shaded cells grey where two tribes are known to cross with members of the same third tribe.In Figure 1, inter-tribal grass hybrids join only twelve of 46 tribes. At first glance, 12 out of 46 seems like poor baraminic evidence, but the 12 hybridizing tribes comprise approximately 7,220 species.
Consequently, I can assign 72% of the Poaceae to one hybridization-defined monobaramin. The remaining tribes that are not connected to the rest by hybridization are mostly small (half of the grass tribes contain less than 20 species). In his analysis of the duck baramin, Scherer noted the same pattern. Of the 13 tribes of the duck family Anatidae, hybridization connects eight. The remaining five represent tribes of 1–3 species each. Despite a lack of hybridization to connect the five small tribes with the remaining eight, Scherer still concludes that all Anatids (ducks, swans and geese) form a single basic type (or monobaramin; see below).41Even though most of the non-hybridizing grass tribes are small, two tribes—Bambuseae (the bamboos) and Stipeae (including ricegrasses)—are quite large. This illustrates a limitation of hybridization: Lack of recorded hybridization is ambiguous baraminic evidence. Although I could find no hybrids between bamboos or ricegrasses and other grass tribes, my search for grass hybrids was cursory. A more comprehensive search may reveal hybrids that join all grass tribes. At this stage, I would advance the conservative hypothesis that 72% of grass species in 12 tribes form a monobaramin. Additive and subtractive evidence: baraminic distance Since hybridization is only additive evidence, I need more data to determine the apobaraminic status of Poaceae. Fortunately, Robinson and Cavanaugh developed statistical methods for examining baraminic relationships without hybridization data.6 They base their methods on thebaraminic distance, a metric that summarizes systematic data. The information in systematic data sets is organized in columns where each column represents a particular characteristic, such as tooth shape or head size. The rows represent the taxa and the particular character states of those taxa. For example, oat flowers (character) are bisexual (character state 1) while maize flowers are unisexual (character state 2). For convenience, character states are almost always coded numerically (1=bisexual, 2=unisexual).Systematic data sets can be challenging to locate. Systematists are aware of this limitation and have begun to archive their datasets in internet databases. You can use two different databases to search for datasets for your group of interest, TreeBASE (www.herbaria.harvard.edu/treebase/index.html) and Cladestore (palaeo.gly.bris.ac.uk/cladestore/default.html). Since the databases are relatively new, they only have a few datasets. You may need to dig further to find a useful dataset for your group. Specialty journals likeCladistics, Systematic Biology, and organism-themed publications (like Herpetologica or Journal of Mammalogy) often publish data sets to accompany articles on systematics. Although many published data sets exist, they are not always baraminologically useful. They may exclude taxa deemed baraminologically significant, or they may simply have too few taxa or characters to give reliable baraminic information. As mentioned previously, we creationists should strive to generate our own datasets by direct observations of living or preserved specimens. Only in this way can we obtain the precise data needed. In the meantime, published datasets can offer useful information in many cases.Because of the importance of the grass family, the Grass Phylogeny Working Group (GPWG) placed a large data set online so that anyone with Internet access can analyze it (www.virtualherbarium.org/grass/gpwg/). The GPWG dataset contains 7,025 characters scored for 62 grass genera and four outgroup genera. The 62 grass genera represent 36 tribes. Most importantly, the large tribes excluded from the hybridization-defined monobaramin are present in this dataset; therefore, their baraminic status should be clearer. For more information about the GPWG dataset, consult their website. Figure 2. Baraminic distance correlation test. The R2statistic is the square of the correlation. In this example, the correlation coefficient (R) would be the square root of 0.9646, or 0.982 (A and C are probably closely related). Click here for larger view Space prohibits a detailed explanation of the baraminic distance method, but a short description of the metric is in order. The baraminic distance between two species is the percentage of characters in which the two species differ in their character states. The simplicity of this metric is very important, because most evolutionary phylogenetic methods make assumptions of common ancestry to calculate similarities and distances. With a percentage, no prior assumptions are made, so identifying both significant similarity between species (implying baraminic relationship) and significant differences between other species (implying discontinuity) should be straightforward. For a detailed discussion of the baraminic distance method, consult Robinson and Cavanaugh’s original paper.6I developed the computer program BDIST to perform the baraminic distance calculations on the large GPWG dataset. BDIST is available at the BSG website (www.bryancore.org/bsg), where you will also find detailed documentation on how to use the software. Because BDIST is written in Perl, it will run under any operating system. BDIST first sorts through the characters and calculates character relevance. Relevance is the percentage of taxa for which a character state is known, and BDIST includes relevance figures for each character in its output file. Robinson and Cavanaugh recommend that character with relevance less than 95% should be eliminated from baraminic distance calculations.6 After calculating relevances for every character, BDIST eliminates characters that have less than 95% relevance. Finally BDIST calculates baraminic distances from the remaining characters and outputs the distance matrix to a plain text file, which can be cut-and-pasted into a spreadsheet or other mathematical software for further analysis. BDIST eliminated 4,906 characters from the GPWG dataset because of low relevance. The remaining 2,119 characters were used for the baraminic distance calculations. Baraminic distances can be analyzed in a variety of ways. I will illustrate the correlation test, one application of baraminic distances.Robinson and Cavanaugh recommend calculating the Pearson product-moment correlation between all possible pairs of taxa. 6 If the distance between taxa A and B is similar to the distance between taxa C and B, and if this similarity of distances holds for taxa D, E, and F, then A and C are probably closely-related (Figure 2). By calculating the correlation of baraminic distances for taxa A and C, we can test whether the distances are similar enough to be statistically significant. Robinson and Cavanaugh suggest that significant positive correlation indicates that the two species are members of the same monobaramin and significant negative correlation indicates that the two species are discontinuous (members of different apobaramins). You should consult their paper for more information on baraminic distance correlation tests. 6 I did not implement a correlation test in BDIST because these tests are more efficiently done by any number of statistical software packages. You can even use a simple spreadsheet, like Excel or QuattroPro. I use the S+ package, available from Insightful Corporation (www.insightful .com).
Click here for larger view Figure 3. Summary of baraminic distance correlation tests for (A) molecular and morphological data and (B) morphological data only. Filled squares indicate significant positive correlation. Circles indicate significant negative correlation. Black horizontal and vertical lines separate tribes. Labels for columns are same as for rows. Click here for larger view In the GPWG dataset, the 62 grass genera yield 1,891 unique species pairs for which baraminic distances and correlations can be calculated. Using the baraminic distances from BDIST, I found that 98% of the species pairs had significant positive correlation. Curiously, I also found that 53% of the 248 species pairs between the grasses and outgroup species also displayed significant positive correlation, and only 6% had significant negative correlation (Figure 3A). Based on Robinson and Cavanaugh’s original discussion of the distance correlation test, I did not expect a high frequency of significant positive correlation between the grass and outgroup species. These results suggest that the non-Poaceae genera included in the dataset might also be members of a monobaramin together with the grasses. If correct, this result would be very surprising, since grasses are widely acknowledged to form a well-defined group.To re-evaluate these results, I removed molecular characters from the GPWG dataset and re-calculated the baraminic distances. Systematic data derived from DNA sequence comparisons may not be very useful for baraminology because so many DNA/DNA comparisons are done on genes that are very similar between many species. Consequently, species appear much more similar than they would if you examined their morphology, thus the use of DNA sequence information biases the systematic results towards similarity that is purely genetic.Of the 7,025 characters in the GPWG dataset, only 53 are morphological. The remaining 6,972 characters come from DNA analyses. After eliminating the DNA characters, the baraminic distance calculations were very different. With the morphology-only dataset, 21 characters were eliminated due to low relevance, and 32 characters were used to calculate baraminic distance. From the Pearson correlation analysis, I found that nearly every one of the grasses shares significant positive correlation with all the other grasses but significant negative correlation with the outgroup genera. Two notable exceptions are the grass generaStreptochaeta and Anomochloa (possibly Pharus as well), both of which have significant negative correlation with most other grasses but significant positive correlation with the four outgroup genera and with each other (Figure 3B).From the morphological analysis, I draw several conclusions. First, the Poaceae (excluding tribes Streptochaeteae and Anomochloeae) form a coherent monobaramin and apobaramin, suggesting that the majority of grass species are members of a single holobaramin. Second, negative baraminic distance correlation indicates that tribes Anomochloeae (1 sp.) and Streptochaeteae (2 spp.) are not members of the grass holobaramin. The position of Pharus and the Phareae (14 spp.) is presently unclear. Third and perhaps most important for the advancement of baraminology methods, heavy reliance on molecular sequence data biases baraminic analysis towards too much similarity. I strongly suggest that researchers do not rely too heavily on sequence similarity for determining baraminic relationships. Conclusions The final step of any baraminology paper is interpreting the analyses and presenting your conclusions. The considerations that went into selecting the group to study should now come back into play. You might consider the geographical distribution of the modern members of your baramin and how it relates to their Flood survival mode. You might also discuss possible diversification theories for an exceptionally large baramin. Finally, compare your results with the results of other creationist researchers. If you are dealing with a completely new group, discuss the general characteristics of your baramin, such as the number of species, the fossil record or how it compares with conventional taxonomic catagories (such as family, order or tribe).Interpreting the grass holobaramin is a monumental task, so I will limit my comments to a few points. Junker previously assigned basic type status to the tribe Triticeae. 20 Because basic type biology considers only hybridization and lacks a method of identifying discontinuities, a basic type is a monobaramin. Junker found no records of hybridization between species in the Triticeae and other tribes of the grasses. Since I found several intertribal hybridization records involving the Triticeae using the journal Plant Breeding Abstracts, I would broaden Junker’s basic type to include all the grasses except Anomochloeae and Streptochaeteae. In a report on the grass species Ring Muhly, the authors speculate that the boundaries of the ‘created kind’ lie within the genus Muhlenbergia.42 My results demonstrate that the holobaraminic boundaries of the grasses (including Ring Muhly) are much broader than any single genus.Lastly, I want to address the question of the diversification of the grass holobaramin, the largest holobaramin identified to date. With 10,000 species, the grass holobaramin easily outnumbers even the biggest mammalian baramins. For example, a recent study places 150 fossil horse species into a single monobaramin.22 The great number of grass species is unlikely to be caused by excessive ‘splitting’ by over-zealous systematists. Instead, the large number of tribes indicates that the diversity is real. The fact that grasses are plants gives a possible clue to the origin of the extreme diversity. It is therefore possible that some of the grass diversity dates from before the Flood, possibly even from created diversity from the begining.Pre-Flood grass diversification would help to make sense of the early grass references. Some cereal grains might have arisen after the Flood. Archaeological evidence of a post-Flood domestication of barley (Hordeum vulgare) could be interpreted as merely diversification within theHordeum genus.43 To clarify the issue of grass diversification, we will need to evaluate the post-Flood fossil record of the grasses.With the Internet and the BDIST software, nearly any student or professional in biology can do a baraminological analysis of their favorite creatures. As we accumulate more baraminological studies, we will get a clearer picture of what baramins look like and how to identify them better. I pray that this article will help researchers become more familiar with baraminology and that biologists reading this article will seriously consider joining this exciting work.
Identification of species within the sheep-goat kind (Tsoan monobaramin) by Jean K. Lightner Animals were created according to their kind with the ability to reproduce. Since variations in climate exist, it follows that animals will have the ability to adapt so this could be accomplished. Hybrid dataindicate that sheep (Ovis aries) and goats (Capra hircus) belong to a monobaramin (or basic type, a group belonging to the same kind). Further hybrid data indicate that other species in the genera Ovis, Capra,Ammotragus, Hemitragus and probably Rupicapra fall within this monobaramin as well. An alleged hybrid between sheep and European roe deer suggests that this monobaramin may actually include several ruminant families; however, a better documented example is desirable before reaching strong conclusions. The variation seen within this monobaramin, at least some of which are adaptive changes, indicate that mutation and chromosomal rearrangement have contributed to the development of currently existing species. Figure 1. Variation within the Tsoan monobaramin. A) This Dall’s sheep (Ovis dalli) exhibits tightly curved horns that curl at the sides of the head typical of Ovis species. B) This alpine ibex (Capra ibex) exhibits horns with a more gentle curve that grow up away from the head. C) The large male Barbary sheep (Ammotragus lervia) has horns with a different curvature as well as a mane (shaggy hair under the neck) and chaps (shaggy hair down the front of the legs). D) This Swaledale, a breed of domestic sheep (Ovis aries), exhibits the heavy growth of underfur known as wool that is typical of most domestic sheep breeds. Many creationists believe that after the Flood there were dramatic changes in climate. This was also a time of rapid speciation as animals spread out over the earth and adapted to new environments. Although animals reproduce within their own kind, characteristics of different populations eventually became divergent enough that they were given different names.4 This concept that creatures were designed according to their kind and with the ability to adapt 5 is in contrast with the molecules-to-man evolutionary idea that all organisms had a single common ancestor and adaptation is the result of chance events.The study of created kinds is called baraminology (from Hebrew bara: create, min: kind). One tool used to determine if two different species belong in a monobaramin (a group belonging to single kind) is to see if they can hybridize with each other or if they can both hybridize with a third species. 6 While such interspecific hybridization* clearly identifies two species as belonging to the same baramin, the absence of such hybridization data is not in itself conclusive. 7 There are a number of differences that can naturally arise between populations that may result in hybridization failure. 8 This study will examine data relating to the baraminic classification of sheep and goats and some of the variation that exists within this monobaramin. Hybridization data Domestic sheep (Ovis aries) and goats (Capra hircus) have been closely associated throughout history. Even today there are many places where they are kept together. Although it is not uncommon to see them mating under these circumstances, live offspring from such a mating are extremely rare. Several hybrids have been confirmed using chromosomal analysis to demonstrate that they had 57 chromosomes (2n = 57) which is intermediate between goats (2n = 60) and domestic sheep (2n = 54) (table 1).12 One study reported a 96% fertilization rate when goats were mated (a buck* with a doe*), and a 90% fertilization rate when sheep were mated (a ram* with a ewe*). However, when rams were crossed with does there was a 72% fertilization rate and the embryos died at 5 to 10 weeks. When bucks were crossed with ewes there was a 0% fertilization rate.13 Thus, the few well documented live hybrids confirm that sheep and goats do both belong to the Tsoan monobaramin. The study cited illustrates how differences have developed within this baramin that most commonly result in a poor fertilization rate and/or a high spontaneous abortion rate in matings between sheep and goats.Within the genus Ovis hybridization occurs quite readily. In fact this is one reason why the species listed in this genus vary depending on the source.14 The mouflon, wild sheep previously classified as O. musimon or O. orientalis, are now often classified as O. aries along with domestic sheep.15 Fertile offspring have been observed from crosses between domestic sheep and the mouflon. Fertile offspring have also been documented between these sheep and Argali sheep (O. ammon, 2n = 56), the Urial (O. vignei, 2n = 58), and bighorn sheep (O. canadensis, 2n = 54).16 It is worth noting that within this genus, differences in chromosome number do not pose a barrier to hybridization.Attempts to artificially cross domestic sheep with the chamois (Rupicapra rupicapra, 2n = 58) resulted in hybrid embryos which died. Similar attempts to cross sheep with domestic cattle (Bos taurus, 2n = 60) resulted in 11 out of 51 sheep eggs cleaving when fresh bull semen was introduced. However, fertilization and cleavage are not sufficient to classify two organisms within the same monobaramin. It is necessary for embryogenesis to continue past the initial maternal phase and for there to be coordinated expression of both paternal and maternal genes.17 Finally, there has been an alleged hybridization between domestic sheep and European roe deer (Capreolus capreolus, 2n = 70).16 European roe deer belong to the family Cervidae, which are characterized by their bony, branched antlers that are shed annually. All other animals previously mentioned in this section belong to the family Bovidae, which are characterized by unbranched horns consisting of a bony core, covered by a keratinized sheath and are not shed.18Domestic goats can hybridize with the Alpine ibex (C. ibex), Nubian ibex (C. nubiana), Siberian ibex (C. sibirica),
Markhor (C. falconeri), West Caucasian or Kurban tur (C. caucasica), East Caucasian or Daghestan tur (C. cylindricornis), and Barbary sheep (Ammotragus lervia, 2n = 58). Many of the hybrids within the genus Capra are fertile. Crosses between domestic goats and the Himalayan tahr (Hemitragus jemlahicus,2n = 48) have resulted in abortions, but no live young. Hybrids between goat and the chamois (Rupicapra rupicapra) have been reported, but a further attempt to produce a hybrid failed.16
Table 1. A hybridogram for sheep and goat hybrids showing all members of the subfamily Caprinae (family Bovidae) and one member of subfamily Odocoileinae (family Cervidae). V = viable hybrid(s); VF = viable, fertile hybrid(s); A = abortion; E = early embyronic death; ? = hybrid of questionable reliability reported; * = the same species. Inferences from other data Within the genus Ovis there are two species for which no clear hybrid data were found. These are Dall’s sheep (O. dalli, 2n = 54) and the snow sheep or Siberian bighorn (O. nivicola, 2n = 52). Both these species are considered to be very closely related to bighorn sheep (O. canadaensis).19 They are mountain sheep which are similar in morphology, habitat, and chromosome number.Within the genus Capra there are also two species for which no clear hybrid data were found. These are the Spanish ibex (C. pyrenaica) and the Eithiopian or Walia ibex (C. walie). These species are closely related to the other ibexes which were all classified as subspecies of C. ibex at one time. As with sheep, there is still controversy over definitions of species and subspecies. The Walia ibex is often included with the Nubian ibex. 20 Since the few species that lack hybrid data are considered so closely related to a species linked by hybrid data, it seems reasonable to conclude that all species of Ovis and Capra fall within the Tsoan monobaramin.Additionally, animals within the same genus would be expected to be more closely related to each other than animals from different genera. Thus, even if there had been no further information on the Ovis or Capra species that lacked hybrid data, it would still seem reasonable to assume that they belong within the monobaramin. When hybrid data shows animals from different genera to be monobaraminic, all animals within the two genera would be expected to be in the monobaramin. Variation within Tsoan Once animals have been identified as belonging to the same monobaramin, variation within the monobaramin can be examined for patterns. There is tremendous variation found within Tsoan (figure 1). For example, horns in sheep generally curl at the side of the head as they grow. Normally there is only one pair of horns, but Jacob sheep (a domestic breed) may have two or even three pairs. Those with four horns have two vertical centre horns that may be up to several feet long (much like goat horns), and two lateral horns which curl down along the side of the head. 21 Goat horns tend to grow upward, and somewhat outward and backward. In some Capra species the horns of adult males 22 form a very large semi-circle as viewed from the side.23 However, the Markhor has tightly curled corkscrew-like horns, 24 while the Daghestan tur has horns which are a rounded triangle shape on cross-section that make an open curl over the head (much like a lyre as viewed from the front of the animal when its head is slightly lowered). Horns in males are usually much larger than those in females.25 Some breeds of domestic sheep are naturally polled*. Thus, there is considerable variation in the size, shape, and number of horns within this monobaramin.The pelage or hair coat of Tsoan is also highly variable. Typically mammals have guard hairs which overlay and protect the underfur. The underfur may be composed of wool, fur and/or velli.26 Domestic sheep are best known for having well developed wool, a growth of underfur that is not shed, and very few guard hairs. This wool ranges from the fine (narrow diameter) wool of the Merino to the longer, coarser wool of the Jacob sheep. Some domestic sheep and most domestic goats have no obvious wool. The length of hair may also vary according to the species, gender and body region of the animal. Bucks often have a beard. Rams in some species have a mane, a fringe of long hair under the throat that runs down to the brisket. In Barbary sheep, the mane divides at the brisket and continues down the legs as chaps.27 In addition to variation in type, diameter and length of hair fibres, there is variation in colour,
colour pattern and density of the hair coat.There is considerable homology among the sheep, goat, and cattle genomes. Both goats and cattle have 60 chromosomes consisting of 29 pairs of acrocentric* autosomes*. Domestic sheep have 3 less chromosome pairs relative to goats and cattle, including 23 pairs of acrocentric and 3 pairs of metacentric * autosomes. Sheep chromosome (OAR) 1 is considered equivalent to goat (CHI) and cattle (BTA) chromosomes 1 and 3. OAR 2 corresponds to CHI/BTA 2 and 8, and OAR 3 to CHI/BTA 5 and 11. These differences are attributed to three Robertsonian translocations.28 A Robertsonian translocation occurs when the long arms of two nonhomologous acrocentric chromosomes combine to form a single chromosome.29 This is a relatively common type of chromosomal change which is nonrandom and appears to have distinct mechanisms that drive the change.30 Conclusions All species in the genera Ovis, Capra and Ammotragus are clearly within Tsoan. Hemitragus is also included because identifiable abortions indicate a significant amount of embryonic development has taken place. Rupicapra is probably included; it appears the major reason for doubting the authenticity of the alleged hybrids with goats was because an additional attempt failed. However, failure is the most common result when goats are crossed with sheep. It is unclear how far the embryos developed when Rupicapra was crossed with sheep. A better documented hybrid would remove the uncertainty. These five genera all fall within Caprinae, a subfamily within the family Bovidae.Although similarities between Tsoan and cattle have been noted, there is currently insufficient hybrid data to place cattle within Tsoan. Cattle belong to Bovinae, a separate subfamily within the family Bovidae. Yet, the alleged hybrid between sheep and European roe deer suggests Tsoan may include not only the family Bovidae, but also the family Cervidae. If this is verified, then Tsoan would likely include Antilocapridae, a family consisting of only the pronghorn (Antilocapra americana) which is intermediate between Cervidae (consisting of over 40 species) and Bovidae (consisting of nearly 140 species). Other ruminant families may be included as well. A better documented Bovidae/Cervidae or other interfamilial hybrid would be tremendously helpful in ascertaining the true baraminological relationship of these families. Since well documented hybrid data is lacking at this time, cattle hybrids will be examined separately in a subsequent paper.The variation present within the Tsoan monobaramin is from both the variety created in this baramin initially and changes that have been acquired throughout history. Some characteristics naturally change as a result of environmental changes, for example growth of a heavier winter coat and moulting. However, the variation within the monobaramin far exceeds this. Mutations, any acquired change within the genome, have historically been considered to be due to random copying errors. As such, they do not significantly add information and often result in disease. However, within the last several decades evidence has been found that some changes within bacterial genomes are directed. Such mutations can be initiated by environmental signals which allow changes in a part of the genome that is likely to help the organism adapt. 31 Much of the variation in pelage could be attributable to similar changes.32 For example, growth in any tissue is controlled by multiple factors; some work to stimulate growth, others to inhibit growth. If directed changes occurred as a result of environmental changes from a post-Flood ice age, mutations may have occurred that increased factors stimulating hair growth and density 33,34 or decreased factors inhibiting it.34 This would easily explain how animals which had no need for heavy coats prior to the Fall were able to acquire them when the need arose. Glossary Acrocentric: a chromosome with the centromere very near one end Autosomes: chromosomes that are not sex (X or Y) chromosomes Buck: an adult male goat Doe: an adult female goat Ewe: an adult female sheep Interspecific forming a hybrid by crossing two different species hybridization: Metacentric: a chromosome with the centromere near the middle Polled: an animal without horns Ram: an adult male sheep Tsoan: an anglicized form of the Hebrew word ( ןאצtsō’n) which is used 275 times in the Hebrew Old Testament to refer to sheep and goats Identification of species within the cattle monobaramin (kind) by Jean K. Lightner Baraminology, the study of created kinds, uses hybrid data to determine what species can hybridize and thus belong to the same monobaramin or basic type. Hybrid data indicate that domestic cattle (Bos taurus) are in a monobaramin with all other species of the genera Bos, Bison, and probably Bubalus. These species are all within the family Bovidae and subfamily Bovinae. Additionally, there are alleged hybrids between cattle and the musk ox (subfamily Caprinae) and cattle and moose (family Cervidae). More data would be helpful to determine the full extent of this baramin. Variation within the genus Bos shows different individuals adapted to extremes in environmental conditions, from the yak which can tolerate extremely cold environments and high altitudes, to the zebu which can tolerate very hot conditions and is more resistant to parasites.
The yak (Bos grunniens) is a member of the cattle monobaramin that is well adapted to cold environments and high altitudes.The study of created kinds is sometimes called baraminology (from Hebrew בראbara’—create, מיןmîn—kind). One technique used to determine if two species belong to the same baramin (created kind) is to demonstrate that they can hybridize with each other or they can both hybridize with a third species. Species that are linked by hybrid data are termed a monobaramin (or basic type 2). However, lack of hybridization is inconclusive since differences can arise during speciation which prevent hybridization.3In vitro (done in a laboratory, outside the animal) fertilization is a well developed technology for a number of animal species, including cattle. This has been a useful tool in attempts to form hybrids. Mere fertilization is not considered sufficient evidence of hybridization. The embryo must develop to the point where there is a coordinated
expression of embryonic genes.2 There is no strong consensus within creationist circles of exactly when this occurs.4Creationists recognize that intrabaraminic (within kind) changes may occur over time. Such changes may be help animals survive in particular environments. Other changes are recognized as being degenerative and the result of the Curse.5 However, the evolutionary notion that all living things have a common ancestor and throughout history have gained new organs and complex, well-integrated biochemical pathways is rejected. The historical accounts and the pattern of changes seen in the real world are in direct conflict with molecules-to-man evolutionary ideas.In my previous paper, 6 I identified a number of species within the Tsoan (sheep-goat) monobaramin. There was insufficient hybrid data to conclude that cattle (members of the genus Bos) belong to the Tsoan monobaramin, so they are examined separately in this paper. Hybridization data Within the genus Bos, hybrids form quite readily. Domestic cattle of European descent (Bos taurus, 2n = 60) hybridize with Indian cattle, or the zebu, (B. indicus, 2n = 60) to form fertile offspring so that the latter is sometimes considered a subspecies of the former (i.e. B. taurus indicus). The yak (B. grunniens, 2n = 60) will hybridize with the above species as well; the resulting females are fertile, but the males are sterile. The guar (B. frontalis, 2n = 58) and the banteng (B. javanicus, 2n = 60) have formed a three way cross with domestic cattle. Other hybrid combinations have been formed as well. With the exception of the first cross mentioned, hybrid males are nearly always sterile while the females are fertile.22 This is in spite of the fact that, except for the guar, they all have the same number of chromosomes.Both the American bison (Bison bison, 2n = 60) and the European bison, or wisent, (Bison bonasus, 2n = 60) have hybridized with various Bos species. Again there is the pattern of fertile females and usually sterile males in the hybrids. Water buffalo (Bubalus bubalis, 2n = 48 or 50) have been observed mating with the gaur and zebu cattle, but no progeny have been observed. Hybrids between water buffalo and domestic cattle (B. taurus) have been reported in China, but they are generally regarded as doubtful because other attempts have repeatedly failed.22 In vitro fertilization has resulted in hybrid embryos that developed until about the 8-cell stage, but then failed and did not express mRNA transcripts found in control buffalo embryos.23 However, at least one study was able to bring hybrid embryos to the advanced blastocyst stage, with cattle oocytes fertilized by buffalo sperm resulting in a significantly larger percentage of blastocysts than the reverse cross.24A report of hybrids between zebu cattle and the eland (Taurotragus oryx, 2n = 31 in males, 32 in females) exists. Further attempts to cross the eland with domestic cattle have failed, so these ‘hybrids’ are considered by some to be eland bulls.22 All hybrids considered thus far are within the subfamily Bovinae, however there are also alleged hybrids between domestic cattle and species outside this subfamily. One is with the muskox (Ovibos moschatus, 2n = 48) which belongs to the subfamily Caprinae. Sheep also belong to the subfamily Caprinae. Attempts to artificially cross sheep with cattle have resulted in fertilization and development to the 8-cell stage, but the embryos failed to transition from maternal to embryonic control as indicated by a lack of RNA synthesis. 25In vitro fertilization of cattle oocytes with sperm from the endangered scimitar-horned oryx (Oryx dammah, 2n = 56–58) from the subfamily Hippotraginae has been reported. However, the embryos were only reported to have reached the 5-to 8-cell stage. 26 The purpose of the study was to evaluate the quality of oryx semen rather than investigate the viability of the hybrid embryos. Until such embryos are documented to undergo further development, this cross should not be considered a hybrid because a coordinated expression of embryonic genes has not been demonstrated.Cattle, sheep and the oryx are members of the family Bovidae. Mating has been reported to occur between cattle and a species of deer (Cervus elaphus, 2n = 68), a member of the family Cervidae. There has also been an alleged hybrid between a cow and a moose (Alces alces, 2n = 68 or 70) which is also in the family Cervidae. Natural variety within the kind Cattle vary in body build (e.g. beef breeds vs dairy breeds), size, coloration, and horn morphology (e.g. longhorn vs shorthorn vs polled (no horn)). The yak has long, coarse hair and a dense, woolen undercoat that grows in the winter. The yak is able to endure colder environments and higher altitudes that any other cattle. 27 On the other hand, zebu cattle, such as the Brahman, have large pendulous ears, a dewlap (folds of loose skin that hang down in front of the chest), a hump over the neck and shoulders from extended dorsal processes, and better developed sweat glands than other cattle. Zebu cattle can withstand hotter environments and are more resistant to parasites than other cattle.28 Conclusions All species in the genera Bos and Bison can be considered part of the cattle monobaramin. Bubalus is probably included since some hybrid embryos have developed to the advanced blastocyst stage. In one study cited, 23 failure around the 8-cell stage was associated with a lack of mRNA transcripts. This suggests that coordinated expression of embryonic genes is necessary for an embryo to develop past this stage into a morula and then a blastocyst. 29The blastocyst stage, at least in cattle, is when the embryo would be placed back into a recipient animal for implantation and further development. More research should be done to determine if the advanced blastocyst stage is really a satisfactory indicator of hybridization in mammals.Alleged hybrids of cattle with members of another subfamily (Caprinae) and family (Cervidae) hint that the holobaramin (all organisms derived from the created common ancestors, whether known or not) could possibly include the entire family Bovidae and several, if not all, of the five other ruminant families. 30Considerable variety is apparent within the cattle monobaramin. In my previous paper on the Tsoan (sheep-goat) monobaramin,6 I suggested that some of the variety may have resulted from directed mutations. These are changes in genes that occur in response to certain environmental clues and help the organism adapt to the new environment. So far, heritable directed mutations have only been documented in microbes. Within the evolutionary paradigm, mutations are essentially the result of random processes. In the creationary paradigm, mutations may be programmed into the genome so animals could adapt to changing environments after the Curse. Further study of variation within monobaramins, particularly looking at the molecular basis of these differences, may reveal programming of an infinitely wise Creator who provides for his creation in ways we had never before imagined. Karyotypic and allelic diversity within the canid baramin (Canidae) by Jean K. Lightner Previous studies suggest that all dog-like creatures (canids, family Canidae) belong to a single created kind. As unclean animals, all modern canids are descendants of two canids survived during the Flood. This pair of canids would have carried a limited amount of genetic diversity. They would be expected to have had a fairly uniform arrangement of chromosomes (low karyotypic diversity) and up to four different versions of any particular gene (allelic diversity). Today there is considerably more karyotypic and allelic diversity within the canids. The patterns imply that more than random mutation and natural selection are involved; instead, certain genetic components appear designed to change and numerous designed mechanisms may be involved in driving many of these changes. This suggests that animals were designed to be able to undergo certain genetic mutations which would enable them to adapt to a wide range of environmental challenges while minimizing risk.
Table 1. List of canid species and their normal diploid (2n) number which were included in a phylogenomic analysis by Graphodatsky et al.7There is a need to more fully describe intrabaraminic (within kind) variation on a genetic level for understanding the basis for the variety we see within baramins today. It has been pointed out that the majority of mutations are near neutral.1 Yet intuitively, I would expect random (chance) ‘errors’ in such a complex system to be more consistently disastrous unless the system was designed to change.2 If genetic systems were designed to allow for such changes, then mutations (changes in the nucleotide sequence of DNA) are not necessarily just ‘errors’ or ‘accidents’. On the contrary, some mutations may be directed to allow animals to adapt in the present fallen world. By examining intrabaraminic genetic diversity, we should be able to discover a clearer picture regarding the role of mutations in the development of the diversity found in animals today.Previous baraminic studies have identified all canids (family Canidae) as belonging to a single baramin. This historical information is important because it suggests there was a limited amount of diversity present in canids at that time. Today, this family is represented by 34 species that are widely distributed around the world.6 There are considerable data available on the karyotypic and allelic diversity in protein coding genes for several of these species. A brief overview of the data is presented here. Karyotype The family Canidae exhibits the most highly rearranged karyotypes* of any family within the order Carnivora. Normal diploid numbers vary from 34 for the red fox (Vulpes vulpes) to 78 for the domestic dog (Canis familiaris) and dhole (aka Asiatic Wild Dog; Cuon alpinus) (table 1). The Arctic fox (Alopex lagopus) is polymorphic for a centric fusion; diploid numbers of 49 and 48 are found in individuals carrying one or two copies respectively of this fusion. Phylogenomic analysis suggests that 82 may have been the ancestral karyotype. Within the 10 species that have been studied in detail it appears that approximately 80 rearrangements have occurred. This includes numerous fusions, both centric and tandem, fissions, pericentric inversions and/or centromere transpositions.7 Several paracentric inversions, and even whole arm (telomere to centromere) inversions, have been implicated based on the differences in loci order among species (figure 1).8,9 Figure 1. Diagrams depicting some of the chromosomal rearrangements reported within the canid baramin. Such rearrangements often result in the loss of relatively small portions of DNA. Fusions (top row) involve combining two distinct chromosomes to form one; to become stable, one centromere must then be silenced. Inversions (bottom row) involve reorienting a portion of DNA within an existing chromosome. There also is evidence that the amount of heterochromatin can be adjusted. These types of rearrangements are too complex to be the result of ‘purely chance events’. While rearrangements do involve some risk, they probably also have purpose, such as adaptation in a fallen world.Evidence of similar rearrangements is present within other baramins and even within some species.10–12 Detailed studies of rearrangements in ruminants strongly suggest that numerous designed mechanisms operate to repair breaks, silence an extra centromere, adjust amounts of heterochromatin and possibly alter the position of the centromere. 13 The fact that such rearrangements often become fixed within a species suggests that they may be beneficial under certain circumstances. However, fixing these rearrangements also likely required a small population, since it is difficult to fix even beneficial mutations in a large population. 14 Thus, rearrangements should not be viewed as a major genetic accident from which animals occasionally may recover. Instead, the presence of multiple designed mechanisms enabling translocations to occur while maintaining viability of the animal suggests that such rearrangements are likely helpful for adaptation in the present fallen world. This is not to say that such rearrangements are without risk. For example, many heterozygous carriers experience some decline in fertility. Occasionally there are more serious results with infertility and/or serious chromosomal aberrations in the offspring. 13 Furthermore, these types of rearrangements certainly don’t explain the origin of chromosomes.The red fox and both subspecies of raccoon dog carry B chromosomes as part of their normal karyotype. 7These small, supernumerary chromosomes can vary in number both within as well as among individuals. Generally their numbers are low, with three to five being typical for the red fox.15 They usually contain significant amounts of repetitive sequences and, until recently, it was thought that they did not contain any protein coding genes. However, the canid B chromosomes have been found to contain the KIT gene, which encodes a transmembrane tyrosine kinase receptor involved in the proliferation, migration and differentiation of hematopoietic, melanoblast, and primordial germ cells. Adjacent sequences were detected, including the RPL23A pseudogene and, in the raccoon dog only, a portion of the more distal KDRgene. This suggests that the B chromosomes were derived from an autosome in a common ancestor and have been lost in other lineages descending from this ancestor. Further studies need to be done to determine if the KIT gene of B chromosomes is actually transcribed.16
Major histocompatibility complex genes The major histocompatibility complex (MHC) consists of a number of genes involved in immune function and which are known for high allelic diversity. Several dog leukocyte antigen (DLA) genes have been evaluated for polymorphisms. As of 2006, there were 90 alleles recognized for DLA-DRB1, 22 for DLA-DQA1 and 54 for DLA-DQB1, with more expected to be discovered.17 High levels of polymorphism are generally considered a sign of a healthy population, although some dog breeds and wild mammals have low MHC diversity with no apparent ill effects. The DLA genes are on dog chromosome (CFA) 12.18 Some DLA haplotypes are associated with various canine autoimmune diseases such as primary immune mediated hemolytic anemia, polyarthritis, hypothyroidism and diabetes. 19 However, it is important to recognize that these haplotypes do not cause disease directly; instead, they may be risk factors that affect the likelihood of disease development. As suggested previously, there is risk in maintaining sufficient variability to adapt in the present fallen world. Dopamine receptor D4 gene There are two portions of the dopamine receptor D4 (DRD4) gene that are variable in dogs. The first is in exon 1 where the two known alleles differ by a 24-base pair (bp) indel. 20 Interestingly, humans also are polymorphic in this region with a 12-bp duplication and a 13-bp deletion having been identified.21 The latter is particularly intriguing as it is found in 2% of the human population and is not associated with any known disease; yet the frameshift is predicted to result in a truncated, nonfunctional protein.22 Figure 2. A representation of the variable number tandem repeat (VNTR) patterns in exon 3 of the dopamine receptor D4 (DRD4) gene for seven dog alleles (after Hejjas et al.23). The nonrandom pattern of mutation suggests designed mechanisms are involved in this mutation. The variability in this region appears to have some influence on personality and behaviour.The second polymorphic region is found in exon 3. There are eight alleles that have been identified in dogs.20 A number of these have been identified in wolves. The alleles differ by variable number tandem repeats (VNTRs) of 12-and 39-bp (figure 2). A similar pattern has been observed in humans, where a 48-bp segment is repeated from 2 to 10 times. These variations are believed to influence behaviour because certain alleles have been shown to be associated with the novelty-seeking personality trait in humans, primates and dogs. 23 VNTRs have been identified in exon 3 of the DRD4 gene of nearly all mammals examined except rodents. The length of the repeated segments varies among taxa, but is consistently a multiple of three. 24This bias of indels, particularly VNTRs, in base pairs that are multiples of three does not appear to be explicable by natural selection. If essentially random, approximately one-third of indels should be multiples of three unless a frameshift, which often results in a premature stop codon and a nonfunctional protein, is lethal or significantly detrimental. It does not appear that frameshifts in DRD4 would be subject to such selection pressure, since a frameshift mutation is carried by a number of normal humans and knock-out mice. 20,22 Furthermore, variability in this gene appears to contribute to variability in personality. The number of alleles in canids (greater than eight, as the raccoon dog has a separate allele identified25) is greater than the maximum of four alleles expected in the pair of canids. Humans also carry more alleles than can be attributed to the first man and woman. This suggests that this gene was designed to vary in a rather unusual way to enhance variability in personality and perhaps other traits as well. Olfactory genes Olfactory (smell) receptor (OR) genes are seven transmembrane receptors. While 1,094 OR genes have been identified in the dog,26 the canine repertoire of odorant molecules is significantly greater than this. This appears to be from a complex combinatorial code. Odorant molecules can bind 20 or more ORs depending on their concentration. ORs can bind more than one odorant molecule. Through interpretation of the complex signalling patterns, dogs are able to detect an incredibly wide array of individual odorants and a large number of mixtures. 27In one study, 16 OR genes were examined in 95 dogs from 20 different breeds. All genes were polymorphic ranging from two to 11 alleles per gene. There was an average of one change per 920 sequenced nucleotides, which is much higher than most coding sequences and a random sampling of non-coding sequences. Of the 98 single nucleotide polymorphisms (SNPs) identified, 55 resulted in an amino acid change and 30 of these involved changes to a different amino acid group. These changes were found throughout the protein (figure 3), mostly in variable or highly variable regions within OR genes. However, two come from highly conserved regions, one in transmembrane (TM) 3 and the other in TM7.28Five of the 16 genes had an allele with a disrupted open reading frame. These were from one of the four indels identified or an SNP introducing a stop codon. Pseudogenization of OR genes is fairly common. In poodles, 18% of ORs are pseudogenes while 20.3% (or 222/1094) are in the boxer. Interestingly, 17 of the OR pseudogenes in the poodle were not found in the boxer, and 22 of those found in the boxer were not found in the poodle. 28It may be premature to assume there is no purpose in mutation or pseudogenization within OR genes.29There is a tremendous amount of redundancy in OR genes which may have been designed to allow for future specialization. For example, a study involving Drosophila sechellia, a highly specialized vinegar fly that feeds solely on fruit from Morinda citrifolia, a shrub which strongly repels related species of flies, suggests that pseudogenization of ORs
and gustatory (taste) receptors has occurred nearly 10 times faster than in the closely related species D. simulans. For those genes which remained intact, D. sechelliaappears to have fixed non-synonymous substitutions at a consistently higher rate than synonymous substitutions compared to the same genes in D. simulans.30 Therefore, the ability of OR genes to be modified or pseudogenized may be an important design element. Conclusion Figure 3. Two-dimensional diagram of an olfactory receptor (OR) indicating positions of 55 non-synonymous single nucleotide polymorphisms (SNPs) and their allele frequencies in dogs, as identified by Tacher et al.28 ‘*’ indicates the SNPs found in highly conserved regions of the OR genes. There are 1,094 OR genes that have been identified in dogs.The two canids that survived the flood would be expected to have carried a fairly uniform karyotype and up to four alleles for nonduplicated genes. This brief examination of present-day karyotypes and several groups of genes indicates that significant diversity has arisen since the Flood. Several different lines of evidence suggest that many of these mutations may have some benefit to the animal. For example, intrabaraminic chromosomal comparisons have implicated numerous designed mechanisms which control chromosomal changes in a way that maintains viability of the animal. The fact that such mechanisms appear to be operating suggests there is purpose to chromosomal rearrangements. The fact that different karyotypes often are fixed in different species within a baramin seems to support this concept as well.The various genes examined here appear to handle mutations very well. In fact, it is generally believed that the high allelic diversity in the MHC genes is important for a healthy population. The redundancy in ORs and the pattern of mutation and pseudogenization in these genes suggests that these genes were designed to vary so that animals can adapt to different environments. Finally, the striking non-random pattern of VNTR mutations, all in lengths divisible by three, when there is no known selection that could produce this non-random pattern, strongly suggests that in some instances there are designed mechanisms driving mutations. The patterns seen here suggest that animals were designed to be able to undergo genetic mutations which would enable them to adapt to a wide range of environmental challenges while minimizing risk. Glossary Autosome:
a chromosome that is not a sex (X or Y) chromosome.
Centric fusion:
combining of two acrocentric (centromere near one end) chromosomes to form a new chromosome with the centromeres adjacent to each other. See figure 1.
Centromere transposition:
a change in the position of the centromere on the chromosome without a change in gene order. This rearrangement can be very difficult to distinguish from a pericentric inversion.
Frameshift:
an insertion or deletion (indel) that shifts the three-base-pair reading frame of the gene. A frameshift will often result in loss of function of the protein.
Haplotype:
a region of DNA usually inherited together; a group of alleles that are closely linked.
Heterochromatin:
sections of DNA containing highly repetitive sequences and few genes. Despite appearing inactive, these regions are important for proper function. The amount of heterochromatin appears to be adjusted following chromosomal rearrangements.
Karyotype:
the appearance of the chromosomes within an individual at metaphase, the time during cell division when the chromosomes are clearly seen.
Open reading frame:
the portion of DNA that is read (copied into RNA) and may be used for protein formation.
Knock-out mice:
mice in which the specific gene under study is disabled (knocked out). Studies with knock-out mice have been very helpful in determining the function of genes.
Paracentric inversion:
an inversion in one chromosome arm that does not include the centromere. See figure 1.
Pericentric inversion:
an inversion in a chromosome that includes the centromere. See Figure 1.
Phylogenomic:
comparison of the genomes of organisms within a group to attempt to reconstruct ancestry.
Single nucleotide polymorphism (SNP):
a difference in a single base in the DNA sequence; a change in which a single base pair differs from the usual base pair in that position.
Tandem fusion:
combining of two chromosomes where the end of one chromosome attaches to the end or centromeric region of another chromosome. See figure 1.
Tandem repeats:
multiple copies of the same base sequence on a chromosome. See figure 2.
Identification of a large sparrow-finch monobaramin in perching birds (Aves: Passeriformes) by Jean K. Lightner In baraminology hybrid data is used to determine which species are able to reproduce with each other and thus logically belong to the same created kind (baramin). Hybrid data from birds in the order Passeriformes was examined. It was found
that there is a large sparrow-finch monobaramin that includes over 1,000 species. One questionable hybrid, if confirmed, would potentially double the size of this monobaramin to include birds such as swallows. Ravens and crows are in a separate taxonomic category within this order and have no hybrid data that would connect them to the sparrow-finch monobaramin. Given the variety within these monobaramins, Male house finch (Carpodacus mexicanus) One goal of baraminology is to identify extant species that belong to a common created kind (baramin). One important method of determining that two different species belong to the same baramin is the ability to form hybrids between them. As long as there is significant embryological development, hybridization is considered, by most creationists, to be conclusive evidence that creatures are from the same baramin.1 Taxa connected by hybrid data are said to be in the same monobaramin. One problem is that a lack of hybrid data does not, in itself, suggest that the two are necessarily from different baramins. This is because barriers can arise which make hybridization difficult or impossible even when creatures are known to be related.Hybrid data is more complete for animals that are domesticated or held in captivity. Indeed, the rare hybrids between sheep and goats would likely never have been identified if these two domestic species were not commonly kept together.2 Several years ago a compilation of all known avian hybrids was published by Eugene McCarthy.3 Again, a very large proportion of the hybrid reports come from animals held in captivity.Several baraminologic studies have been done using this excellent resource. The first was with the order Galliformes (landfowl).4 Hybrid data connected the families in the superfamily Phasianoidea: Phasianidae (pheasants and partridges), Meleagrididae (turkeys), Tetraonidae (grouse), Odontophoridae (New World quail), and Numididae (guineafowl) and the family Cracidae. The inclusion of Cracidae in this monobaramin is somewhat surprising since this family is generally placed in a separate suborder, Craci, which is more closely associated with the remaining family of this order, Megapodiidae (mound builders).5The second baraminologic study involved the order Anseriformes (waterfowl).6 Here the major family, Anatidae (ducks, geese, swans), which includes over 145 species, had hybrid data across subfamilies showing it to be a monobaramin. The other two families, Anhimidae (screamers) and Anseranatidae (magpie goose), are small and include three and one species, respectively. There is no hybrid data connecting these three families.Another order, Passeriformes (perching birds), contains more than half of the world’s bird species. It includes the domestic canary (figure 1), which itself has considerable hybrid data with other species. Other members of finch and sparrow families also have interfamilial hybrid data which reveals a sizable monobaramin.Before beginning the analysis, it should be pointed out that bird taxonomy is in a state of flux. It is common for sources to disagree. Some genera have been lumped from several different families into one; others have been separated out into a new family. One reason is that it is notoriously difficult in birds to distinguish between traits that occur due to common ancestry and those that arise via convergent evolution. For example, a thick, conical bill does not necessarily imply anything about the relationship of two species. This trait is referred to as an analogous trait in that it has arisen a number of times in divergent taxa. 7 Additionally, DNA studies have had a mixed effect. In many cases they have confirmed traditional classification; in other cases they profoundly challenged accepted taxonomy based on morphology and other data.8 Interfamilial hybrids Hybrid data exists (table 1) which connects Fringillidae (finches) with Estrildidae (estrilid finches), Emberizidae (American sparrows and buntings), Passeridae (Old World sparrows), and Icteridae (blackbirds). Further Estrildidae species have crossed with those of Ploceidae (weaver finches) and Emberizidae with Cardinalidae (cardinal and grosbeaks).Many of these interfamilial crosses have multiple well-documented hybrids. However, the documented cross connecting Fringillidae with Passeridae involves the formation of fertile eggs with no comment on a live hybrid being hatched. There are also several other hybrid reports between these two families, but McCarthy considers these latter ones doubtful. Assuming fertility was measured by candling, significant embryonic development would be necessary to identify the eggs as fertile. Thus, I consider the hybrid evidence strong enough to include these families in the same monobaramin.Due to the current state of flux in avian taxonomy, some of the species generally identified as from the family Emberizidae have been reassigned to the family Thraupidae (tanagers). This includes some species involved in the hybrids above. Not all sources accept this taxonomic change, but it is interesting to note that McCarthy groups the families Cardinalidae, Coerebidae (bananaquit), Emberizidae and Thraupidae together in one section when reporting the hybrids. 22 Other sources group these families together as well. 23 Thus, I conclude the monobaramin also includes Coerebidae and Thraupidae.Several other families are connected by hybrid data that McCarthy considers questionable. An old reported cross between Estrildidae and Viduidae (vidua finches and whydahs) is strongly questioned because the details of the original report are so sketchy. A cross between Fringillidae and Zosteropidae (white-eyes) is also questioned because the latter belongs to a separate superfamily (Sylvioidea) than the rest of the Passeroidea hybrids above. Hybrids involving swallows and ravens Swallows are in the family Hirundinidae, which is also in the superfamily Sylvioidea. There have been reports of natural hybrids connecting several genera (Delichon, Hirundo, Riparia and Tachycineta) within this family, but no interfamilial hybrids have been reported.24 Thus, based on the data considered most reliable by McCarthy, swallows currently occupy a separate smaller monobaramin than the sparrow-finch monobaramin. There is no hybrid data connecting the above families with Corvidae (crows, ravens, magpies and jays). Within Corvidae there is hybrid data connecting the many species of Corvus (crows and ravens) and Pica (Magpie),25 forming a small monobaramin. A second monobaramin is present in this family, consisting of Aphelocoma, Calocitta, Cyanocitta, Cyanocorax, and Psilorhinus, genera comprised of various species of jays. 26There are many other families in the order Passeriformes, but they lack well-substantiated interfamilial hybrids. They also contain small
monobaramins similar to what is found among swallows and ravens. They will not be listed in detail here as it would be tedious and not add significantly to this paper. DNA-DNA hybridization Sibley and Ahlquist used DNA-DNA hybridization data in an attempt to clarify avian taxonomy.27 This laboratory procedure involves ‘unzipping’ DNA by heating it. The DNA is then cut into fragments averaging about 500 bases to allow for the removal of the bulk of repeated sequences and to obtain reproducible rates of reassociation. These DNA fragments are then reassociated, either with fragments from the same individual or those from another species. The stability of the resulting duplexes is evaluated by comparing the median melting temperature of a homoduplex (same individual) DNA hybrid with that of a heteroduplex (different species) hybrid.The reassociated DNA duplexes have a lower thermal stability due to base pair mismatches. Thus, a greater difference in thermal stability between a homo-and heteroduplex implies greater sequence differences between the two species. The authors’ analysis assumes that sequence similarity is always from common ancestry. Thus, universal common ancestry for all birds is assumed, which is clearly in conflict with the young age history. This incorrect assumption may explain some radical rearrangements in higher taxa compared to traditional means of classification. A detailed investigation of this is beyond the scope of this paper, which is limited to taxa connected by hybrid data.A second assumption more directly related to this paper is that convergent evolution on a DNA sequence level is negligible. There could be some reason to question this since convergence is so common on a morphological level. Research in color-coding genes has shown that the same nucleotide changes can occur in divergent taxa, but this is not terribly common.28 Further, the same color patterns can be acquired via different mutations in the same gene or mutations in different genes.29 This suggests that sequence convergence should be less of a problem than morphologic convergence. Table 1. A list of successful interfamilial crosses within the sparrow-finch monobaramin. Page
276
276*
293*
FAMILY Genus common name
species X
FRINGILLIDAE Carduelis Eurasian Linnet
FAMILY Genus common name
species
ESTRILDIDAE cannabina Amadina Cut-throat
fasciata
FRINGILLIDAE ESTRILDIDAE Serinus mozambicus Amandava Yellow-fronted Canary Zebra Waxbill
subflava
FRINGILLIDAE Carduelis Grey-crowned Goldfinch
ESTRILDIDAE caniceps Taeniopygia Zebra Finch
guttata
FRINGILLIDAE Carduelis European Goldfinch
EMBERIZIDAE carduelis Emberiza Yellowhammer
citrinella
EMBERIZIDAE chloris Emberiza Yellowhammer
citrinella
FRINGILLIDAE Serinus Domestic Canary
EMBERIZIDAE† domesticus Volatinia Blue-black Grassquit
jacarina
342*
FRINGILLIDAE Serinus Domestic Canary
PASSERIDAE domesticus Petronia xanthocollis Chestnut-shouldered Petronia
339
FRINGILLIDAE Serinus Domestic Canary
ICTERIDAE domesticus Agelaius ruficapillus Chestnut-capped Blackbird
341
FRINGILLIDAE Serinus Domestic Canary
PLOCEIDAE domesticus Foudia Red Fody
297–298*
299
344
276
317
317
FRINGILLIDAE Carduelis European Greenfinch
madagascariensis
ESTRILDIDAE Amadina Cut-throat
PLOCEIDAE fasciata Euplectes Orange Bishop
EMBERIZIDAE Gubernatrix Yellow Cardinal
CARDINALIDAE cristata Cardinalis Northern Cardinal
cardinalis
CARDINALIDAE coronata Cardinalia Northern Cardinal
cardinalis
EMBERIZIDAE† Paroaria Red-crested Cardinal
franciscanus
319
EMBERIZIDAE† CARDINALIDAE Sporophila caerulescens Cyanocompsa Double-collared Seedeater Ultramarine Grosbeak
brissonii
324
EMBERIZIDAE† Paroaria Red-crested Cardinal
ICTERIDAE coronata Agelaius ruficapillus Chestnut-capped Blackbird
324
EMBERIZIDAE† Paroaria Red-crested Cardinal
ICTERIDAE coronata Molothrus Shiny Cowbird
bonariensis
DOUBTFUL HYBRIDS 281
344
ESTRILDIDAE VIDUIDAE Lonchura atricapilla Vidua Southern Blk-Headed Munia Village Indigobird FRINGILLIDAE Serinus Domestic Canary
chalybeata
ZOSTEROPIDAE domesticus Zosterops Green White-eye
Pages are from McCarthy, * indicates fertile eggs, but no mention of † indicates species which are now sometimes classified as Thraupidae.
virens ref. hatched
2. hybrids.
Extent of the sparrow-finch monobaramin Ignoring the hybrids McCarthy considers questionable, it appears the monobaramin would easily include nine families in the Passeroidea superfamily (Fringillidae, Estrildidae, Emberizidae, Passeridae, Icteridae, Ploceidae, Cardinalidae, Coerebidae and Thraupidae). This would include 1,045 species30 and about half of the families generally placed in the superfamily Passeroidea. If the cross between Fringillidae and Zosteropidae is confirmed, then the monobaramin would include Passeroidea and at least some of Sylvioidea, two of three major superfamilies in the infra-order Passerida. 31 This seems to imply that swallows, as members of Sylvioidea, might also belong to the sparrow-finch monobaramin.Using Sibley and Ahlquist’s taxonomy based on DNA-DNA hybridization, the monobaramin includes two families: Passeridae and Fringillidae. The other families are demoted to subfamilies within these two. However, with this regrouping the monobaramin consists of 1,379 species. If Zosteropidae were also included, then a second superfamily, Sylvioidea, would be included in this monobaramin as described above. This would more than double the number of species in the monobaramin and, as mentioned above, include swallows. 32 Regardless of whether this monobaramin actually includes one or two superfamilies, the ravens still occupy a separate parvorder and remain unconnected to the sparrow-finch monobaramin based on current hybrid data. Conclusions Though ambiguity exists within avian taxonomy, there is clear evidence from hybrid data for a large sparrow-finch monobaramin consisting of over 1,000 species from multiple families. These species display an impressive variety of color patterns, beak morphology, and other characteristics. This is particularly notable given the severe genetic bottleneck at the time of the Flood less than 5,000 years ago. There are examples of genes that were designed in a way to allow for genetic changes to occur which are useful and/or add beauty and variety. Given patterns observed in these genes, it was further suggested that the genome is programmed to respond appropriately to environmental factors. 33 This would allow for these non-random changes to appear at appropriate times rather than waiting on chance mutations to supply them. Epigenetic factors may play a crucial role as well. Further study into the underlying basis for variation in this monobaramin would be helpful in determining if similar patterns exist in birds. If interspecific hybridization is a reliable criterion in determining baramins, then much more work is necessary to identify the genetic and environmental mechanisms responsible for generating this tremendous intrabaraminic diversity from one kind. Identification of gene modules or gene regulatory networks and the factors responsible for their differential expression are essential in understanding the mechanisms driving post-Flood diversification. In addition to genomic analysis, phenotypic plasticity and/or ecomorphological studies could lead to important insights and testable hypotheses regarding the innate genetic potential of baramins. WHAT IS SPECIATION.DOES IT TAKE MILLIONS OF YEARS TO OCCUR Brisk biters Fast changes in mosquitoes astonish evolutionists, delight creationists. by Carl Wieland About 100 years ago, bird-biting mosquitoes called Culex pipiens entered the tunnels then being dug for the London Underground (the ‘Tube’). Cut off from their normal diet, they changed their habits to feed on rats and, when available, human beings. During WW2, they attacked Londoners seeking refuge from Hitler’s bombs. Their plaguing of maintenance workers may be the reason the underground variety has been dubbed molestus.British scientists have now found that it is almost impossible to mate those in the Tube with the ones still living above ground, thus suggesting that they have become a new species1 (or almost so). This has ‘astonished’ evolutionary scientists, who thought that such changes must take many times longer than this.2 Informed creationists have long pointed out that the young age model of earth history would not only allow for the possibility of one species splitting into several 3 (without the addition of new information, thus not ‘evolution’ as commonly understood), but would actually require that it must have happened much faster than evolutionists would expect. The thousands of vertebrate species emerged into a world with large numbers of empty ecological niches, often as varied as the two worlds of our mosquito example here. They must have split many times into new species in the first few centuries thereafter, as the bear population, for example, gave rise to polar bears, grizzlies, giant pandas and more.5 The observations on these underground mosquitoes are thus exciting news.Actually, creationists have long suspected that organisms had ‘built-in’ genetic mechanisms for rapid variation—even beyond the normal processes of adaptation where genes, reshuffled by sexual reproduction, are selected in various environments. 6 Thus, recent discoveries
of such mechanisms being still viable today are of very great interest.For example, there are genes which can ‘jump’ around the chromosome. These are normally kept in check, but Drs Jenny Graves and Rachel O’Neill of La Trobe University in Melbourne, Australia, have found that in hybrids, these can undergo ‘rampant’ changes.This may even be ‘the general mechanism for speciation in all multi-cellular creatures’ (by making it impossible to ‘back-breed’ with a parent population). Graves says, ‘We thought it took millions of years of long-term selection for a jumping gene to be activated. We’ve now shown that it can happen maybe in five minutes after fertilization.’7 These are exciting times to be a creationist.We think that expanding genetic research will likely reveal even more examples of built-in, ‘pre-fab’ mechanisms for rapid change in response to environmental pressures. Ironically, as more such created mechanisms (very far from normal Darwinian ideas) are discovered, they will probably be misconstrued as support for evolution. Darwin’s finches Evidence supporting rapid post-Flood adaptation by Carl Wieland Thirteen species of finches live on the Galápagos, the famous island group visited by Charles Darwin in the 1830s. The finches have a variety of bill shapes and sizes, all suited to their varying diets and lifestyles. The explanation given by Darwin was that they are all the offspring of an original pair of finches, and that natural selection is responsible for the differences.Surprisingly to some, this is the explanation now held by most modern creationists. It would not need to be an ‘evolutionary’ change at all, in the sense of giving any evidence for amoeba-to-man transformation. No new genetic information would have been introduced. If the parent population has sufficient created variability (genetic potential) to account for these varied features in its descendants, natural selection could take care of the resulting adaptation, as a simplistic example will show.Say some finches ended up on islands in which there was a shortage of seeds, but many grubs were living under tree bark. In a population with much variation, some will have longer, some shorter, beaks than average. Those birds carrying more of the ‘long-beak’ information could survive on those grubs, and thus would be more likely to pass the information on to their descendants, while the others would die out. In this way, with selection acting on other characters as well, a ‘woodpecker finch’ could arise.The same thing is seen in artificial selection, with all the various modern breeds of dogs being more specialized than the parent (mongrel) population, but carrying less information—and thus less potential for further selection (you can’t breed Great Danes from Chihuahuas). In all these sorts of changes, finches are still finches and dogs are dogs. The limits to change are set by the amount of information originally present from which to select.Creationists have long proposed such ‘splitting under selection’ from the original kinds, explaining for example wolves, coyotes, dingoes and other wild dogs. The question of time has, however, been seized upon by anti-creationists. They insist that it would take a much longer time than the young age frame allows. Artificial selection is quick, they admit, but that is because breeders are deliberately acting on each generation. The usual ‘guesstimate’ of how long it took for Darwin’s finches to radiate from their parent population ranges from one million to five million years.However, Princeton zoology professor Peter Grant recently released some results of an intensive 18-year study of all the Galápagos finches during which natural selection was observed in action.1 For example, during drought years, as finches depleted the supply of small seeds, selection favoured those with larger, deeper beaks capable of getting at the remaining large seeds and thus surviving, which shifted the population in that direction.While that is not very surprising, nor profound, the speed at which these changes took places was most interesting. At that observed rate, Grant estimates, it would take only 1,200 years to transform the medium ground finch into the cactus finch, for example. To convert it into the more similar large ground finch would take only some 200 years.Notice that (although the article fails to mention it) such speedy changes can have nothing to do with the production of any new genes by mutation, but are based upon the process described, that is, choosing from what is already there. It therefore fails to qualify as evidence for real, uphill (macro) evolution — though many starry-eyed students will doubtless be taught it as ‘evolution in action’.Instead, it is real, observed evidence that such (downhill) adaptive formation of several species from the one created kind can easily take place in a few centuries. It doesn't need millions of years. The argument is strengthened by the fact that, after the Flood, selection pressure would have been much more intense — with rapid migration into new, empty niches, residual catastrophism and changing climate as the Earth was settling down and drying out, and simultaneous adaptive radiation of differing food species. Dogs breeding dogs? That’s not evolution! by Don Batten Museums, and school, college and university courses in biology, emphasize variation within a kind as ‘evidence’ for evolution. For example, the Natural History Museum in London says that breeding of dogs shows evolution. Presumably all you have to do is breed dogs for long enough and you will get something which is not a dog—something that is basically different. To the uninformed this can seem convincing—after all, there are many and varied breeds of dogs. However, the evidence from breeding and the science of genetics actually presents a huge problem for evolution. In spite of much breeding and the generation of many varieties of dogs, from chihuahuas to Great Danes, dogs are still dogs. Dogs have only ever bred dogs. Roses have only ever bred roses. As a biologist with a Ph.D. in plant physiology and over 20 years research experience, including the breeding of fruit trees, I believe genetics holds major problems for evolutionists. Why? Because there is no mechanism for the acquisition of new, more complex characteristics in living things. There is no means of
generating the new genetic information required. Evolution from microbes to man requires such a mechanism.A recent survey of students before and after a genetics course at Central Michigan University (USA) showed that the number of students believing in evolution declined from 81% before the course to 62% after, although the course was almost certainly taught from an evolutionary perspective.1If the course had been taught without the inevitable evolutionary bias, the shift in attitude towards creationism might have been even greater! Pigs breed pigs! How can one basic kind of organism change into something fundamentally different? A pig farmer in the UK heard an evolutionist academic talk about how breeding of farm animals shows evolution. At the end of the lecture the pig farmer said, ‘Professor, I don’t understand what you are talking about. When I breed pigs, I get pigs—if it were not so I would be out of business!’The evolutionist Dr Keith Stuart Thompson said: ‘Evolution is both troubled from without by the nagging insistence of anti-scientists, and nagged from within by the troubling complexities of genetic and developmental mechanisms, and new questions about the central mystery: speciation itself.’ 2 In other words, how can the incredibly complex biochemical systems in living things come about by any conceivable natural process? And then how could random changes in such complex systems change them into something else—something fundamentally new?What Thompson said 13 years ago has been amplified by the studies in molecular biology since then. Every new discovery should be another nail in the coffin of naturalistic origins (evolution). As a graduate student at the University of Sydney I sat in on a biochemistry course covering the operation of a bacterial gene which coded for the enzyme complex which breaks down lactose, the milk sugar. The enzymes are produced only if lactose is available. I found it fascinating. The system was so beautifully designed and finely tuned to do what it did. An end-of-course discussion time saw a student ask the lecturer how such a system could evolve. The answer? ‘It couldn’t.’ Such integrated and complex systems cannot come about through chance, random processes (mutations etc.). Spelling it out Dr Michael Denton, a molecular biologist, spelled out the problem in his book, Evolution: A Theory in Crisis.3 Dr Denton, although not a Christian or a creationist, acknowledges the problems for the idea of chance processes generating living things or generating new genetic information. Denton’s book was published in 1985, but it has not dated in any substantial area. Although written by an expert in his field, the book is quite readable.There is no known natural process for generating new, more complex, traits. If a reptile changed into a bird, the reptile would have to, along with many other improbable changes, acquire the ability to produce feathers. To get a reptile to produce feathers requires new genes to produce the proteins necessary for the production of feathers. The chance of natural processes creating a new gene coding for a protein fundamentally different to those already present is essentially zero. New ‘species’? New ‘species’ can and have formed, if by definition we mean something which cannot breed with other species of the same genus, but this is not evidence for evolution. The new species have no new genetic information! For example, a ‘new species’ has arisen in Drosophila, the ferment fly so popular in undergraduate genetics laboratories. The new ‘species’ cannot breed with the parent species but is fertile with its own type, so it is, by definition, a new ‘species’. However, there is no new genetic information, just the physical rearrangement of the genes on one chromosome—technically called a ‘chromosome translocation’.To get evolution ‘from bacteria to Bach’ requires incredible amounts of new information to be added. Typical bacteria have about 2,000 proteins; a human has about 100,000. At every upward step of evolution there needs to be new information added. Where does it come from? Not from mutations—they degrade information.Carl Sagan, ardent evolutionist, admitted: ‘… mutations occur at random and are almost uniformly harmful—it is rare that a precision machine is improved by a random change in the instructions for making it.’4 … But no new ‘kinds’ There are many breeds of pigeons, cattle, horses, dogs, etc., but they are all pigeons, cattle, horses, dogs, etc. Recombination of existing genes can produce enormous variety within a kind, but the variation is limited by the genes present. If there are no genes present for producing feathers, you can breed reptiles for a billion years and you will not get anything with feathers! Polyploidy (multiplication of the number of chromosomes), chromosome translocations, recombination and even (possibly) mutations can generate ‘new species’, but not new information, not new characteristics for which there were no genes to start with.It is possible for mutation ‘breeding’ to generate new varieties with traits which are ‘improved’ from man’s point of view (e.g. shorter wheat plants, different protein quality, low levels of toxins, etc.). Where such ‘improvements’ have been investigated on a molecular basis, researchers have found that the ‘new’ trait is not due to the appearance of a new protein, but the modification of an existing one, even when it seems to be a new trait, such as herbicide resistance.Herbicides often work by fitting into an enzyme—a bit like a key in a lock. The presence of the wrong key stops the protein or enzyme from accepting the correct key, the chemical compound that it normally works on, and so the plant dies (see diagram). Herbicide resistance can be due to a mutation in the gene coding for the enzyme so that a slightly modified enzyme is produced which the herbicide molecule no longer fits. The enzyme may still do its usual job sufficiently well for the plant to survive. However, such a mutant is normally less fit to survive in the wild, away from the herbicide, because the modified enzyme is no longer as efficient at doing its normal job.In the whole creation/evolution debate, keep in mind that variation within a kind, such as through breeding or adaptation, is not evolution. All the biological / genetic ‘evidence’ for evolution is actually variation within a kind, not evolution at all. This includes peppered moths, bacterial resistance to antibiotics, insecticide resistance, horse ‘evolution’, Galápagos finches, Arctic terns, etc. Creationists recognize the role of natural selection in today’s world, in changing gene frequencies in populations,
but this has nothing to do with the evolution of some mythical ‘simple’ life form into a human over billions of years, because natural selection cannot generate new information. Nor can mutations, polyploidy, etc.Evolutionists often call the natural variations in living things ‘microevolution’. This misleads people into thinking that since such variations are real, therefore evolution itself—from molecules to man—is proven. There is no logical connection between varying gene frequencies in populations of peppered moths, for example, and the origin of the genes themselves, which is what evolutionists claim the theory explains.In a recent paper, evolutionist Dr George Gabor Miklos summed it up nicely when he said: ‘We can go on examining natural variation at all levels … as well as hypothesising about speciation events in bed bugs, bears and brachiopods until the planet reaches oblivion, but we still only end up with bed bugs, brachiopods and bears. None of these body plans will transform into rotifers, roundworms or rhynchocoels.’ 5All kinds of living things were created tohave the genetic capacity for variation by the rearranging of the genetic information, the genes, through the reproductive process. However, the variation is basically limited to that available in the created genes, with the addition of some extra variation due to non-lethal mutations in the original genes. The extra variations in humans caused by genetic mutations probably include such visible things as freckly skin, blue eyes, blond hair, inability to roll the tongue, lack of ear lobes, and male pattern baldness. Genetic engineers unwind species barrier But have they ‘reversed evolution’? by Philip Bell Imagine hearing that scientists had managed to genetically engineer one species of living creature so that it could now successfully breed with a totally distinct species; i.e. whereas the offspring of this union are usually sterile, they are now fertile. Well that is exactly what a team of scientists from several British academic institutions have done (reported in the journal Nature)1—albeit with the humble baker’s yeast. 2This yeast is one of a group of six related species (all Saccharomyces) that are able to cross-breed, but form sterile hybrids. By ingeniously tinkering with the genome of this single-celled fungus, the scientists managed to ‘create’ a new strain that was able to form fertile crosses with a distinct, but similar species.3 This is the first time that this has been observed in these yeasts. 4
In this cousin of the baker’s yeast, portions of its sixth and seventh chromosomes have apparently swapped places at some point in the past.5 This change did not involve the input of any new information—just a reshuffling of what already existed. Nevertheless, the researchers concluded that it contributed to the inability of the different species to interbreed, once the species formed.6 Believing this rearrangement of genetic information was ‘wrought by evolution’, one science writer claimed that the genetic engineers had actually succeeded in undoing what evolution had achieved! 7 She even quoted a Ph.D. scientist from the brewing industry, claiming that fermentation failures were similarly due to ‘evolution in the vat’!Apparently, when yeasts with new chromosome arrangements arise during the brewing of beer,8 they drop uselessly to the base of the vat. Now, this is hardly evidence for evolution. Who benefits? It’s certainly not the yeasts, which are now less fit to survive. As far as the brewers are concerned, these mutant yeasts are useless and the brewers have to start over with new yeast cultures.Evolutionists often delight in pointing to such speciation as an example of evolution in action, thinking that this contradicts the young age account. The fixity of species is an erroneous belief that was held by several early biologists 10 but which we know to be false today.11In fact, a young age of the history of life would seem to require that speciation not only happens, but does so rapidly. The wolf kind, for example, would need to have been able to rapidly diversify into the different ‘species’ seen today—the various types of wolves, jackals, coyotes and dogs, which are adapted to a wide range of different climates, from Arctic to tropical. These can hybridize, indicating that they came from the same original created kind 12 (see pp. 19–22).So—just variation within the created kinds—but a surprise to the evolutionists, who are wedded to their millionsof-years dogma.13 In addition, evolution from molecules to man would have had to involve massive additions of new information. However, all known examples of modern-day speciation (and the assumed speciation that occurred in the past in the case of these yeasts) involve a loss or reshuffling of existing information.So if speciation is not evidence for evolution, reversing it obviously has nothing to do with undoing evolution. If all it takes to cause two species to become one is a reshuffling of genes, then a gene reshuffle presumably caused the original Saccharomyces species to split into isolated species. Since this involves no new information, it cannot legitimately be used as evidence that yeasts can become yaks, given enough time.Examples like this one show that evolutionists are really clutching at straws. Past events are unobservable and unrepeatable, so trying to reconstruct vanished history is (for the evolutionist, at least), rather like investigating a crime for which there are no witnesses. Ironically, in a commentary on the yeast speciation paper (same issue of Nature), the author said, ‘Research into evolution is a bit like forensic detective work. Because it’s impossible to carry out million-year experiments, we instead look at what evolution has produced and try to figure out what happened and why.’ 14This reveals the faith of the evolutionist, which can be summarized as follows: ‘We cannot go back in time to observe evolution happening, but although we weren’t there, we’re sure evolution happened. We just don’t know how or why!’Of course, this will not prevent claims that a greater understanding of speciation mechanisms will show how evolution happens—in spite of the scientific and logical objections to the contrary. Ultimately, if a person chooses a worldview that redefines science to say that only natural processes have ever occurred, that person will be forced to the irrational conclusion that any change in the genome (even if it is downhill) is evidence of big-picture (uphill) evolution—the sort that supposedly changed single cells into scientists. The Heliconius hybrid butterfly: speciation yes, evolution no by David Catchpoole 23 June 2006 The news headline proclaimed ‘Evolution simulated in the lab’.1 The article then went on to say that a research study published in the prestigious journal Nature last week2had successfully recreated the South American butterfly Heliconius heurippa,
Changes in butterflies do not demonstrate bog sludge-to-butterfly evolution as there is no observed increase in genetic information.
which has red-orange and yellow-white stripes on its wings. They did this, the article said, by seeking to ‘recreate the evolutionary pathway’ that had given rise to it. Other news media carried the same theme, with BBC News reporting the study demonstrates that ‘two animal species can evolve to form one’.3 But is it really ‘evolution’? A closer look at the facts shows otherwise. Researchers had suspected that H. heurippa might be a hybrid of Heliconius cydno, which has a yellow stripe, and Heliconius melpomene, which has a red one. So the researchers interbred these two species, ‘creating a butterfly with the two-stripe pattern of H. heurippawithin just three generations.’ And there was no need to physically separate the two-stripe butterflies from the others, in order to maintain the ‘purity’ of the newly bred H.heurippa. ‘Butterflies tend to choose partners that look like themselves’, said one of the researchers, Chris Jiggins of Edinburgh University. ‘So, once the new pattern was established, these individuals have tended to mate with one another and shunned their parental species.’This is a fantastic example of rapid speciation—no surprise to creationists. However, it is not evolution, as no The patterns on butterfly wings are new genetic information has been produced. The butterflies are still butterflies, with mosaic pictures, made up of the hybrid species simply having an assortment of genes inherited from the two thousands of individual, vividly parent species. coloured dermal scales (often due to diffraction rather than pigment). On a single square millimetre of wing surface, there can be as many as 600 of these, arranged in straight lines as if drawn with a ruler and systematically overlapping each other like roofing tiles.
DAILY ARTICLES Comparative cytogenetics and chromosomal rearrangements by Jean K. Lightner
Figure 1. Chromosomal rearrangements involve the repair of double stranded breaks. They may be followed by changes in heterochromatin or centromeres, which suggest designed mechanisms are involved in the modifications. A better understanding of chromosomal rearrangements is necessary to developing both a more robust creation model and better reasoned apologetic arguments.Creationists accept that creatures can change over time, but a clearer understanding of the types of changes involved is necessary for a robust creation model. In creation apologetic arguments, many genetic changes are assumed to be “accidents” and the degenerative nature of these changes are commonly pointed out. However, there is no reason why all genetic changes must be “accidents” or even degenerative. Related to this issue is a critical need for a reasonable estimate of genetic similarity between various kinds at Creation. For example, evolutionists often point to human-chimp similarities to support their model’s assumption of common ancestry. Creationists commonly respond that similarity can be from a common designer and then list genetic differences between humans and chimps. Which of these differences are differently and which are from changes that have been acquired since then? If we point to differences that can reasonably be attributed to changes since Creation, our arguments will be weak and misleading. A proper use of evidential arguments depends on a robust creation model which requires a more detailed understanding of genetic changes that have occurred during history. Chromosomal rearrangements Comparative cytogentics has been important in establishing that many mammals have undergone significant chromosomal rearrangements during their history. A diversity of karyotypes may occur within a genus 3-5 or even a species.6-8 All rearrangements involve the repair of double stranded breaks. Additionally, many rearrangements are associated with alteration of heterochromatin, silencing of a centromere, and/or the formation of a new centromere. 10 Because of the precision necessary to accomplish such changes while maintaining viability of the animal, it appears there are designed mechanisms in place to accomplish such rearrangements. Creating comparative genome maps Comparative genome maps based on chromosome painting are useful and have been performed using more than eighty eutherian species. Yet chromosome painting has some significant limitations when comparing divergent species. There can be reduced hybridization efficiency of the probes from increased sequence divergence between these species (e.g. eutherians and marsupials). Comparative genome sequence analysis based on direct genome alignments has been used to overcome this problem. However, when evolutionists attempt to construct maps of a putative eutherian ancestor, the results are quite different between the two methods.A new in silico method of comparison, called electronic chromosome painting (E-painting), has been developed to overcome limitations of the previously mentioned techniques and reduce the complexity of whole genome sequence alignments. First, orthologous (corresponding) genes are identified using various means such as reciprocal BLAST best-hit searches.11 Comparative mapping of these orthologous genes allows for identification of regions with conserved gene order (syntenic segments). These can be used to infer details about past chromosomal rearrangements. E-painting makes comparisons easier because it ignores intergenic regions. This also means the method cannot be applied to telomeric, centromeric, or non-genic portions of the genome.A recent study using E-painting has revealed some interesting results.12 The genomes of six different mammalian species (human, mouse, rat, dog, cow, opossum) and the chicken were compared. The mammalian genomes have been sequenced with a 7-fold or greater coverage. The chicken genome was included because previous studies had shown it remarkably similar to eutherians in genome organization. Altogether 526 evolutionary breakpoints (EBs) were identified and mapped with a resolution around 120 kb. There was a positive correlation between EB frequency and gene density. Unlike some previous studies, these EBs did not significantly correspond to well known breakpoints in cancer and other disease related rearrangements. Primatespecific rearrangements occurred preferentially in regions containing segmental duplications and copy number variants. The
authors concluded that EBs were not random and show evidence of reuse. Their reconstruction of a putative ancestral eutherian genome based on this technique showed remarkable similarity to previous ones based on comparative chromosome painting. Usefulness of comparisons across baramins At this point some readers may be questioning the relevance of the above study. After all, the results are interpreted within an evolutionary framework where all life is considered to be related. Further, these results may make some people feel uncomfortable. If rearrangements do occur, and evolutionists can show how a chimp genome can be rearranged to fit the order found in a human, doesn’t that lend credence to evolution?First, chromosomal rearrangements themselves do not change one type of animal into another. Carriers of balanced chromosomal rearrangements generally have a normal phenotype, although they may have reduced fertility.13 Additionally, intergenic regions, genes without orthologs, and the specific sequence of orthologous genes are not considered in these comparisons. One cannot turn a mouse into a man by simply aligning its genes in the same order as ours. Second, genomic comparisons, whether within or between baramins, can provide useful information on genomic structure. This information is essential for further building the creation model.The identification of syntenic segments shows that genes commonly appear in a specific order. If there is an advantage to a specific order of genes, then chromosomal rearrangements may provide a mechanism for new gene associations that are advantageous in a different environment. Intrabaraminic E-painting investigations would be useful in investigating this idea further. It would also be interesting to note any overlap between EBs and breakpoints required by the creation model.This study should also force creationists to address the issue of genome organization similarity between baramins at creation. Decades ago it was thought that karyotypes were fixed, at least at the species level. Historically, many creationists have assumed that different kinds with different karyotypes were created . In light of what is now known about rearrangements, this assumption needs to be reassessed. Understanding interbaraminic similarity at Creation will add robustness to the creation model and aid in interpreting interbaraminic investigations that exist in the literature. Baranomes, VIGEs and chromosomal rearrangements Peer Terborg has suggested that baranomes were created, pluripotent uncommitted genomes, within created kinds. 14 These genomes were designed to adapt rapidly, facilitated by the presence of variation inducing genetic elements (VIGEs). VIGEs include repetitive sequences and various mobile elements. 15 Interestingly, another recent study identified a significant enrichment of certain endogenous retrovirus (ERV) and long interspersed nucleotide (LINE1) elements in EBs in humans and marsupials.16 Studies of phylogenetic trajectory of orthologous chromosomes have shown many EBs are coincident with ancient centromere activity or the appearance of new centromeres.16 Thus the identified ERVs and LINE1s may be acting as VIGEs which play an important role in chromosomal rearrangements. Conclusion Creationists need a more complete understanding of the types of genomic changes that have occurred throughout history. This includes a more detailed understanding of chromosomal rearrangements. Identification of patterns of intrabaraminic chromosomal diversity should help clarify what types of rearrangements are consistent with the creation model. It may also help uncover underlying mechanisms for rearrangements and allow for reasonable inferences about the designed purpose of such rearrangements. This improved understanding of genomic structure and function may inform conjecture about interbaraminic similarities at Creation and aid in interpreting interbaraminic comparison that appear in secular literature. Epainting is a recently developed tool that can aid creation research in this area as genomic data continues to accumulate. Inheritance of biological information—part I: the nature of inheritance and of information by Alexander Williams Creationists need to rethink their understanding of inheritance. The current secular view is based on the inadequate Mendelian (genetic) paradigm and the inadequate statistical theory of information. The new understanding needs to be based on young age model and Werner Gitt’s multidimensional theory of information. The key element in the multidimensional theory is apobetics and this explains the failure of Darwinists to come to grips with the reality of biological information, because they reject the idea of purpose. Two different purposes can be identified in the yong age view of biology—stasis of created kinds and variety within kinds. We therefore need to look for two corresponding types of informational structures—one to explain stasis and one to explain variation. The cell may be the basic unit of inheritance that provides stasis, for its extra-nuclear contents pass unchanged from parent to daughter generation. Coded information on the chromosomes is also strongly conserved, but in addition it provides controlled variation within the created kind. The new science of semiotics may provide some useful tools for implementing the multi-dimensional approach to biological information. The nature of inheritance
The five dimensions of biological information. Statistics concerns the states of the four bases, semantics concerns the meaning of codons, syntax concerns the order of codons and the stop and start positions, pragmatics concerns the function of proteins, and apobetics concerns the purpose of the genetic code.The current view of inheritance taught in our schools and colleges is Mendelian. Darwin imagined inheritance to occur by a blending of the characters of each parent, but Mendel showed that inheritance was particulate—it was carried by discrete particles in discrete states. These particles became known as genes, and genes were eventually found to be coded segments on the DNA molecules that make up chromosomes in the nucleus of cells. Darwinists today view all of inheritance as genetic, and because genes can change more or less indefinitely, they identify this as the obvious means to explain how everything has evolved from something else during the supposed millions of years of life on Earth.But Mendel’s work only explained the things that changed during inheritance, not the things that remained the same. For example, he used varieties of pea plants that had round or wrinkled, green or yellow seeds. He simply took for granted, and thus overlooked, the fact that the peas produced peas. Darwinists
today still remain blind to this fact and insist that peas will eventually produce something other than peas, given enough time. There is certainly enormous variability in all forms of life, yet all our experiments in plant and animal breeding still show the same result—peas produce peas, dogs produce dogs and humans produce humans. Unfortunately, creationists today still tend to do their reasoning on the subject of inheritance in Mendelian terms. It is time that we developed a theory of inheritance, and this article (in three parts) is an attempt to outline some principles required for such a theory. Here, in Part I, the nature of inheritance and of information will be considered, emphasising the 5-dimensional Gitt theory of information. In Part II, the ‘information challenge’ (where did the new information come from in ‘goo to you’ evolution?) will be reformulated in terms of the Gitt theory of information. And in Part III the biological mechanisms for control of information transfer and change will be examined in the light of the young age principles. Static and variable inheritance structures If inheritance was totally Mendelian, this would indeed favour the Darwinian model because, in principle at least, any and every part of a chromosome can be chopped and changed, and therefore variation should be unlimited. The ‘in principle’ rider is important because both internal and external constraints operate in practice. One external constraint, for example, is the survival of the organism, which requires practical limitations on the amount of change that can occur in any one generation. One internal constraint is that choices made at any particular stage in a selection process will shut off the deleted options for later stages in that lineage. Furthermore, the two sexes need to be genetically compatible for reproduction in order to pass on any change to the next generation.But this argument leads to a paradox—chromosomes are potentially infinitely variable, while organisms are not infinitely variable. Is this just a matter of practical constraint, as Darwinists would argue, or is something more fundamental at work? Could it be that chromosomes are not the sole determinants of inheritance?Cytoplasmic inheritance1 is now well documented. Organelles such as mitochondria, chloroplasts and the centriole all have DNA of their own that is passed on directly to the daughter generation in the cytoplasm of the mother’s egg cell, independently of chromosomal DNA. But this kind of inheritance is still particulate, coded and Mendelian. There is another kind of inheritance that is quite different—structural inheritance.Living cells are extraordinarily complex in their structural and functional organization, as modern textbooks on cell biology testify.2 However, the more we study cells, the more we discover of their complexity. There seems to be, as yet, no end to their astonishingly intricate designs. Not only are they intricate and complex, they are amazingly fast and accurate in what they do. For example, the enzyme carbonic anhydrase can break down a molecule of carbonic acid in under 2 millionths of a second. Chemical reactions that go so fast need to be precisely controlled and integrated with other cell reactions, otherwise they will just as quickly go wrong and wreak havoc in the cell. And fatal diseases such as progeria and Tay Sachs disease can be produced by no more than one single mistake in the structure of just one single kind of molecule. Not every molecule is so intolerant of error, but the fact that some are means that not only can the cell avoid mistakes, but it can also normally correct them when they do occur to the supreme standard of 100% accuracy.Such incredibly fast and accurate biochemistry at a submicroscopic level requires a wondrous array of minute transport, communication and control systems, otherwise chemical chaos would produce a plethora of unwanted (and fatal) cross-reactions. All of this structure is contained in the mother’s egg cell and is passed on in toto to the daughter cells. As a result, the fast and accurate biochemistry of the mother’s cell continues, seamlessly, to occur in the daughter cells without any interference from mutations or recombinations that might have occurred in the chromosomes.If mutations or recombinations have occurred in the chromosomes in such a way as to modify the behaviour of the daughter organism relative to its ancestor, then such effects will come into play during the subsequent development of the offspring as nuclear information is used by the cell to guide the development and behaviour of the new organism.Most of this structural inheritance has been overlooked by biologists. Until recently it was thought that cellular components moved passively from parent to daughter cells during cell division, carried along by the cell-division mechanism that duplicated the chromosomes and pulled them apart into the daughter cells. However, in 1999, Yaffe3 found that there was a complex of cellular machinery associated with the cytoskeleton that coordinates the distribution and movement of mitochondria throughout the cell. Recent developments in microscopy have allowed these structural components and their movements to be viewed in live cells. 4 If mitochondria are catered for in this way, then obviously other cellular components are equally well catered for when it comes to cell division. Organelles such as mitochondria, peroxisomes, etc. then divide and proliferate in the daughter cell, once again independently of the replication that goes on in the nucleus and in the whole cell.Mutations can occur in mitochondrial DNA, and this has been used to trace ancestral lineages in humans and other species, on the assumption that no recombination occurs in mtDNA. However, the recent discovery that recombination also occurs in mitochondria casts these types of studies into doubt.5 Such studies show that inheritance goes beyond the nuclear chromosomes, but it still ignores the microstructure of the cell that is so essential for all of these processes to occur. Cellular inheritance Genes can no longer be seen as the cause of biological inheritance because we now know that control over their expression (i.e. their being switched on and off when needed or not needed, respectively, and the timing of these events) comes from epigenetic mechanisms operating in the cell. 6 This suggests that the DNA simply provides a ‘library’ of information and the use of that information is controlled not by the genes themselves but by the cell.If the cell, and not the genes, control inheritance, then certain observations that puzzle Darwinists become explicable. For example, Australian rock hopper wallabies display an incredible array of chromosomal aberrations, yet all within a group of species that are so similar to one another that most people cannot tell them apart.7 The chromosomes have been grossly scrambled, yet the cell is still able to extract the information it needs for survival. If the genes had been in control during such a scrambling process, Darwinists would expect it to take about a hundred million years, but the evidence suggests quite recent divergence of these species.A similar pattern of cell stability in the face of genome change is constantly at work in bacteria. It has been found that new gene sequences are continually being brought into bacterial cells and spliced into the bacterial genome. 8 The bacterial genome does not keep getting bigger, however, because it also has a complementary method of getting rid of unwanted or useless sequences. The result is that the bacterium is continually ‘sampling’ its genetic environment, looking for new gene sequences that might be useful in the ever-changing world around it. Throughout all this change, the bacterium maintains its integrity as a bacterium. For example, a study of the bacterium Escherichia coli over 10,000 generations found that at the end, ‘almost every individual had a different genetic fingerprint’, yet they were still Escherichia coli.9Only if the cell is in control can we explain these observations.Another kind of evidence comes from the architecture of cells. When cell membranes were transplanted by microsurgery in ciliates, for example, the transplanted membrane pattern was inherited even though the DNA had not changed.10 This provides direct evidence for inheritance of cell architecture from cell architecture.An illustration of how cell architecture and DNA interact is provided by an organelle called a ‘peroxisome’, which detoxifies cells by breaking down hydrogen peroxide. Peroxisomes self-replicate by binary fission and, like all other organelles, are passed directly from mother to daughter in the cytosol. Certain chromosomal mutations will suppress peroxisome development and it was originally thought that such mutant cells therefore lacked peroxisomes altogether. Further study, however, showed that a structural remnant of the peroxisome continued to be present, and was inherited, and
it could be resurrected in subsequent generations by reversal of the chromosomal mutation. 11 Thus, it seems that the cell passes on structural components upon which the genes act in a cooperative way to reproduce the architecture of the mature daughter cell.So here we have an obvious source for the fixed information that maintains the integrity of the created kinds. When reproduction occurs, it is not just chromosomes that are passed on to the offspring, but whole cells—complete with cell walls, cytoplasm, organelles and the elaborate and extensive transport and communication and control networks that connect cells inside and out. These things are passed on independently of the genetic shuffling that occurs on the chromosomes. Thus, it is biologically possible (and perhaps blindingly obvious) to identify the cell as the unit of inheritance, not the chromosomes. Since cells appear to pass unchanged from parent to daughter generations, this could explain why organisms reproduce ‘after their own kind’ and are not infinitely variable as Darwinists assume. The nature of information Inheritance occurs by the transmission of information from parent to daughter generation. Because genetic information (i.e. that which is coded on the DNA molecule) is superficially easy to understand, it has dominated scientific thinking on inheritance. Yet the concept of information itself is quite complex and this complexity has limited creationists’ ability to break away from the Mendelian mould.Information theory only began as a discipline in 1948 with the publication of Claude Shannon’s classic paper, entitled A Mathematical Theory of Communication.12 He was working on electronic communication (radio, television, telephone) and needed to create a high signal-to-noise ratio that would ensure accurate transmission of messages. While he acknowledged that messages ‘frequently have meaning’, he went on to say that ‘These semantic aspects of communication are irrelevant to the engineering problem.’ He quantified information statistically, in terms of all possible ways of arranging the symbols that carried the messages.Another approach to quantifying information is called algorithmic information theory. In this view, the information content of any object is defined as the shortest binary computer program that would adequately describe it. In one of the pioneering papers in this field, Gregory Chaitin claimed that his method was theoretically capable of describing biological systems, but he also acknowledged its practical limitations: ‘We cannot carry out these tasks [i.e. biological descriptions] by computer because they are as yet too complex for us—the programs would be too long.’ 13 Creationist biophysicist Lee Spetner used an algorithmic approach to enzyme specificity to determine whether genetic mutations could produce new information. 14 While he concluded that mutations could not do so, others have claimed that a more rigorous application of his method shows the opposite result, that mutations can produce new information.15 This illustrates the potential complexity of information arguments.Intelligent Design theorist William Dembski has identified his work on complex specified information as constituting a theory of information different to the former two. 16 He defines information in its most general sense as ‘the actualization of one possibility to the exclusion of others’ and claims that ‘this definition encompasses both syntactic and semantic information’. He thus treats information as a multidimensional entity, not just a one-dimensional entity as Shannon and Chaitin treated it. His first dimension is statistical—he defines complex as being ‘an improbable arrangement of elements’. He then includes dimensions of syntax (ordering rules) and semantics (symbolic associations or meanings) when he defines specified as ‘conforming to a predetermined pattern’. But Dembski’s work stops there. Information specialist Werner Gitt goes on to show that information actually has five dimensions.17 The Gitt theory of information In his book In the Beginning was Information, Gitt did not apply his analysis to biology in any detail, so I will here explain it by applying it to biological information and to information as expressed in the English language. The genetic code consists of four bases (the genetic alphabet) taken three at a time (the genetic words). The four bases are guanine (G), adenine (A), cytosine (C) and uracil (U).18 Four bases taken three at a time yield 64 possible three-letter genetic words (there are no one-, two-or four-letter genetic words). There are twenty amino acids and each three-letter ‘codon’ (word) represents one amino acid or a ‘stop’ or ‘start’ sign. Several different codons can represent the same amino acid (since 64 is greater than 20) but each codon represents only one amino acid. For example, GCA, GCC, GCG and GCU all represent alanine, and UAA, UAG and UGA all represent the ‘stop’ sign, but AUG alone represents methionine.Let’s now consider some three-letter English words for comparison. Cat, mat, bat, hat, fly and sky are all three-letter English words that carry approximately similar Shannon-type statistical information content. Yet we all know that these words carry much more information than just the statistical properties of their letter frequencies. The most obvious extra dimension is their semantic content. ‘Cat’ represents a furry, four-legged mammal, ‘bat’ represents a flying mammal, ‘hat’ is a shading device placed on human heads, etc. In an exactly parallel fashion, the genetic codons UUU and CGA have semantic content as well—the former represents the amino acid phenylalanine, and the latter represents arginine.The next dimension of information is syntax—the place value or ordering rules of the words. The English sentence ‘A bat can fly in the sky’ is meaningful, but ‘The sky can fly in a bat’ is not. Likewise, syntax is a component of the meaning of genetic words. For example, the correct sequence of amino acids in the enzyme hexosaminidase A can produce a healthy human child, but a single error in that sequence can produce a child with the fatal Tay Sachs disease.A fourth dimension of information is pragmatics—the practical functionality of words. For example, ‘a bat can fly in the sky’ is a statement about the capability of bats. This statement could have a practical application in a children’s book, for example, to teach children about the world around them. Information always has some practical application; it does not just float around in the air waiting for somewhere to settle and become meaningful. In an exactly parallel way, the amino acid sequence in hexosaminidase A has a practical function in preventing the abnormal build-up of fatty substances in human brain cells.The fifth dimension of information is apobetics (teleology or teleonomy)— the overall purpose for which a particular word sequence is produced. In the case of the children’s book cited above, the overall purpose is that parents want their children to learn about the world around them so that they will grow up to be good citizens (and perhaps look after their parents in their old age). In the case of the amino acid sequence in hexosaminidase We can now see that Shannon’s statistical approach to information ignores all four of these ‘extra’ dimensions of information. The reason is quite straightforward—Shannon was originally interested in quantifying the concept of information, and there is no easy way to quantify semantics, syntax, pragmatics or apobetics. They are no less real, however, and this is the challenge that creationists face. We cannot simply say, as Shannon did, that ‘[the] semantic aspects of communication are irrelevant to the engineering problem’. They are certainly not irrelevant to the biological problem. The higher dimensions of biological information Fifty years of molecular biology have produced enormous advances in knowledge, but you won’t find any discussion about these ‘extra’ dimensions of biological information in any standard textbook on biology. No doubt, progress could continue without ever addressing the issue. But no biologically realistic worldview can develop without addressing this question, because it is here that we find ‘meaning’, ‘order’, ‘practical application’ and ‘purpose’. To incorporate these extra dimensions into our understanding of biology, we first need to know more about them. Semantics The essence of semantics is symbolism. The English word ‘cat’ has no statistical, alphabetical or biological relationship with the furry mammal that it refers to. The relationship is purely arbitrary. The equivalent (and different) words in Russian, Chinese and Arabic are entirely as satisfactory for the intended purpose as the English word. English speakers at some time
in the past chose to use the word ‘cat’ and we continue to use it by convention in order to maintain effective communication. In every language the relationship between the furry mammal and the word that represents it is purely symbolic. Symbolism is an activity of the mind that does not have any physico-chemical basis in biology. A multilingual human can speak about a cat in several different languages, yet say exactly the same thing using different symbols. The mind—and nothing else— makes the connection between the words and the objects that they symbolize.In the genetic code, the relationship between UUU and phenylalanine is likewise symbolic. There is no physicochemical or biological reason why UUU should not represent glycine, lysine or serine rather than phenylalanine. At some point, ‘someone’ made a choice and decided that UUU would represent phenylalanine. And in order to maintain effective communication between parent and daughter cells, the convention has been strictly maintained ever since. While some variations from the standard code do exist in some microbes and mitochondria, the symbolism is strictly maintained within each such lineage. Indeed, the slight variations in the code highlight the purely arbitrary nature of the relationship between codon and amino acid—the symbols can be changed! Since semantics is based on symbolism, and symbolism is a purely mental connection between object and symbol, this may explain why evolutionary biologists have ignored the matter of the ‘extra’ levels that exist in biological information. They do not want to admit any such anthropomorphisms (or worse) into their naturalistic biology.
Syntax The essence of syntax is structure. As already mentioned, the English sentence ‘A bat can fly in the sky’ is meaningful, but ‘The sky can fly in a bat’ is not. Word order in English is crucial to meaning. Yet the rules of English syntax are arbitrary—the rules are different in other languages. In Greek, for example, word order can be changed without changing the meaning, but different word orders will give different emphases to that same meaning.Syntax in the genetic code is like the English language where word order is crucial to meaning. One of the smallest biologically useful protein molecules is insulin. It contains 51 amino acids. Now there are 2051 = 1066 ways of arranging 51 amino acids into chains, but only a very small number of these are biologically useful. For example, beef insulin differs from human insulin in only two places, and pork insulin in only one place. Even fish insulin is close enough to human insulin to be effective in humans. Hexosaminidase A is about an average-sized molecule and it contains 529 amino acids. There are 20 529 = 10688 different ways of arranging 529 amino acids into a protein chain, but just one single error in the sequence can be sufficient to produce the fatal Tay Sachs disease. Other proteins can be much larger—the muscle protein titin, for example, consists of 27,000 amino acids. The number of wrong ways in which the amino acids in these proteins could be assembled is approximately 20 27,000 = 1035,127. So the fact that they are usually assembled in precisely the correct order, and only allow the most minute variations, testifies that cells are extremely sensitive to syntax in the genetic language. Pragmatics The essence of pragmatics is context. The English sentence ‘A bat can fly in the sky’ tells us something about the capabilities of the small, furry mammal (it can fly) and where it can exercise that capability (in the sky). But this sentence has no function on its own. It is entirely dependent upon the context of an English-speaking writer and/or reader to become functional. Its function is also likely to be just one component part of some larger work that describes batsin greater detail. Just as an English sentence requires a context (writer and/or reader) to be functional, so the function of a protein molecule is entirely dependent upon the cell. Life does not exist outside of cells. Viruses are simpler than cells but they can only reproduce inside functional host cells. Some microbes can have acellular stages but they retain a full complement of cell contents and mechanisms and require a cell stage to complete their life cycle.The biological function of a protein does not come just from its amino acid sequence, but from its three-dimensional shape. The precise amino acid sequence in a protein chain determines the ways in which it is able to fold into that three-dimensional state. The wrong amino acid in the wrong place may produce a 3-D structure that is out of shape and so fails to achieve its required function. Furthermore, other proteins, called chaperones, are necessary for the correct folding of many proteins; so the amino acid sequence only generates the correct shape in the context of a cell with chaperones. Moreover, the context within which each molecule in a cell exercises its function is extremely dynamic—the molecule must appear when and where it is needed and then disappear when and where it is not needed. If, for example, hexosaminidase A does not appear at the right time and place and/or does not function properly, then fatty ganglioside molecules build up in brain cells, causing the brain cells to degenerate and the child to die. Apobetics The essence of apobetics is inverse causality—present processes occur because of some future goal. All human languages have a purpose—communication between individuals. A vast range of other organisms (perhaps all organisms) also communicate in many and varied ways, and each has a purpose in doing so, but only humans use syntactic language. For example, white-tailed deer communicate alarm by flicking up their tails. The flash of the white tail has semantic content—it means danger is near. But it has no syntax capability like in the English language, where 26 letters can be combined in different ways to form hundreds of thousands of words that can be then arranged in an infinite number of ways to communicate unlimited different ideas and messages. In further contrast, apes can learn hundreds of symbols and can communicate quite a range of semantic content, and their communications also show pragmatic and apobetic content, but they have no syntax capability like humans.The language of DNA also has purpose. The discipline of embryology would be incomprehensible without apobetics. For example, the large, bony plates on the back of the stegosaur are of no practical
use to the embryo, yet the stegosaur embryo develops these plate structures. The reason it does so is for the benefit of the adult (it is currently supposed that the adult used them for temperature control). The end (the benefit to the adult) determines the means (the development in the embryo). Non-biological causality usually proceeds the other way around— the cause precedes the effect. But in biology, the effect (embryonic development) precedes the cause (the needs of the adult organism). This inverse causality is the essence of apobetics. In Part II of this paper, when we use the Gitt theory to analyze information change, we will find that apobetics is the major determinant of information change. Applying the Gitt theory of biology It is genetic engineers, not Darwinists, who are using biological information to its fullest extent. They are the ones who look for semantic content (i.e. what protein a particular codon sequence refers to), whereas Darwinian phylogeneticists simply use the overall similarity between DNA sequences (irrespective of semantic content) to construct phylogenetic trees. Genetic engineers are the ones who are working out the syntax of genes (i.e. where they occur on the chromosomes and what their relationship is to adjacent and/or internal non-coding sequences). They are the ones discovering pragmatics (i.e. what the genes actually do). And they are the ones who are applying their knowledge to novel purposes (apobetics) such as gene therapy and improved crop production. Such an analysis of biological information is lethal to Darwinism because what Darwinists dismiss as ‘the appearance of design’ becomes ‘intelligent design’ in the hands of the genetic engineers. Yet even the genetic engineers, it seems, are mostly oblivious to the implications for intelligent design that their work entails. But the fact that genetic engineers are forging ahead without producing any new biological theory of information illustrates how difficult it is to grasp and implement these concepts. However, Italian biologist Marcello Barbieri believes he has found a way of moving on from the ‘statistics only’ view of information through what he calls the semantic theory of biology.19 He argues that we cannot make progress in this area until we find a mechanical model from which we can develop a mathematical model, which we can then use to integrate and organize the information and make experimentally verifiable predictions.By way of explanation, Barbieri points out the mechanical and mathematical models underlying Darwin’s theory. Darwin developed his theory of natural selection by bringing together the experimental results of plant and animal breeding (i.e. organisms reproduce with slight variations that are subsequently inherited) with the population model of Thomas Malthus (i.e. populations grow exponentially, forcing a competition for resources). Barbieri then uses a computer as a mechanical model of the Mendelian (genetic) view of life. A computer with its hardware and software is a good analogy, taking the cell as the hardware with the genome as the software. But computers do not ceaselessly repair and reproduce themselves, as cells do, so this clearly exposes the inadequacy of the genetic view of life. Something more is needed.Barbieri has brought together the problem of embryonic development (i.e. how can one cell differentiate into something as complex as a tree or a human being?) with an ingenious mathematical solution that he developed to the problem of reproducing computed tomography images from a less-than-complete set of data. Analytical solutions (that is, straightforward exact solutions) to the computed tomography problem exist, but only for impractically small data sets. For real life (large) data sets, an iterative method is required. But working iteratively with a complete set of tomographs is deadly slow and uses huge amounts of computer memory. Barbieri discovered that by adding a memory matrixto his results matrix (i.e. not only keeping track of the current best picture, but also remembering highlights from the past) he could rapidly converge onto the required image with as little as 10% of the full complement of tomographs.Applying this principle to embryological development, Barbieri argues that growth from zygote to adult is a process of reconstructing the adult organism from incomplete starting information (i.e. only that which is in the zygote). His model predicts the existence of biological memory matrices that assist the process, and he is able to name at least some of them. For example, when embryonic cells differentiate they remain differentiated for life. A memory of differentiation must therefore be lodged somewhere within each cell. Similarly, the location of each cell within the body plan of the organism is remembered for life (and can be considerably rearranged during insect metamorphosis), so a memory of body plan must exist somewhere. He cites other examples as well.Now for a memory to be a functional part of an organism (or a computer) there must be a code that relates each item in the memory to its functional complement in the organism. As an example, the genetic code relates DNA codon sequences (i.e. the genetic memory) to functional amino acid sequences in proteins. In a similar way there must be a differentiation code that relates the information in the ‘differentiation memory’ to the repair mechanisms in the cell that ceaselessly maintain the cell in its differentiated state.Barbieri admits that much work needs to be done to develop and test these ideas, but he certainly seems to have opened a door to new ways of looking at life. The three main points of his semantic theory are:The cell is fundamentally an epigenetic, rather than a genetic, system (i.e. cells and not genes control inheritance). While the genes provide a genetic memory for the cell, there are other memories (waiting to be discovered and described) that assist in many aspects of embryonic development. Each memory has its associated code—an arbitrary but irreducible and essential semiotic (see below) system—to enable the memory information to be implemented within the ceaseless self-maintenance of the cell. Conclusion The Gitt theory of information provides a whole new way of looking at biology. Purpose (apobetics) becomes the primary concern, rather than chance, as in Darwinism. Stasis of the created kinds requires the conservation of biological information, not the continual change that is required in Darwinism. Multi-dimensional information is also a very complex subject and requires a new way of thinking about life. Barbieri’s semantic theory of biology may provide a way ahead.In Part II of this article, I shall reformulate the ‘information challenge’ (where did the new information in ‘goo to you’ evolution come from?) in terms of the Gitt theory. In Part III (to appear in a future issue of JoC), I shall look at experimental evidences for the way information is transferred and changed in biology.A parallel can be drawn between information, as expressed in the English language (left), and biological information (above). The five dimensions in Werner Gitt’s theory of information (see previous image) can be applied to understand both the genetic code in DNA and the English language system. Inheritance of biological information—part II: redefining the ‘information challenge’ by Alex Williams The ‘information challenge’ (Where did the new information for ‘goo to you’ evolution come from?) raises lots of questions for creationists when viewed in the light of Gitt’s multidimensional theory of information. It highlights Creationists need to develop a new attitude towards biological information, and develop new tools for discovering its multiple levels of meaning. Despite this challenge, however, the Gitt theory provides a stunning confirmation of a creationist position because the true nature of biological information rules out a chance origin and requires intelligent design.
Figure 1. The late Stephen Jay Gould used Scilla’s coral as an icon to illustrate the structure of Darwinian theory. The trunk represents natural selection.In Part I of this article I pointed out that information is conventionally treated as a onedimensional statistical entity, but creationist Werner Gitt has shown that information is a five-dimensional nominal entity. By nominal we mean that information can be named (i.e. identified) but it cannot be explained in terms of matter or energy so it is a third fundamental component of the universe after matter and energy. Despite this revolutionary new understanding of information, creationists appear not have made any progress in applying it to biological problems. In this article, I use the Gitt theory to redefine the ‘information challenge’ that creationists have been bringing against evolutionists. And in a third article in this series, I will look at control of information transfer during inheritance in the context of the Gitt theory. Darwinian treatment of biological information Creationists commonly challenge evolutionists to explain how vast amounts of new information could be produced that would be required to turn a microbe into a microbiologist (or ‘goo to you’ and other catchy alliterations). We shall look at this challenge in detail shortly, but before we proceed, it is instructive to look at how leading Darwinists have handled the problem of information in their own worldview. They seem not to have dealt with it at all, and perhaps have deliberately ignored it.No Darwinist appears to have developed a full theory of information—it took a creationist to do so. Indeed, a prominent cause of Darwinism’s survival is that the true nature of information has not been properly understood (and perhaps even suppressed). One reason for this is that Darwinian evolution is a mechanical theory that was born in a mechanical age (the Industrial Revolution) and information theory only began in the mid-twentieth century. Darwin’s theory is based on four main propositions: organisms produce offspring that differ slightly from themselves; they produce more offspring than survive to reproductive age; there is a struggle for survival; and those individuals most suited to their environment are naturally selected and they pass on their genes to future generations. Although information is passed on in this process, no information is needed to drive it, just the ‘blind forces’ of nature. This has allowed Darwinists to occupy themselves with the ‘blind forces’ and to ignore the true nature of information.Let’s look at some examples. In a review of evidence presented for evolution in ten biology textbooks, 1 the best example that addressed the ‘information challenge’ is the case of four-winged fruit flies being produced by mutation from two-winged fruit flies. But the extra wings arose from three mutations that switched off existing developmental processes. No new information was added. Nor was any new capability/functionality achieved—the extra wings were non-functional and the fly was a cripple.One of the most authoritative works in print at present on evolutionary theory is the late Stephen Jay Gould’s 1,433page The Structure of Evolutionary Theory. After a lifetime of challenging Darwinian gradualism and its adaptationist storytelling, Gould’s opus magnum reveals that the foundation of all evolutionary theory is still natural selection. 2 Everything that has happened since Darwin, has served to change the downstream details that flow from natural selection, but nothing has displaced natural selection from the foundation. While he does use genetic arguments when they suit his purpose, not one of the 348 headings in his table of contents deals directly with subjects like information, genetic code or DNA, nor do these words appear amongst the 2,600 items in the Index. At no point does he formulate evolution as an information-creating process.Darwinian philosopher of science Michael Ruse also recently addressed the issue of design in biology.3 He, like Gould, covered the history of biological thinking in great detail, but failed to even mention the subject of biological information.When asked by creationists if he knew of any biological process that could increase the information content of a genome, Oxford Professor Richard Dawkins could not answer the question. 4 He later wrote an essay on the subject titled The Information Challenge5 but even in the essay he could not give a single example of a mutation that could increase the information content of a genome. This is not surprising, for both Gitt 6 and Dembski7 have independently shown that no naturalistic process can produce new information. Gitt has also pointed out that information is a non-material entity, which further elucidates why naturalistic material processes cannot create it. This theorem has the status of a natural law that Dembski calls the ‘Law of Conservation of Information’. It states that naturalistic processes can use, transfer or degrade information, but they cannot create it. Information only comes from information, and ultimately from an intelligent source.Dawkins’ failure to have any answer at all when first questioned on the subject illustrates that his information analysis, as published in his essay, is completely uninformative. He based his analysis on the Shannon theory, which deals only with the statistics of information systems. This theory defines information as a numerical property calculated from the number of ways in which the system can be configured. In this concept, a random string of letters can have more ‘information’ than a meaningful sentence.Evolutionary physicist Hubert Yockey has been investigating the role of information in biology for many years. He has not been able to progress beyond the Shannon theory, but he does appear to recognize the impossible barriers that information poses to the naturalistic origin of life. He has come up with a quasi-solution that it is undoubtedly a matter of chemistry, but the actual mechanism may be beyond the scope of human reason to grasp. He writes,‘There is nothing in the physico-chemical world that remotely resembles [the genetic code]. The existence of a genome and the genetic code divides living organisms from non-living matter. … [Neils] Bohr argued that life is consistentwith but undecidable by human reasoning from physics and chemistry.’ 8Which, interpreted, means they have no idea how the genetic code could arise spontaneously from non-living chemicals.Evolutionary quantum chemist John Avery has recently published a book on ‘Information theory and evolution’ which summarises quite well how evolutionists misinterpret and misrepresent the evidence on information.9 Avery defines information in terms of Shannon’s theory, and points out that ‘thermodynamic information’ is coming to us continually in photons from the Sun, and he attributes the origin of life to this source (p. ix). He then ‘explains’ that it is only ‘Gibbs free energy’ (a favourable energy balance between reaction terms in chemistry) that can drive a chemical reaction, and ‘life maintains itself and evolves by feeding on Gibbs free energy’ (p. 174). The implication (for the unwary reader) is that ‘information’ in sunlight can explain the information in living organisms and the information needed for evolution from microbe to man.However, in chapter 5 he admits that there is a difference between thermodynamic and cybernetic information (although he does not say what the difference is). Cybernetics is the field of communication and control in machines and living organisms. So Avery’s admission means that the information in sunlight cannot explain the information in intelligently designed machines and living organisms. Indeed, the full sentence quoted above is:‘Life maintains itself and evolves by feeding on Gibbs free energy, that is to say, by feeding on the enormous improbability of the initial conditions of the universe.’In admitting that the ‘initial conditions of the universe’ were ‘enormously improbable’ he is inadvertently admitting that it was intricately designed, because ‘enormously
improbable’ events don’t happen by chance. The evidence for special creation is right there in front of him but he cannot (or will not) see it. The information challenge When viewed in the light of the multidimensional nature of information, the ‘information challenge’ that creationists commonly throw up to evolutionists, is not at level, the information challenge can be stated in two parts as follows:The human genome is much larger and contains more genes than that of a microbe.What naturalistic mechanism does an evolutionist have to explain the increase in information content from microbe to man?This seems to be a reasonable wellformulated question, but is it really? Consider the following facts. The genome of the Anthrax bacteriumBacillus anthracis contains about 5 million base pairs while the human genome contains about 3 billion base pairs. Thus, at a statistical level, it seems to take almost a thousand times more information to make the human. This kind of analysis seems to be confirmed when we look at an intermediate-scale organism such as rice (Oryza sativa) the genome of which contains an intermediate value of 466 million base pairs.However, the reasoning starts to fall apart when we look at genes rather than base pairs. The bacterium contains about 5,500 genes, but humans have only 20 to 25 thousand genes. 10 Surely humans are more than four times more complex than bacteria! Furthermore, the rice plant has an estimated 46,022 to 55,615 genes,11 so it appears to take more genetic information to make grass (rice belongs to the grass family) than it does to make a human! Suggested solutions to this paradox lie in two main areas. On the one hand, perhaps the rice genome is heavily redundant and contains a lot of repeated information. On the other hand, human genes (and probably rice genes as well) can be read in different ways (a process called ‘alternative splicing’) and edited in different ways to produce numerous different products from the same gene. 12 Also, humans, and others of the more complex eukaryotes, have a huge amount of DNA that does not code for proteins. What this does is only slowly starting to be discovered. A recent paper implicated quite a bit of it in regulating embryo development in mice. 13 Whatever the final resolution to this apparent contradiction, however, it illustrates that our ignorance still far outweighs our knowledge in these areas and we need to be careful.Human gender provides us with another challenging example. The X and Y chromosomes determine gender. XX yields a female, and XY yields a male. Now the Y chromosome (with about 50 million base pairs) is only one-third the size of the X chromosome (with about 150 million base pairs), but it contains a mosaic of ‘maleness’ genes that are not present in the X chromosome.14 So, does it take more, or less, information to make a male than a female?From the point of view of statistics (total amount of DNA code), it takes about 100 million base pairs less to make a male than it does to make a female. However, if we go the extra step up the information ladder and look at genes, we come to the opposite conclusion, that it takesmore genes to make a male than it does to make a female.Let us now see what happens when we take semantics, syntax, pragmatics and apobetics into account (Gitt information theory—see part I, p. 29).Since the X chromosome is always present (in healthy individuals), the default configuration is XX. Both male and female components occur in every embryo, but the XX chromosome combination will cause them to develop into a female. Only when the Y chromosome is present do the embryonic structures develop into a male. The XX pair of chromosomes are duplicates (one from the father, one from the mother) that may contain different copies of comparable genes (alleles). but they will carry essentially the same amount of total (statistical) information. From asemantic point of view, X means female and Y means male (with the implied condition that a complementary X is always present).In regard to syntax, the X chromosome has regions associated with more than 100 genetic disorders, while the Y chromosome is involved in only two disorders. Therefore, correct syntax in the X chromosome appears to be far more important than in the Y chromosome. Alternatively, the Y chromosome may be much less prone to mutations, due to the palindromic error-correction system that seems to operate in much of the sequence.14 Lack of variation in the Y-chromosome sequences has surprised researchers. 15In regard to pragmatics, the previously mentioned statistics illustrate that the X chromosome has enormous practical importance in constructing a healthy child of either sex. Male diseases such as prostate cancer and male breast cancer result from defects on the X chromosome, while it is clear that the SRY gene complex on the Y chromosome is crucial in developing male gonads, hormones and other sexual characteristics.And what about apobetics? What was the purpose in gender differences and sexual reproduction? This is a great enigma in evolutionary biology, because the enormous investment in sex that organisms have to make (the peacock tail is an extreme example), coupled with the dilution of an individual’s genes by 50% in the mating process, would surely cause natural selection to weed out such inefficiencies—or at least natural selection would not permit mutations to invent it (if it were possible) in an asexual organism. While some advantage comes from added variation in cross-fertilization and getting rid of some deleterious mutations, the advantage is not likely to exceed the 50% loss incurred in meiosis and the halving of the number of reproducers. In a number of cases, asexual species appear to be just as successful as congeneric sexual species.Given that there is a purpose in sex, however, that purpose finds its expression in the embryological implementation of the genetic blueprint. Since the purpose is to produce humans of two kinds, then from an apobetic point of view the two kinds are entirely equivalent. So the apobetic answer is ‘No, there is no more information required to make a male than a female.’ The information is simply packaged and dispensed in such a way that one combination (XX) produces a female and the other combination (XY) produces a male. Semiotics—the new science of signs As pointed out in Part I, the enormous gap between the true nature of information and that which is passed off as ‘information’ in our colleges and universities has not gone unnoticed. Workers on this problem in many different fields have recently discovered one another and have come together under the heading of ‘semiotics’.16 Semiotics is the study of signs, meaning and communication. The basic concept is the ‘semiotic triad’—a sign represents an object that has some significance to an interpreter. In genetics, the codon is the sign, the amino acid that it represents is the object, and the interpreter is the cell mechanism that implements the genetic instructions.This very simple recognition of what actually goes on in cells (as opposed to the Darwinian phylogenetic treatment of genomes merely as strings of symbols that are compared statistically) has created a minefield of controversy. One reason for the controversy is that the relation between the sign and object is arbitrary and cannot be explained in terms of the laws of physics. Thus, information is revealed to be a fundamental entity in its own right, not reducible to matter, energy or the forces that govern them. This principle is the first of Werner Gitt’s thirty theorems on information,17 and has been recognized by pioneer in biosemiotics Marcello Barbieri, 18 who therefore classed information as nominable (that is, it can be named) alongside the more familiar quantitative and qualitative entities of physics.Another reason for controversy is that the relation between the sign and the object is entirely dependent upon the context, and is independent of the nature of the sign or the object. A sign in one context might signify something entirely different in another context. This leads to the conclusion that the cell is the unique and crucial context for the meaning of genes, which appears to contradict Dawkins’ notion of the ‘selfish gene’. It also contradicts the notion that cellular life could arise from something other than cellular life (e.g. chemical evolution). Yet another reason for controversy is that the need for an ‘interpreter’ highlights the concept of ‘mind’ as something distinct from matter. Materialists vigorously dispute such conclusions, but they have offered no viable alternative explanations.A pioneering book (published on-line) in this field is The Organic Codes: the birth of semantic biology, by Marcello Barbieri, founder and president of the Italian Association for
Theoretical Biology.19 Barbieri cites Karl Popper and René Thom among his mentors, and he quotes the former as saying his semantic theory is ‘revolutionary’. While Barbieri is a committed evolutionist, his theory appears to be wide open to creationist interpretations.For example, his theory of semantic evolution says:.‘The origin and the evolution of life took place by natural selection and by natural conventions. The great events of macroevolution have always been associated with the appearance of new organic codes’ (p. 227).By ‘organic codes’ he means the protocols or conventions that exist within cells for reconstructing organisms from their originating cells, and these include things like the genetic code, the translation code, the splicing code, the patterning codes and (in humans) the linguistic code. His definition of the origin of an organic code is a gift to creationists:‘The origin of an organic code is the appearance of a complete set of rules, because when that happens it also appears something totally new in nature, something that did not exist before’ (p. 225).Creationists merely have to point out the irreducible complexity of the semiotic triad and the best explanation of ‘evolution’ (the origin of biological complexity) becomes special creation.In explaining why others have not uncovered what he calls the ‘organic codes’ he says that‘They can be discovered only if we are looking for them, and we can look for them only if we believe that they can exist. In order to build a semantic biology, therefore, the first step is a new mental attitude towards nature, even if this will probably be possible only with a new generation of molecular biologists’ (p. 233). Figure 2. The semiotic triad. In genetics, the amino acid is the object that is symbolically represented by the codon, which the cell interprets via the translation mechanism (the ribosome). One of the great challenges of ‘semantic biology’ find a way of treating ‘meaning’ in a quantitative way. Barbieri points out that the study of linguistics is producing a theory of group properties that may be relevant to biosemiotics (pp. 230–232). This again has creationist implications because the ‘universal grammar’ of human language is built-in at birth, and becomes particularised only when the child learns an actual language (p. 217). Research into artificial intelligence faces the same challenge of quantifying meaning. Recent use of the Internet is relevant here. The meaning of a word can be thought of as a point in the multidimensional space of all word meanings, and the relationship between any word and any other word can be gauged by putting each pair of words into a Google search on the internet. Word pairs for which Googlereturns a large number of hits are clearly more closely related than word pairs for which it only returns a small number of hits. Thus a quantitative measure of meaning emerges as a statistical association between words of related meaning. 20As outlined in Part I, the centrepiece of Barbieri’s theory is a model of development as a process of reconstructing the adult organism from anincomplete set of information (i.e. that in the zygote). He believes this is achieved by the zygote using one or more memories ancillary to the chromosomes (genes are just one kind of memory) that are each linked to development by an associated code (the genetic code is just one kind of code). Differentiation is one of several examples that he gives. When a cell differentiates in the embryo it retains its identity throughout the life of the organism, so there must be a memory of this lodged somewhere, together with a code that ensures the cellular repair mechanisms always maintain this identity. While the model still requires extensive investigation and validation, it provides creationists with a much more information-rich template to build upon than the naïve Mendelian model. It also makes testable predictions that we can possibly join with starting assumptions. Conclusion The expectation of those that have used the ‘information challenge’ seems to have been that evolutionists cannot answer it, but creationists can. There is certainly a huge information problem for evolutionists, but when it comes to a rigorous definition of biological information, creationists have a lot of work to do. In particular, when we try to formulate the question in terms of Gitt’s 5-dimensional theory of information, we encounter vast gaps in our knowledge of the way that cells store, use and pass on biological information. Clearly, a lot more theoretical and experimental work is required. However, defining information in terms of apobetics (purpose), which even the new secular field of semiotics does, seems to provide a stunning confirmation of creationist thinking—because the true nature of biological information rules out a chance origin and requires intelligent design. In Part III of this article, I will use the Gitt theory as a framework for understanding the experimental evidences for the control of information transfer and change in biology. Inheritance of biological information—part III: control of information transfer and change by Alexander Williams When viewed in the light of Gitt’s multidimensional theory of information, Darwinian evolution falls apart. The structure of life, thought by Darwinians to be purposeless, is revealed to be awash with purpose. There is a surprising amount of experimental support for the idea that cells (as well as genes) control inheritance, and this contradicts neo-Darwinism because the extra-nuclear cell contents are passed on unchanged during reproduction. It also provides the foundation for a creationist theory of baramin stasis. The concept of baramin stasis does not exist in secular biology, so creationists need to develop it.
Figure 1. The cross-species clone of a young gaur bull from a cow ovum does not represent a cross-baramin clone, for gaur (right) and cattle (left) probably came from the one baramin. In Part I of this article, I outlined the poverty of the Shannon theory of information as used in biology by evolutionists, and illustrated the 5-dimensional Gitt theory of information in biological terms. In Part II, I used the Gitt theory to redefine the ‘information challenge’ (where does the information come from in ‘goo to you’ evolution?) in creationist terms, showing that there is a vast gap in our knowledge of information storage, use and transfer in biology. Here, in Part III, I review experimental evidence on control of information during inheritance, and endeavour to develop a new perspective within a young age framework. How does biological information change? As Darwinists struggle to find answers to the ‘information challenge’ using only the one-dimensional statistical view of information, creationists now have a powerful 5-dimensional argument to bring to bear on the problem. Here are two examples. Antibodies and new enzymes The human immune system can conjure up new antibodies (which are protein complexes) to deal in a very specific way with just about any foreign organic material that enters the body. 1 Moreover, microbes can produce new enzymes (by changing existing enzymes) to metabolize synthetic organic molecules that did not exist prior to their manufacture by humans.2 Evolutionists have used both these lines of evidence to answer the ‘information challenge’ and argue that new information can arise by random mutations in existing biochemical pathways.But can new information really be produced by a random mutation? We can address this question using a comparison with human language.Let’s imagine that Romeo sends Juliet an email every day saying ‘I love you.’ But suppose that one day a spontaneous error occurs in the system and the email reads ‘I love Lou.’ Juliet goes out and kills herself because she thinks that (a) Romeo no longer loves her, and (b) he now loves someone else called Lou. But has any new information arisen from the spontaneous error? No. Romeo still loves Juliet, not someone called Lou, and Lou does not even exist. All that the error has done is to degrade the integrity of the intended information.In this scenario there is a change at the statistical level that appears to lead to a change at the semantic level—‘you’ and ‘Lou’ appear to refer to different people—but this is an illusion, because there is not a corresponding change at the apobetic level. That is, there was no change in the purpose of the message. Romeo’s intention in sending the email remained the same. For the new message to be true, Romeo’s intention would have had to change, but it did not, so the change to the message was an error, not a change in information content.In contrast, something quite different can happen in cells. For example, one of the steps in the degradation of the pesticide pentachlorophenol in the bacterium Sphingomonas chlorophenolica involves a reductive dehalogenase enzyme that may have evolved by random mutation of a maleylacetoacetate isomerase that is normally involved in degradation of the amino acid tyrosine.3 Why the difference between biology and the English language? One reason for the difference is that in common usage the English language is not generally designed to produce useful information by the random shuffling of its components, whereas cells have a number of systems that are designed to produce useful outputs via the random shuffling of components. Does this constitute new information? No, it doesn’t, as an analysis of the higher levels of information content will reveal.To do this, a more relevant example in English might be a soccer scoreboard. Let’s imagine that the scoreboard contains the information ‘Home Side 1, Visitors 0’. When the score changes to ‘Home Side 1, Visitors 1’ has the amount of information changed? No, it has not. The information content has changed, but no extra information has been added because the purpose of the information structure at the outset was to record varying score numbers. In a similar way, bacteria have informational structures in place to produce enzymes with the capability of changing their amino acid sequence. Some will be useless, some will be useful. Natural selection may ensure the survival of the useful ones, but a new, useful enzyme will not contain more information than the original system because the intention remains the same—to produce enzymes with variable amino acid sequences that may help in adapting to new food sources when there is stress due to an energy deficit.So, the Darwinian arguments are without force, since it is clear that organisms are designed to vary. When they do vary, they produce nothing new (at the apobetic level), they merely illustrate that the variable design is being implemented. Apobetics controls information change, not statistics.The challenge for creationists, on the other hand, is to identify the two different kinds of informational structures that are present in living organisms. In the soccer scoreboard analogy, the ‘Home Side’ and the ‘Visitors’ structures remain conserved, while the score values can vary according to the progress of the game. What is it that maintains the integrity of the created kind, and what components lead to the different species within the created kind? Structural information Cells and their structural components were created de novo, and (we might reasonably infer) have been passed down more or less unchanged since then, maintaining the integrity of the created kinds. Organisms today therefore contain an enormous amount of non-coded (primordial created) information in these structural components, as compared with the coded information that we find on the DNA molecule and elsewhere.How much non-coded information is contained in the structure of the cell? The algorithmic approach could be used here, and may be illustrated with a parallel question in human endeavour such as ‘How much information is contained in the Empire State building?’ Computer specialists could answer by calculating the length of the computer program that would be needed to specify the composition and manufacture of all the components, to direct all the building work, install all the services, establish and conduct all the businesses that use the building, and direct the finances and maintenance work that keeps the building running. In short, an architecturally
complex entity (a cell is actually more like a city than a building, but even more complex still because it can reproduce itself) carries an enormous amount of structural information. We are still in the same boat as Chaitin (see Part I) when he said in 1974 that ‘the programs would be too long’.So when we ask questions about biological information, it is naïve to simply look at the genetic component of information. Three billion base pairs of coded information in the human genome may well be miniscule compared with the enormous amount of non-coded structural information built in to the organism at creation. Information transfer We are now in a position to specify how information is transferred in a young age model of biology. The chicken came before the egg. Biology begins with an initial deposit of non-coded structural information in adult baramins. We could, in theory, quantify this information using an algorithmic approach, but for practical purposes it is enough to note that it isenormous and non-coded. Then there is created coded information in the chromosomes, with further smaller amounts in mitochondria and some other organelles. If we accept the Barbieri model (see Part II), then further codes also exist within the various memories that underlie development, but we should perhaps ignore them for the present, for we cannot deal with what we do not know.If we now ask ‘How is information transferred?’ there must be two parts to the answer. Baraminlevel information must be passed on unchanged, and species-level information must be subject to change. Since the purpose of coding is to provide a flexible information system capable of change, it seems fairly straightforward to propose that coded information in cells is the locus of species-level change. On the other hand, cell architecture is passed on unchanged and is thus the likely source of baramin stasis, although there also is much evidence that regions of DNA are highly conserved as well.How can this information change? The coded information can change by mutation or by enzymemediated recombination. By mutation, in this context, I mean a random change caused by a copying error or by some physical damage to the DNA caused by radiation or chemical insult. By recombination I mean crossing-over, insertions, deletions, transpositions, jumping genes and any other enzyme mediatedprocess. Since recombinations are enzymemediated, it reasonably implies that recombination are created to be the primary means of variation within baramins. Since mutations are arbitrary, and thus generally likely to be deleterious, it is reasonable to infer that the error correction systems were created to eliminate mutations.Can structural information change? Even though the initial deposit of cell architecture comes in toto from the mother, its further growth (replication of organelles, extensions to microstructures, synthesis and destruction of metabolites) presumably involves DNA transcription and is thus subject to variation. As the peroxisome example quoted in Part I of this article showed, however, there do appear to be structural components in the cell that are not deleted when the complementary genes are deleted. This is perhaps an area for further research. Error correction systems The widespread existence of error correction systems in cells argues powerfully for stasis because things will remain the same if random change is averted. However, there is a functional rider to this claim. Error correction is also required to keep the cell functioning. As anyone knows who regularly works with machines (e.g. cars, computers) errors cause chaos, and in the cell’s case, death. How much of the error correction machinery is aimed at function and how much is aimed at maintaining integrity of the baramin? Or perhaps the two aims are in fact one—are baramins functional peaks in an otherwise ‘flatland’ of non-functionality?Error correction and/or avoidance mechanisms operate at many levels, and their ubiquity and utility seems to contradict the neo-Darwinist claim that mutational errors are the driving force behind evolution and are thus central to the whole scheme of life. At the ground level, there is the redundancy in the three-base genetic codon arrangement that provides 64 codons to represent only 20 amino acids. This allows more than one codon to represent one amino acid, so any single mutation has a lesser chance of knocking out or changing an amino acid in the resulting protein. The mutation may simply change one codon to another which codes for the same amino acid.Sexual reproduction is another level of defence against mutational change. Adult organisms that reproduce sexually have the ‘diploid’ chromosome condition. In humans, for example, we each have 46 chromosomes that consist of 23 pairs, one copy of 23 from each parent. If there are defects in the copy from one parent, then the uncorrupted copy from the other parent can override the defect to produce a normal child. This mechanism provides a challenge for neo-Darwinists, because without it, and given enough time, asexual organisms should go extinct via mutational overload (called Muller’s Ratchet). Yet there are many asexual organisms surviving today. But even if both copies are faulty, there appears to be a ‘revert to saved’ function in some cases that does not use DNA as a template. 4 A leftover genetic imprint in the cell somewhere may provide the template, and if this is so, then it further supports the cellular control hypothesis.The next level of protection comes in the form of error correction routines in the chromosome copying process. In humans, the system is so effective that only about one error slips through in around 40,000,000 nucleotide copies.5 Then we have DNA repair systems that check the integrity of DNA strands and repair any damage. Cells that have unrepaired DNA are prevented from undergoing cell division, so this is yet another level of protection again. And if the mutation is severe enough, the cell kills itself by apoptosis, 6 thus providing yet another level of protection.Another level of protection comes with redundancy within the chromosomes themselves. Large stretches of the chromosomes consist of repeated segments so any mutations in these areas are likely to be insignificant because there still remain multiple copies of the original.The cell also gives special attention to certain regions of chromosomes that are known to be highly conserved. In contrast, others regions of chromosomes seem to be mutational hotspots. That is, during cell division, mutations are much less likely to occur in the highly conserved regions and much more likely to occur in hotspots. The cell thus appears to be able to control the mutation pattern to some extent. Insights from cloning experiments Some interesting insights into control of information during inheritance have come to us in recent years through experiments in cloning and chimera production. A clone is produced when the nucleus (i.e. the genome only) of one individual is transferred to an ovum from another individual (from which the nucleus has been removed) to produce a genetically identical individual to the first one. 7 A chimera is produced by inserting one or more whole cells (stem cells) of one organism into the early embryo of another organism to produce an adult that carries cells and tissues of both kinds. Figure 2. Chlamydomonas rheinhardtii, a single celled alga widely used in research. Photo by Yuuji Tsukii, Protist Information Server,
Dolly the sheep was the first reproductively viable mammal to be cloned.8 Dolly’s biological mother was a Scottish blackface ewe. The nucleus was removed from one of her egg cells, then the nucleus from a body cell (i.e. not a gamete, but a differentiated adult cell, in this case from the udder) of a Finn Dorsett (white faced) ewe was inserted into the vacant egg cell, and implanted into the womb of a third blackface ewe. The embryo grew normally and white-faced Dolly was born. When she grew up, she was mated and produced lambs of her own showing she was reproductively normal (although she aged and died prematurely).Inheritance at the subspecies level
(blackface/whiteface) was thus determined by the nucleus. But because both parents came from the same species (sheep, Ovis aries) this does not tell us about how the integrity of the created kind is maintained.Is it possible to produce cross-species clones? On 8 January 2001, a baby gaur bull (Bos gaurus) was born to a domestic cow (Bos taurus).9 The gaur is an endangered Asian ox and a skin cell nucleus was implanted into a cow egg cell to produce the baby bull. However, it is almost certain that the gaur is of the same created kind as domestic cattle, so while this is a cross-species clone it is not a cross-baramin clone.Cross-baramin ‘clones’ of a ‘lesser’ kind have been widely produced in which only a gene or DNA fragment has been incorporated via recombinant technology. For example, a Canadian company has produced artificial spider silk in the milk of transgenic goats.10 In this case, the cell maintains the integrity of the baramin (the goats are normal goats and the milk is normal milk but with extra proteins in it), but of course the inserted genetic component is only a fragment and not a whole genome. The real test of inheritance requires a full-genome cross-baramin clone.The closest report so far is a cross-genus experiment with common carp (Cyprinus carpio) and goldfish (Carassius auratus).11 The seven offspring (from 501 attempts) were virtually identical to the nuclear donor species (carp) in appearance and in most physical traits, but the number of vertebrae was in the range of the recipient species (goldfish). The authors speculated that a ‘segmentation clock’ early in embryonic development directs segmentation of the body and is controlled by the egg cytoplasm. This suggests Note on nuclear reprogramming that the ground plan for the body is controlled by the cell, Cloning experiments illustrate the extraordinary ability of and the details of the external morphology are controlled the nucleus to be ‘reprogrammed’ when transferred from an from the nucleus. This is consistent with the hypothesis adult cell to an ovum. In normal development, a zygote that baramin integrity is maintained by the cell and divides into the billions of cells of an adult mouse (for species-level variation is produced in the nucleus. example) and each of those cells differentiates and takes In regard to chimeras, the basic principles are best on very specific characteristics (e.g. eye, hair follicle, 12 illustrated with different strains of mice, because in epidermis, etc). The repair mechanisms in each of these chimeras of unrelated kinds some of the potential cells maintain this differentiated state for the lifetime of the offspring combinations are non-viable. When an 8-cell body. That is, the repair and replacement processes always embryo of strain A is combined with an 8-cell embryo of repair the skin cell as a skin cell, not as a toe bone or an strain B (or just with cells from the embryo of strain B) inner ear cell. However, when the nucleus of any one of and is implanted into a strain A mother, then a strain A those differentiated cells is removed and inserted into a offspring results, but having certain organs and tissues mouse egg cell from which the nucleus has previously been consisting wholly or partly of strain B cells. But by removed, the inserted nucleus gets ‘reprogrammed’ and chemically tricking the strain A embryo into doubling its the egg behaves as a fertilized zygote and goes on to chromosome number (thus turning the normal diploid into differentiate (again) into a whole new mouse. What controls a tetraploid) and then inserting strain B stem cells into it, this reprogramming—the cell or the nucleus? It must be the an exclusively strain B offspring is produced. This cell, because it is only the cell (ovum in this case), and not happens because the strain A tetraploid cells are unable the nucleus, that is in reproductive mode. to develop normally and thus the strain B cells ‘take over the drivers seat’.Chimera’s tell us at least two important things about inheritance. First, since pig/human and mouse/human chimeras have been produced, then it means that whole cells of one baramin are able to be ‘reprogrammed’ to function happily inside the body of a different baramin. 13 Second, the cell in the ‘driver’s seat’ (the inner cell mass of the pre-implantation embryo) determines the baramin of the offspring. Either cell line can (theoretically, at least) take over the reins of development. The distinction between baramins is maintained in the body of the chimera, yet they can function harmoniously together.Does this extraordinary discovery provide evidence of a Master Designer who can seamlessly interface different operating systems? The challenge is well illustrated by the history of personal computers. In the early days, there were many manufacturers in the marketplace, but none of the different machines could ‘talk’ to any other. Only two systems survived the competition (PCs and Macs) and they have gradually learned to ‘talk’ to one another. Producing a viable cell is one thing, but getting different kinds of cells to function together is a very much more advanced achievement. Patterns in embryology Embryogenesis provides us with incontrovertible evidence of maternal control over reproduction. In most animals (except mammals) everything that happens in the zygote up to the 128-cell stage (the blastula) is under the control of the maternal cell cytoplasm. No transcription of DNA from the zygote nucleus occurs until the mid-blastula transition (MBT) point. All the early cell divisions (called ‘cleavage’) occur within the existing mass of cytoplasm that was delivered with the maternal egg—no new cytoplasm is made. The only processes that occur are mitosis and DNA replication, and the resources needed for these come from RNA stored in the maternal cytoplasm. Indeed, the zygote nuclei can even be removed and the ovum will still produce a blastula.14 Only after the MBT does transcription from the zygote nucleus begin and the new organism begins to make its own RNA and remaining maternal RNA is broken down and removed.In insects, where there is too much yolk to allow full cell division, ‘superficial cleavage’ occurs and only the nucleus divides. When about 5000 daughter nuclei are produced, they migrate to the perimeter of the yolk, encapsulate themselves in a membrane, and only then do the homeotic control genes become active and start coordinating the activity of other genes in embryo development.This clearly shows that zygote DNA is only brought into operation after the cell has prepared the ground plan for it. This order of events seems to be confirmed by the carp-goldfish clone, 9 where the early development (vertebra number) was determined by the cytoplasm and the later development (external morphology) was determined by the nucleus.In mammals, transcription of zygote DNA begins after the first or second cleavage division in order to provide proteins required in the cleavage process. But whereas in other animals cleavage begins only a matter of minutes after fertilization, in mammals it does not begin until 12–24 hours afterwards. The cell is still in control in this period because it arranges the onset and early progress of cleavage, and it then co-opts the zygote DNA into providing construction materials for the continuing cleavage process. As in other animals, the real work of transcription—production of the genetically new offspring—does not begin until after the MBT. According to Gao et al.,‘Early development in mammalian embryos is supported entirely by [egg cell cytoplasmic] factors before embryonic genome transcription commences, and genetic variation in [egg cell] composition can have profound effects on early development.’15Thus, the groundwork of embryonic development is laid entirely by the mother cell, before it starts to implement the information contained in the nucleus of the zygote.In the single-celled bi-flagellate
alga Chlamydomonas, development is very brief—the zygote simply divides into four new vegetative individuals. But two of the most important post-fertilization processes are known to remain under cytoplasmic rather than nuclear control. First, two sets of DNA are carried in each gamete—the nuclear DNA and the chloroplast DNA. The nuclear DNA of both sexes (actually, strains called plus and minus) are amalgamated to produce the zygote nucleus, but only the plus chloroplast is transferred to the zygote—the minuschloroplast is digested and destroyed. The latter is accomplished by a nuclease enzyme present only in the plus gamete cytoplasm that is transferred to the zygote and then selectively imported into the minus chloroplast. Second, there are genes in the nuclear DNA that only become active when the zygote forms. This activation is accomplished by a homeodomain protein16 already present in the cytoplasm of theplus strain, which binds with an as yet unidentified protein delivered by the minus gamete. The new complex then activates transcription of the zygotespecific genes.17 Figure 3. Drosophila melanogaster, the fruit fly that provided the fundamental insights into genetics. Used with permission from J.A.T. Dow . Photo by Dow/Davies Laboratories, Glasgow. In the flowering plant, Arabidopsis, ‘embryogenesis generates only a less complex core structure, the seedling, while virtually the entire adult plant morphology is generated by the activities of the apical meristems.’ 18 The apical meristem is a group of actively dividing cells in the growing tip, which only appears and begins to function once the seedling is in place. The seedling develops entirely under the control of maternal cell factors. An inheritance model based on speciation data The creationists history of biology is that a vast array of original kinds were created. Then extinction on a global scale occurred during the Flood, and the new world after the Flood was re-populated by a surviving subset of the original kinds. These surviving kinds proliferated in a glut of post-Flood speciation that resulted in the vast array of species that we see on Earth today.If we ignore, for the moment, the very interesting question of how this might have happened and simply focus on the number of species that resulted from it, we can gain some insight into the nature of the information inheritance problem. For example, humans went through this catastrophic history just like every other created kind, yet there are very few named species of humans and they probably all belonged to just one biological species. 19 In contrast, the majority of the flowering plants are generally thought to have speciated in the post-Flood period, and we see numbers amongst them in the order of 30,000 orchid species, 20,000 daisy species and 10,000 grass species. The beetles are the superstars of the animal kingdom, with over 350,000 named species coming from probably about 150 created kinds (taken as the number of families).From an apobetic point of view, perhaps it was the designer`s purpose to create mankind to be like Himself and to retain that likeness consistentlythroughout human history. In contrast, it is clear that the purpose for vegetation (e.g. grass) was to cover the land, and for creeping things (e.g. beetles) to feed upon vegetation. Lots of grass and beetle species would thus be needed to fill the innumerable ecological niches that the Earth provided.This model makes testable predictions. We would expect human inheritance to be dominated by structural and conservative components, and grass and beetle inheritance to have more emphasis on variable components. Perhaps the existence of more genes in the rice genome than in the human genome may fit this picture, although further research may show what we have discovered elsewhere, that the simple statistics are misleading. For example, since rice is an autotroph and has to manufacture and operate a photosynthesis system, extra genes would be required for this purpose. There may also be major differences in the levels of alternative splicing. How did speciation occur? Any theory of inheritance has to explain speciation, and the yong age worldview requires an enormous glut of speciation to have occurred in the immediate aftermath of the world-destroying Flood. How is this possible, given that modern species are fairly stable, and that stasis is the norm in the fossil record? 20Wild populations today may often be morphologically stable, but they can also be genetically quite diverse.21 A classic series of papers on the fruit fly Drosophila melanogaster shows that speciation can occur in just one generation from the wild. 22 A culture of wild flies from an orchard was developed, and pupae from the culture were put into a habitat maze. Newly emerged flies had to negotiate the maze to find food. The flies faced three choices of which way to go through the maze, in the following order: light or dark, up or down, and scent of acetaldehyde or of ethanol. The flies were further characterized by the time of day when they emerged from the pupae. Two strains exhibiting opposite behaviors were chosen and allowed to breed together in the maze. One strain emerged early, flew upward and was attracted to dark and acetaldehyde. The other emerged late, flew downward and was attracted to light and ethanol. After 25 generations of continuing to live together, mating tests showed the two populations remained reproductively isolated and behaviorally distinct.Two kinds of forces are at work here, the external environment (maze) and the internal metabolism (early/ late emergence) and behavior (preference combinations). Organisms that find a balance between these internal and external factors survive best. But very few characteristics of organisms are determined by single genes. One gene often influences several or many organ systems, and particular characteristics are often determined by multiple genes. Genetic engineers are therefore beginning to think in terms of gene ‘modules’ and a whole new field of ‘modular genomics’ is opening up to try to cope with this complexity.23 When a change in environment creates a selective pressure on a population, the genetic changes that result will sometimes be disruptive to some organisms but not, or less so, to others. Those that can balance the inner factors with the outer factors are the ones more likely to survive and reproduce.Changes to the internal factors may also be accompanied by morphological changes (depending which ‘modules’ are involved) that would cause a taxonomist to call them a different species. We can view a species therefore as a population of interbreeding organisms that have reached an equilibrium between their environment and their internal constitution. Sometimes this equilibrium may be narrowly defined and the individuals will be all alike and easy to identify, and sometimes the equilibrium may range rather broadly and individuals will vary more from one another and be harder to identify.After the Flood, as Woodmorappe has pointed out,24 there was a whole world of vacant ecological niches available, a rapidly changing climate (into and out of the ice age), and lots of opportunities amongst pioneering populations for founder effects, geographic isolation, and population bottlenecks that together would create a very rich landscape for rapid speciation. Towards a yong age semantic model of inheritance Let me now summarize. First, the naïve one-factor Mendelian model of inheritance (genes alone) is not consistent with the young age view of biology—(and real, as opposed to Darwinian, biology) requires a two-factor model. At one level, organisms were designed to reproduce ‘after their kind’, but at a second level they were designed to diversify and adapt into a multitude of different ecological niches and changing environments. The most obvious experimental correlates with this two-level system are the cell and the chromosomes. Cells pass on their architecture and contents unchanged from mother to daughter, but chromosomes can vary from mother to daughter. Cells and their chromosomes do not act independently, however, and many areas on the chromosomes are highly conserved. The existence of multilevel error correction and error avoidance mechanisms also points to stasis in the chromosomes. Perhaps both cell and chromosomes together control stasis. Indeed, so much of the structure of life is devoted to information conservation that there is very little room left for random variation.Baramin stasis is a concept alien to secular biology, so creationists need to develop a clear understanding
of it. The evidence is there for those who want to see it. For example, Stephen Jay Gould said at the end of his distinguished career in paleontology,‘ … the central fact of the fossil record [is] … geologically abrupt origin and subsequent stasis of most species. … the last remnants of a species usually look pretty much like the first representatives. … Paleontologists have always recognized the longterm stability of most species.’25Likewise, the mechanism of inheritance was acknowledged to be fundamentally unexplainable in Darwinian terms when Richard Dawkins wrote,‘The theory of the blind watchmaker is extremely powerful given that we are allowed to assume replication and hence cumulative selection’26 [my emphasis].Dawkins’ theory did not even begin to operate until all the complex machinery of reproduction and inheritance was already in place. Thus the great champions of evolution are telling us virtually all we need to know to formulate the young age model of baramin stasis!Second, information is a 5-dimensional nominal entity that cannot be explained in terms of matter, energy or the forces that influence them. The ‘information challenge’ is thus a challenge for creationists as well as evolutionists. But since information comes from information and ultimately from an intelligent source, and an intelligent designer can account for its dimensions of semantics, syntax, pragmatics and apobetics, then creationists are in a leading position to make progress in this field.Third, the Barbieri semantic model (see Part II) appears to provide a means of progressing towards an implementation of Gitt’s 5-dimensional theory of information. This model identifies cells as primarily epigenetic rather than genetic systems—that is, stable inheritance is not primarily controlled by genes but by the cellular and chromosomal systems that control genes. Moreover, it predicts the existence of several other cellular memories apart from genes, each with its own code system apart from the genetic code. These have yet to be discovered experimentally, but they should provide a strong test of the validity of the model. Some could, for example, reside within the 97% of the human genome that does not code for proteins.Fourth, since organisms are designed to change at the species level, Darwinist attempts to support their theory with statistical arguments are irrelevant. When organism lineages change through their builtin mechanisms of variation (together with natural selection) no increase in apobetic information content occurs. The organisms are simply doing what they were designed to do—survive in the face of a changing environment. Apobetics, not statistics, controls information change. Conclusion The concept of baramin stasis does not exist in secular biology, so creationists need to develop an answer to the question of what maintains baramin integrity and what allows for variation. There is a surprising amount of experimental support for the idea that cells, not just genes, control inheritance. This provides an obvious foundation for stasis because extranuclear cell structure and content is passed on unchanged from mother to daughter cell. Furthermore, the high levels of information conservation in chromosomes also suggests further mechanisms of baramin stasis. Baramin stasis fits well within the Gitt theory of information, and together they provide a powerful refutation of Darwinism and a resounding affirmation of yong age model. The 3 Rs of Evolution: Rearrange, Remove, Ruin—in other words, no evolution! The genetic changes observed in living things today could not have turned bacteria into basset hounds—ever by David Catchpoole Evolution textbooks cite variation as being something upon which ‘evolution depends’.1 However, when one examines closely the claimed ‘demonstrable examples’ of ‘evolution’, they actually fall into three categories, which we can label here as the ‘3 Rs’. Let’s look at each of these in turn. ‘R’#1: Rearrange existing genes Careful examination of many purported instances of ‘evolution in action’ shows that such ‘variation’ actually already exists, conferred by genes that already exist.Here’s a simplified example that shows this, and also how such genetic variety might be misconstrued as ‘evidence of evolution’. The two dogs in the top row of Figure 1 are a male and a female. They each have a gene that codes for short hair (inherited from its mother or father) and a gene that codes for long hair (inherited from the other parent). In combination, this gene pair for fur length results in medium length hair.2
Figure1. The red bars represent the genes for hair length (short and long hair). One of each gives medium length hair. By re-arranging (recombining) the parents’ genes (top) in reproduction, variety is generated in the appearance of the offspring, but no new genes are involved.Now when these two dogs are crossed, what new combinations of the genes are possible in the resulting offspring? The second row of Figure 1 shows this:The dog at the far left has inherited its father’s short-hair gene and its mother’s short-hair gene. Result: short hair.The two dogs in the middle have each
inherited a long-hair gene from one parent and a short-hair gene from the other parent. Result: medium-length hair (just like the mother and father).The dog at the far right has inherited its mother’s long-hair gene and its father’s long-hair gene. Result: long hair.A casual observer, looking only at the outward appearance, i.e. unaware of what is happening at the genetic level, might think: “There were no long-hair dogs in the parents’ generation. This long hair is a new characteristic— evolution is true!”But such a view is incorrect. The only thing this ‘evolution’ has done is to rearrange existing genes. There’s simply been a sorting out of pre-existing genetic information. There’s no new information here of the kind needed to have turned pond scum into poodles, Pekingese, pointers and papillons. ‘R’#2: Remove genetic information What about natural selection, adaptation and speciation? None of these represent the generation of any new microbes-to-mastiff genetic information either. In our ‘hairy dog’ example, if we were to send our new population of dogs, some with short hair, others with medium or long hair, to an icy, very cold location, we wouldn’t be at all surprised to see natural selection at work, killing off any dog that didn’t have long hair (Figure 2, Line 1). When the survivors reproduce, the only furlength genes passed on to the offspring are those that code for long hair (Figure 2, Line 2). Thus we now have a population of dogs beautifully adapted to its environment. Biologists encountering our ice-bound population of dogs, observing them to be isolated3 from other populations of dogs, could argue that they be given a new species name.So here we see natural selection, adaptation, and possibly even speciation— but no new genes have been added. In fact, there’s been a loss of genes (the genetic information for short-and medium-length hair has been removed from the population). Note that such examples of natural selection, adaptation and speciation are often portrayed as evidence for evolution, but the only thing this ‘evolution’ has done is to remove existing genes. If this population of exclusively long-hair dogs were now forcibly relocated to a steamy tropical island, the population could not ‘adapt’ to the hot climate unless someone reintroduced the short-hair gene to the population again, by ‘back-crossing’ a short-or medium-length hair dog from elsewhere. This is exactly the sort of thing that our crop and livestock breeders are doing. They are scouring the world for the original genes created but which have subsequently been ‘bred out’ (lost) from our domestic varieties/breeds of plants and animals because of breeders artificially selecting certain characteristics, which means other features are de-selected (lost). ‘R’#3: Ruin genetic information In the above examples, we see that natural selection, adaptation and speciation are real and observable. And that these simply demonstrate the rearranging and/or removing of dog genes that were originally present the beginnig. Figure 3: Dogs with the floppy ear mutation, such as bassets, are much more prone to ear infections (e.g. from food scraps) than dogs with erect ears (they clearly can’t hear as well either!)However, there are forms of dog genes today which were not present at Creation but have arisen since. But those have not arisen by any creative process, but bymutations, which are copying mistakes (typos, we might say) as genes are passed from parents to offspring. You would expect such accidental changes to wreck the existing genes, and that’s what happens. For example, the dog pictured in Figure 3 has just such a mutated gene, resulting in ‘floppy ear syndrome’. 5Dogs with this genetic mutation have weaker cartilage and cannot lift up their ears. So they just hang, floppy before dinner, and sloppy after it—unless their owners are diligent in cleaning them. Such regular attention to ear hygiene is necessary, as dogs with floppy ears are prone to serious ear infections, which can even lead to hearing loss. 6 Not that their hearing was especially good anyway. As you might expect, dogs with erect ears are far superior to floppy-eared dogs at detecting prey by sound. 7I can remember reflecting on this when I was an atheist/evolutionist, and wondering how such floppy-eared dogs could have ever evolved and survived in the wild. I now know that they didn’t. Instead this mutation in the genes has arisen since the original “very good” world . The floppy-eared mutation in dogs is but one example of how a post-Fall world is very much “in bondage to decay”. So common is this mutational defect in modern domestic dogs that many people have naïvely come to think of floppy-eared dogs as ‘normal’. But the first people, if they were alive today, would no doubt be shocked to see such deformity. The original dogs, probably something like today’s gray wolves, would have had erect, superbly functional, ears.Why is this so important to consider, in the context of evolutionary claims that no intelligent designer was necessary? Evolutionary biologists, when pressed with the facts about natural selection, will concede that natural selection by itself can only remove existing genetic information. However, they argue that in tandem with mutations, natural selection would be a creative process.But the floppy-ear mutation, for one, is a classic example of the widespread degradation of the genome— a downhill process. For microbes-to-man evolution to be true, evolutionists should be able to point to thousands of examples
of information-gaining mutations, an uphill process, but they can’t.8 Mutations overwhelmingly ruin genetic information. Therefore evolutionists looking to mutations as being evolution’s ‘engine’ do so in vain. 9 Thus they are left with no known mechanism capable of ever turning microbes into mutts—i.e. no way of ‘climbing’ up the supposed evolutionary ‘tree’.Note that while mutations degrade genetic information, sometimes an advantage arising from such degradation can outweigh the disadvantage vis-à-vis survival. While a floppy-eared mutant mutt might not last long in the wild, under human care—i.e. with regular ear cleaning—the equation changes. And what about the key moment when a buyer is looking for the ‘cutest’, friendliest pup in the pet shop window? Indeed, there is increasing evidence that the floppy-eared characteristic is strongly associated with tameness.10,11 Little wonder then, that floppy-eared dogs are so common today. 12Conclusion: 3 Rs = no new information = no evolutionThe above examples of changes in fur length and ear structure of dogs are not evolutionary changes, though they are often claimed as such.Rearranging genes, Removing genes, and Ruining genes are not the sort of genetic changes that could have turned bacteria into basset hounds—ever. These ‘3 Rs’ are repeatedly cited as evolution in a host of other settings, too, e.g. in antibiotic and pesticide resistance, and in sticklebacks, beetles, mosquitoes, worms, sheep, and codfish.13 But none of these are evidence of evolution. The ‘3 Rs’ could never add up to mosquitoes, mesquite, mutts and man from microbes (let alone from molecules!).The evidence instead fits with the young age account of a universal designer having created a multiplicity of ‘kinds’, each programmed to reproduce according to its kind. Geneticists recognize that the diversity of dog breeds we have today could have arisen quickly, in recent history.14 As we’ve seen in our fur length example, long hair and short hair can appear in just one generation, arising from the in-built canine genetic variation—variation that was built-in to dogs at the beginning The Island rule—recipe for evolution or extinction? by Garry Graham Biologists have for many decades observed and recorded that animals isolated on islands away from mainland populations ‘evolve’ into smaller or larger species. Generally, smaller animals tend to become larger, and larger animals become smaller when isolated populations become established on islands. Biologists have coined this phenomenon the ‘island rule’. Examples include giant tortoises native to the Seychelles and Galápagos Islands, Komodo dragons, miniature frogs, Madagascar’s giant hissing cockroach, dwarf elephants, and various rodents, lizards and snakes from islands around the world. In a recent study, a species of lizard has been observed to ‘evolve’ shorter legs over a period of only six months when introduced onto an island where it did not previously occur.1,2For the two most prominent figures in the development of evolutionary theory, Charles Darwin and Alfred Wallace, consideration of the animals on islands played an important role in developing their evolutionary ideas. 3For evolutionists, any changes that can be observed in populations are good news. But does the island rule demonstrate the sort of evolutionary changes that have created biologists from bacteria over millions of years? As creationists have demonstrated, diversification into species cannot be claimed as evidence for evolution into new kinds of animals. Speciation arises from the interplay between inherent genetic variety and natural selection and enables animal populations to adapt to changing habitat or climate. The field of baraminology investigates the boundaries between the created kinds of organisms, and helps us understand the limited, yet valuable role that speciation within kinds plays in biological diversity. 4Let’s look a little more closely at what the island rule really shows when changes to isolated populations are observed. The diagram below 5 demonstrates how a large elephant can reduce in size, or a shrew can increase in size on an island. Changes in the size of sea snails can occur when they form isolated populations at different depths, in similar fashion to the island rule.Notice something very important about the changes occurring in these simple examples. The large elephant has been replaced by a smaller elephant when isolated on the island, and the small shrew has become a larger size shrew on the island. But the elephant is still an elephant and the shrew is still a shrew. There is absolutely no suggestion that a new form of animal will ever be created by changes observed under the island rule. It is simply preposterous to use the island rule to support evolution in terms of the creation of novel genetic information, increasing genetic complexity and diversity. It simply is not observed.Imagine for a moment the elephant scenario. The genetic variety of the elephant naturally includes differences in size. Any population of genetically diverse elephants will include individuals of all sizes, from large to small. If placed onto a smaller habitat such as an island, selective pressures can gradually lead to smaller average size over a number of generations—because of factors such as restrictions of food and possibly space for a given herd size. The genes for smaller size were already there, but were selected because smaller elephants would be better able to survive. The possibility also exists that mutations could cause stunted growth, through a reduction in growth hormone production, for example. 6What would happen, however, if the genes for large size are lost from that isolated population? Would the population of elephants somehow be more genetically diverse? Of course not! The population would be genetically impoverished. In fact, they would be liable to extinction if moved off the island or if a large predator invaded the island. Their much smaller gene pool would make them less able to adapt to environmental change. Can we therefore conclude that genetic loss, local reduction of genetic diversity and no increase in complexity is proof that Darwinian evolution created all the life on earth? No!
Shrew The same can be said for the shrew. The little shrew would have natural variation in size. Predation or other pressures on the mainland may select for smaller size in the population as a whole. Remove some to an island, and the isolated population may become larger, because the larger type may be better suited. Perhaps an absence of predators and competition for food would bring about the size change. But evolution? Again, we see only a reduction in genetic diversity, and no increased complexity. Only pre-existing genes are involved. They are still only shrews, since shrews only reproduce more shrews. Molecules-to-man evolution is not occurring. Natural variation and natural selection have modified the population morphology, but not produced anything truly novel. And if either the elephant or the shrew are returned to their mainland habitat before genetic diversity is permanently lost, they are likely to revert to the original size distribution.Real life examples confirming this can be readily seen in classic evolutionary icons. Charles Darwin used the speciation of finches on the Galápagos Islands as evidence for ‘evolution’. But he failed to realise that populations fluctuate back and forth with changing climatic conditions, and no net evolutionary progression actually occurs.7 Similarly, the famous peppered moth, so often paraded as ‘evolution in action’, only ever demonstrated that moth populations could adapt to their environment (not to mention that aspects of the studies were staged!). 8A famous evolutionary paleontologist, the late Stephen Jay Gould, used the ‘geographical isolation principle’, or island rule, to develop his own ideas of evolutionary processes from which he coined the term ‘Punctuated Equilibrium’. He incorrectly suggested that the rapid changes in isolated populations are where the bulk of evolution has occurred throughout history. He saw islands as ‘our great laboratories of evolution’ that were the driving forces of biological radiation. 9 In 1996 he wrote, ‘ … evolutionary events are concentrated in episodes of branching speciation within small, isolated populations.’10But how can this be? As demonstrated by the examples discussed above, if anything, the island rule offers a stronger explanation for extinction of organisms than for ‘evolutionary’ radiation. Ironically, in an essay on the study of land snails on the Tahitian island of Moorea, Gould reported that they were driven to extinction in the 1960s, following the introduction of a predatory snail to control an agricultural snail pest.9The idea that adaptations are quickly acquired by isolated populations in response to environmental conditions, which leads to evolutionary radiation and increased diversity, is false. It is precisely the problem of small isolated populations of low genetic diversity that threatens many organisms with extinction today. It is true that in some cases geographical isolation on an island has enabled some species to survive, safe from predators, while their mainland cousins have perished. A good example is the quokkas of Rottnest Island off Western Australia. However, history is also littered with examples of extinctions of genetically isolated and vulnerable species. Of 23 Australian bird species that became extinct since 1788, 17 are from continental or oceanic islands! 11,12Also, geographic isolation results in a subset of the original complete population reproducing locally. This subset will not have all the variety of genes from the parent population and will therefore display a narrower range of features. This can result in a distinct variety of the animal or plant developing, if it can survive the isolation (not having the full range of genetic variety, it may not be able to adapt). Such geographic isolation could have contributed to the development of sub-types within the created kinds after the Flood.Modern instances of the island rule in action have nothing to do with molecules-to-man evolution, but only with the natural variation already present within the genes of the pioneering animals.Isolated populations are more likely to suffer eventual extinction, rather than herald a new age of increased diversity and radiation. Therefore, the island rule, while demonstrating natural variation inherent in a population, offers no hope for evolutionists desperately needing a mechanism for the myth of Darwinian Evolution. Molecular limits to natural variation by Alex Williams Darwin’s theory that species originate via the natural selection of natural variation is correct in principle but wrong in numerous aspects of application. Speciation is not the result of an unlimited naturalistic process but of an intelligently designed system of built-in variation that is limited in scope to switching ON and OFF permutations and combinations of the built-in components. Kirschner and Gerhart’s facilitated variation theory provides enormous potential for rearrangement of the built-in regulatory components but it cannot switch ON components that do not exist. When applied to the grass family, facilitated variation theory can account for the diversification of the whole family from a common ancestor—as baraminologists had previously proposed—but this cannot be extended to include all the flowering plants. Vast amounts of rapid differentiation and dispersal must have occurred in the post-Flood era, and facilitated variation theory can explain this. In contrast, because of genome depletion by selection and degradation by mutation, the potential for diversification that we see in species around us today is trivial. Darwinian evolution Figure 1. Potential for variation in modular regulatory control systems. The hair dryer (A) and the vacuum duster (B) consist of similar components, but one is wired up to blow air, the other is wired up to suck air. The axolotl (C) is an adult salamander that has retained its juvenile gills; if thyroxin is given at the right time, it develops into a normal salamander (D) with lungs.Charles Darwin will always be remembered for turning descriptive biology into a mechanistic science. His famous 1859 book The Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life argued persuasively that species are not immutable creations but have arisen from
ancestral species via natural selection of natural variation. Two main points contributed to Darwin’s success:he presented a simple, testable, mechanical model that enabled other scientists to engage experimentally with the otherwise overwhelming and bewildering complexity of life;unlike others, Darwin approached the subject from many different angles, examined all the objections that had been raised against the theory, and provided many different lines of circumstantial evidence that all pointed in the same direction.He went wrong in four main areas, however. First, he proposed an entirely naturalistic 1 mechanism, but we now know that it must be intelligently designed. 2 Second, he extrapolated his mechanism to all forms of life, but we will soon see that this is not possible. Third, he went wrong in proposing that selection worked on every tiny advantageous variation, so it led to the continual ‘improvement of each creature in relation to its … conditions of life.’3 By implication, deleterious variations were eliminated. We now know from population biology that selective advantages only in the order of ≥10% have a reasonable chance of gaining fixation. 4 The vast majority of mutations are too insignificant to have any direct influence on reproductive fitness, so they are not eliminated and they accumulate relentlessly like rust in metal machine parts. The machine can continue to function while the rust accumulates, but there is no improvement in the long term, only certain extinction. 5Fourth, he proposed that reproductive success—producing more surviving offspring than competitors—was the primary driving force behind species diversification. If this were true, then highly diversified species in groups like the vertebrates, arthropods and flowering plants would produce more surviving offspring per unit time than simpler forms of life. This is not generally true—quite the opposite. The ratio of microbial offspring numbers per year compared with higher organisms is in the order of billions to one. Facilitated variation theory Kirschner and Gerhart’s facilitated variation theory provides a far better explanation of how life works. In a companion article,2 I showed that this requires an intelligent designer to create life with the built-in ability to vary and adapt to changing conditions, otherwise it could not survive. This leads us to the important question of the limits to natural variation.The limits of natural variation today are extremely narrow, being evident only at the variety and species level. History requires a far greater capacity for diversification in the ante-diluvian world to be available for rapidly repopulating the Flood-destroyed Earth, and quickly restoring the ecological balances crucial to human habitability. Baraminologists have identified created kinds that range from Tribe (a sub-family category, e.g. Helianthus and its cousins within the daisy family), 6 to Order (a super-family category, e.g. cetaceans—the whales and dolphins).7 Theoretical limits to natural variation Scope for change in core structure According to facilitated variation theory, the capacity to vary requires: functional molecular architecture and machinery, a modular regulatory system that maintains cellular function but provides built-in capacity for variation through randomly rearranged circuit connections between machines and switches, a signaling network that coordinates everything. Most variation occurs between generations by rearrangement of ‘Lego-block-like’ regulatory modules. Over this timescale, we can emphatically say that no change at all occurs in the molecular architecture and machinery, because it is physically passed in toto from mother to offspring in the egg cell. Variation between generations must therefore be limited to the regulatory and signaling systems. Scope for change in regulatory modules The law of modules2 says that the basic module of information has to contain functionally integrated primary information plus the necessarymeta-information to implement the primary information. This information has to be kept together so that the module retains its functionality.Genes only operate when they are switched ON. Their default state is to remain OFF. Genes don’t usually work alone, but as part of one or more complexes. Even the several different exons (the protein-coding segments) within a gene can participate in different gene complexes, some being involved with up to 33 other exons on as many as 14 different chromosomes. 8 And genes are not just linear segments of DNA, but multiple overlapping structures, with component parts often separated by vast genomic distances.9Sean Carroll, a leading researcher in developmental biology says, ‘animal bodies [are] built—piece by piece, stripe by stripe, bone by bone—by constellations of switches distributed all over the genome.’10 Evolution, he believes, occurs primarily by adding or deleting switches for particular functions, for this is the only way to change the organism while leaving the gene itself undamaged by mutation so that it can continue to function normally in its many other roles. Carroll considers this concept to be ‘perhaps the most important, most fundamental insight from evolutionary developmental biology.’ 11Diversification via Carroll’s proposed mechanism consists of rearranging the signaling circuits that connect up genes, modules and switches, while retaining functionality of both the modules and the organism. Carroll tells us that gene switches are extremely complex, comparable to GPS satellite navigation devices, and easily disabled by mutations, so if switches can be spliced into and out of regulatory circuits, then it must happen via a cell-controlled process of natural genetic engineering (the law of code variation2).Regulatory areas within gene switches are hotspots for genetic change. An average gene switch will contain several hundred nucleotides, and within this region there will be 6 to 20 or more signature sequences. These signature sequences are similar to credit card PIN numbers—they allow the user to operate the bank account—and they are easy to change. The result of such change is that different signaling molecules will then be able to operate the ‘bank account’ of natural variation.There are about 500 or so ‘tool-kit proteins’ that are highly conserved across all forms of life and that carry out a wide range of basic life functions. For example, bone morphogenetic protein 5 (BMP5) regulates gastrulation and implantation of the embryo, and the size, shape and number of various organs including ribs, limbs, fingertips, outer ear, inner ear, vertebrae, thyroid cartilage, nasal sinuses, sternum, kneecap, jaw, long bones and stature in humans, and comparable processes in other animals including the beaks of Darwin’s Galápagos finches.The signature sequences recognized by such tool-kit proteins are usually about 6– 9 nucleotides long. A 6-nucleotide sequence can have 46 = 4096 different combinations of the nucleotides T, A, G and C, and a 9-nucleotide sequence can have 49 = 262,144 different combinations. But there are 6 to 20 or more signature sequences that can be recognized by the 500 different tool-kit proteins, which gives somewhere between 500 6 (~1016) to 50020 (~1054) different possible combinations.An obvious limitation to change in regulatory circuits is that switches can only switch ON functions thatalready exist. It is easy to switch OFF an existing function, but it is impossible to switch ON a function that does not exist.Two examples of regulatory variation are given in figure 1. The hair dryer and the vacuum duster both use similar materials—motorized fan, plastic housing, power circuit and switch. In one, the control circuit is wired up to blow air; in the other, the circuit is reversed, and the machine sucks air. A biological example is the axolotl, a salamander that has retained its juvenile gills into adulthood. This can happen if there is an iodine deficiency in the diet, or if a mutation disables thyroxin production. By adding thyroxin, the axolotl will develop into a normal salamander. Both these switch-and-circuit rearrangements seem to be simple changes, but they are possible only because complex mechanisms of operation already exist within the system. Scope for change in signaling networks
While there is enormous potential for variation built-in to the circuitry that connects up regulatory modules, it is signals that trigger the switches and their functional modules. What scope is there for diversification in signal networks?Signal networks are compartmented. They operate as a cascade within each compartment—one signal triggers other signals, which trigger other signals etc. Each compartment cooperates with its adjacent compartments so that the unity and functionality of the organism is maintained, but they do not influence activities beyond their local neighbourhood. Figure 2. Embryonic switching cascades represented as a ‘domino cascade’. The domino cascade is set up on the left so that when the ‘Start’ domino is toppled, the sequential falling of dominoes will trigger the next activity in the series, but also trigger other developmental modules in the outer circles, until the ‘Stop button’ is hit. Once the cascade is complete, an organism does not need any of the sequence again so it is permanently shut down, as on the right where all the dominoes have fallen and will not get up again. There is no coded information in this signal network because everything that has to be done has been designed into the pattern of dominoes. With no coded information, no mutations or recombinations can occur, so this kind of signal network probably marks a limit to natural variation.The two examples I used to illustrate this point in the companion article ‘How Life Works’2 were the propagation of plants from cell culture, and the regeneration of double-headed and double-tailed planarian flatworms. In both these cases, a single signal molecule triggered a dramatic developmental cascade (shoot/root growth in the former, and head/tail growth in the latter) that was completely independent of, but cooperative with, the other half of the whole organism.Some signals are hard-wired into the cell, while others are soft-wired. An example of a hard-wired signal occurs within theapoptosis cascade for dismantling cells and recycling their parts. In a normal cell, apoptosis is extensively integrated with a wide range of functional systems and can be triggered by a variety of causes through a complex signaling network. However, in human blood platelets the system is isolated from its normal whole-cell environment and we can see it operating in a much simpler form.A complex of two proteins, Bcl-xL and Bak, performs the function of a molecular switch. When Bcl-xL breaks down, Baktriggers cell-death.12 In a normal whole cell, homeostasis maintains the balance between Bcl-xL and Bak, but platelets are formed by the shedding of fragments from blood cells and there are no nuclei in them. Once the platelets are isolated from homeostatic control, Bcl-xLbreaks down faster than Bak, so the complex provides a molecular clock that determines platelet life span—usually about a week. No signal is sent or received in this hard-wired system, so there is no room for diversification.Hard-wired signaling networks are probably a major component of stasis. We can visualize them by using a domino cascade model, illustrated in figure 2. In this case, embryogenesis is symbolized as a series of events in the main circle, which trigger other peripheral cascades as they proceed. Each cascade continues until it meets a STOP signal, at which point the whole circuit is shut down. A similar thing happens in individual cells when they differentiate. Embryonic stem cells have the potential to become any cell in the body, but once the cascade is traversed, all options but one are shut down.In contrast, a soft-wired system sends actual signal molecules, raising the possibility of adaptive change—e.g. sending a different signal molecule. A recent study of red blood cells investigated cell fate decision making—whether to proliferate, to kill themselves or to call for help. This decision lies at the very heart of homeostasis because it determines the robustness and stability of the organism in the face of change and challenge. Figure 3. Grass flower (spikelet) structure and some common variations. A—conventional spikelet on the tip of a branch. B—exploded view of spikelet: a = lower glume; b = upper glume; c = lemma; d = palea; e = ovary (black oval) with bifid filamentous stigmas, surrounded by 2 or 3 translucent lodicules and 3 anthers. C—apex of lemma may elongate to produce a straight awn, or corkscrew several turns to produce a twisted column with a straight or curved terminal bristle.The researchers discovered that they did not need to know the detailedstructure of the decision-making system, just a knowledge of its network of signaling interactions was sufficient to identify which components were the most important.13 This finding was confirmed in another study in which a wide range of perturbations were applied to white blood cells and the effect upon the cell fate decision was examined. The decision came not from any particular target of perturbation, but as an integrated response from many different nodes of interaction in the signaling network. The authors suggested that computations were carried out within each node of the signaling network and the combination of all these computations determined what the level of response should be from any particular perturbation.14Does this indicate a potential for adaptive change? Or does it suggest a system that is designed to resist change?The primary role of the signaling system is to coordinate everything towards the goal of survival. Life can survive only by maintaining a balance between contradictory objectives. On the one hand, it has to achieve remarkable results as accurately as possible—e.g. plants turning sunlight into food without the high energies involved killing the cell. On the other hand, it has to do it in an error-tolerant and constantly variable manner to maintain its adaptive potential and its robustness and stability.The solution to this dilemma is error minimization. All possible routes will involve risks of error, but the optimal solution will minimize those risks. A computer simulation study of regulatory networks found that using an error minimization strategy leads to the formation of control motifs (gene switching patterns) that are widely found in very different kinds of organisms and metabolic settings.15 When applied to the ‘noise’ in yeast gene expression that results from the ON/OFF nature of signaling, it was found to also be the case in real life. Genes that were essential to survival exhibited the lowest expression-noise levels when compared with genes
that were not directly essential. The author concluded that ‘there has probably been widespread selection to minimize noise in [essential] gene expression.’ But there is a down side—noise minimization probably limits adaptability.16 Figure 4. The grass inflorescence consists of (A) the basic unit of a single terminal flower (spikelet) on a short stalk (pedicel) which is repeated in a terminal group of branches (B). This terminal group structure is then repeated on side branches (C), with the lower branch(es) including further internal branching. This basic inflorescence type is called a panicle.Since the goal of signal coordination is survival, I suspect that the large, interconnected signaling networks in all forms of life contribute more to stasis than to change. Practical limits to natural variation It is impossible to describe the full range of natural variation across all life forms in a journal article, so I will focus just on variation within the grass family (Poaceae), and between it and other families of flowering plants (Angiosperms).The grass family comprises about 10,000 species in about 700 genera. Is it possible that maize, lawn grass and bamboo all arose from a common ancestor? Baraminologists believe so.17 Grass morphology The easiest way for us to conceptualize the extent of natural variation is through illustrations of morphological variations. We need to keep in mind that much more than morphological variation is involved in speciation, but it can serve as a convenient surrogate for our present purpose. The basic structure of a generalized grass flower (spikelet) is illustrated in figure 3. Figure 5. Ordination and classification of specimens of the three native Puccinellia species identified in Western Australia, based on 34 morphological characters. Principle Coordinates 1 and 2 provide a 2dimensional representation of the differences between the specimens and a clustering algorithm identified groups of similar specimens (ellipses). A common variation on the standard structure is the development of an awn upon the apex of the lemma (or glume) in figure 1C. This transformation is fairly straightforward. The apex of the lemma is extended into a long straight awn, then a regulatory change causes the edges to grow faster than the centre, which causes the base part of the awn to spiral around into a twisted column, leaving a straight or curved bristle at the top.Grasses generally have a multitude of spikelets, arranged into a terminal structure called theinflorescence, as shown in figure 4. Species-level variation in the Australian salt grass Puccinellia Salt grasses of the genus Puccinellia are distributed worldwide, from the Antarctic to the Arctic, and they occur right across southern Australasia (Australia and New Zealand) in marine salt marshes, around the edges of inland salt lakes and on salinised pasture lands. They have a quite generalized grass morphology, with no special adaptations for dispersal, as many other grasses do, so they may represent a typical primordial grass.The most widespread species, found right across Australasia, is Puccinellia stricta. When Edgar18 described the New Zealand species in 1996 she noted some differences between Australian and New Zealand populations of P. stricta and suggested that further detailed study was warranted. I was fortunately able to undertake that study,19 with results that are quite typical of many widespread plant genera. My study focused on the genus in Western Australia (WA), where three native species were identified—P. stricta, P. vassica and P. longior. An ordination and classification of specimens based on their morphological characteristics is shown in figure 5. Figure 6. Ordination and classification of specimens of Puccinellia stricta from across Australasia. The group labeled perlaxa had been identified as a subspecies of P. stricta. Four geographically isolated regions were sampled: WA = Western Australia, SE Aus = South East Australia (Victoria, South Australia and New South Wales), Tas = Tasmania, NZ = New Zealand. The axes of ordination and the ellipses of classification have the same meaning as Figure 3 and were based on the same 34 morphological characters.The plot shows that all three species are well separated from one another, with members of each species being more closely similar to members of their own species than to other species.I then needed to know how our specimens of Puccinellia stricta compared to specimens of the same species from right across Australasia. Loan specimens were obtained from other herbaria and the same analysis was carried out as for the WA specimens. A very different plot resulted, as shown in figure 6.In this case, a new species was clearly separated out from the rest, while the remainder spread broadly right across the ordination space. The group labeled perlaxa (occurring only in southeast Australia) had previously been identified as a subspecies of stricta, but from this analysis it was clear that it warranted species status, so we named it Puccinellia perlaxa.The big picture of the native Australasian species of Puccinellia that emerged from this study was of a single widespread species, P. stricta, that varied in a continuous manner right across the whole region, and then localized species with restricted distributions that could generally be explained in terms of local ecological and/or geographical factors.Historically, therefore, it is most likely that the widespread species was the progenitor of the all the other species. It has retained at least some of its capacity for variation, and certainly a greater capacity (wider dispersion in the ordination space) than any of the other species that I studied. Morphological variation in Australian Puccinellia
Figure 7. Panicle variations within Australian species of Puccinellia. The contracted panicle with a variety of branch lengths at A is typical. B has numerous spikelets crowded along very short branches, while C has very few spikelets on very short branches, and D has few spikelets that are mainly on the ends of very long branches. Images were scanned from dried herbarium specimens; in life, D would have had straight branches and a more symmetrical shape. Figure 8. Variations in upper glume length (marked with black bars) in spikelets of some Australian species of Puccinellia. Figure 9. Paleas from five different Australian species of Puccinellia. Note the variation in hair development on the margins, ranging from glabrous (no hairs) on D, a few hairs near the apex of E, the top half of B with hairs and the lower region glabrous, with A and C having hairs extending into the lower half. Figure 10. Retrogression of Panicoid grass spikelets. The characteristic condition in the Tribe is to have one terminal fertile floret subtended by one sterile floret. The primordial condition at A has the sterile floret male. Condition B has lost the anthers of the sterile floret. Condition C has lost the palea of the sterile floret. Condition D has lost the lower glume. The series E, F, G and H illustrate the same pattern of retrogression but with the spikelet axis rotated in relation to its adjoining branch. Figure 11. Transformation of a panicle into wheat. The side branches of A are eliminated to give B, the number of spikelets is increased to form C, then the pedicels are reduced to form D. Australian Puccinellia species vary most markedly in their panicle structure, a few of which are illustrated in figure 7. Puccinellias have multiple florets per spikelet, ranging from 3 or 4 up to 10 or more. One feature that varies significantly in spikelet structure is the length of the upper glume, illustrated in figure 8. The palea also varies significantly, particularly in the extent of hairs on the margins, as shown in figure 9. Genus-level variations in Tribe Paniceae The grass family is divided up into Tribes of genera that (ideally) reflect their common ancestry. The largest Tribe is Paniceae, and Häfliger and Scholz have suggested that the spikelet variations within this Tribe follow a fairly simple pattern of retrogression from the original Paniceae spikelet,20 as illustrated in figure 10. Sub-family variation within Poaceae Argentinian researchers Vegetti and Anton have shown that if we begin with a panicle as the primordial grass inflorescence, then every other generic form can be derived simply by adding, subtracting, shortening or lengthening the components of the panicle.21 I will take just three types of transformations that represent different sub-family groups within Poaceae— wheat, maize and silkyhead lemon grass. Wheat The hypothesized transformation of a panicle structure into the reduced seedhead of a wheat plant via the Vegetti-Anton theory is illustrated in figure 11. Maize Figure 12. Transformation of a panicle into maize. The middle branches of the panicle A are replaced with leaves and leafy bracts, and the lower branches are transformed into a spike (like wheat, Figure 9) to form B. The upper spikelets lose their female parts, and the lateral spikelets lose their male parts to form C. The male spikelets multiply, and the female spikelets elongate their pollen receptors to form a tassel that emerges from the enveloping leafy bracts, to formD. Transformation of a panicle into the compact seedhead of maize is more complex, but still conceivable, as illustrated in figure 12. The primordial panicle could have been divided by the panicle branches being switched OFF in the midsection, and leaf modules being turned ON. A leaf within the inflorescence is called a ‘spathe’ leaf. Apical dominance is a common mechanism in all
plants for repressing growth below the apex until conditions are appropriate. This normally controls the proliferation of fertile seeds within grass spikelets. It represses female organ development more strongly than the male parts, so in many grasses the apical florets within a spikelet will be either male or sterile, and only the lower florets (those furthest away from the dominating apex) will produce fertile seed. This mechanism is already in place to suppress female organ development in the top branches of the maize plant, making them all male. But the lower branches of the inflorescence are now far distant from the apex, so apical dominance is eliminated and the female organs grow uninhibitedly, perhaps out-competing the male organs and suppressing them altogether. Leaf and bract growth in the lower parts is stimulated and they cover the female spike entirely. This causes the female florets to lengthen their pollen receptors so that they can reach the open air and receive wind-dispersed pollen, making the silky tassel at the end of a corn-cob. Silkyhead lemon grass Figure 13. Transformation of a primordial panicle into the spatheate panicle of Cymbopogon obtectus. The branching pattern in A is reduced to a repeating set of branches in which a sessile fertile spikelet with an awn occurs at each secondary branch point, accompanied by a pedicellate awnless sterile spikelet (B). Pairs of these branched structures are subtended by a spathe leaf, from which they emerge at flowering time (C) to produce the complex mature panicle (D).Transformation of the panicle into silkyhead lemon grass (Cymbopogon obtectus) can be hypothesized by reducing the pedicel of alternate spikelets so that they occur in pairs—one pedicellate, the other sessile. The pedicellate spikelet retains apical dominance and is sterile or male, and the sessile spikelet is fully fertile, but it also develops an awn on its lemma (see figure 3). The paired branching structures occur also in pairs, and a leaf growth module is switched ON within the developing inflorescence to produce a spathe leaf surrounding each pair of branched structures. Hairs are normally present in many parts of the inflorescence, and are usually short, but in Cymbopogon obtectus, the hairs are abundant and long, producing a fluffy white ‘silkyhead’ at flowering time, as illustrated in figure 13. Origin of the angiosperms Within the grass family, diversification from a common ancestor seems to be fairly straightforward, and could have occurred via numerous rearrangements of parts that were already present in the primordial grass ancestor. But can we continue this process back to a common ancestor with daisies, orchids and all other flowering plants?A recent review of the subject was entitled ‘After a dozen years of progress the origin of angiosperms is still a great mystery.’ 22 The ‘progress’ referred to was the enormous effort put into DNA sequence comparisons, in the belief that it would give us the ‘true’ story of life’s origin and history. While such comparisons have proved of great value in sorting out species and genus relationships, the results for family relationships and origin of the angiosperms has often been confusing and/or contradictory—thus the remaining ‘mystery’.Recent discoveries of fossil flowers show that angiosperms were already well diversified when they first appeared in the fossil record. The ‘anthophyte theory’ of origin, the dominant concept of the 1980s and 1990s, has been eclipsed by new information. Gnetales (e.g. Ephedra, from which we get ephedrine), previously thought to be closest to the angiosperms, are now most closely related to pine trees. To fill the void, new theories of flower origins have had to be developed, and ‘Identification of fossils with morphologies that convincingly place them close to angiosperms could still revolutionize understanding of angiosperm origins.’22 Conclusions Theoretically, the greatest scope for natural variation appears to lie in the almost infinite possible permutations of the Kirschner–Gerhart ‘Lego-block’ regulatory module combinations, and these could rapidly produce the enormous diversification implied by the young age history. In contrast, there is no scope at all for change in the machinery of life from one generation to the next because it is passed on in toto from the mother in the egg cell. Signaling networks appear to be limited in their scope for diversification, particularly those that are hard-wired (designed into the system) into compartments and cascades that have symmetry and functional constraints. The elaborately interconnected signaling networks are very robust in the face of perturbation, and provide a crucial component of stasis. There is some potential for variation in the signaling molecules that are sent, but error minimization limits its functional scope.From a practical point of view, diversification of the whole grass family from a common ancestor is conceptually feasible via switching ON and OFF the original component structures within a primordial grass. It is not possible to switch ON components that don’t exist, however, so this mechanism cannot be extrapolated to include a common ancestor between grasses and other angiosperms such as daisies and orchids.Flowering plants display an enormous amount of differentiation and dispersal (between 250,000 and 400,000 species in 400 to 500 families worldwide) and appear only in the upper levels of the fossil record. Most of this diversification appears therefore to have happened rapidly, possibly in the post-Flood era. A possible reason for this is that the flowering plants were originally planted in the Garden of Eden and radiated worldwide mainly after the Flood.23 This is not Darwinian evolution. It is intelligently designed, built-in potential for variation in the face of anticipated environmental challenge and change. The word ‘evolution’ is still useful in describing processes of historical diversification, but its Darwinian component is now only a minor feature. In contrast to Darwin’s proposed slow development of variation, the evidence supports a vast amount of rapid differentiation in the past, degenerating into only trivial variations today—a far better fit to Kirschner–Gerhart theory and the young history. Galápagos with David Attenborough: Evolution by Russell Grigg Published: 18 April 2013 (GMT+10) Galápagos with David Attenborough is the title of a three-part Sky 3D TV series that was shown in Australia with the revised title, David Attenborough’s Galápagos. Here we examine the third episode,1 in which Sir David claims that “Galápagos is a crucible where evolution proceeds at extraordinary speed.” And we also test his claim that the discoveries on Galápagos “inspired an idea that changed our understanding of life on Earth—evolution” And in particular, “Charles Darwin’s evolution by natural selection”. What evolution is and what it’s not Whether or not evolution has occurred on Galápagos (or anywhere else on Earth for that matter) depends very much on what is meant by the term ‘evolution’. The theory that creationists oppose is the idea (and consequent atheistic worldview) that all living things on Earth have arisen from a single source (which itself came from non-life). The key issue is the type of change required. For example, to change microbes into marine iguanas would require massive successive increases in the genetic information of the genome. However, none of the examples of change over time that Attenborough calls ‘evolution’ in this series involve the addition of new genes. Rather, they all
involve sorting and/or loss of existing gene information. Hence they do not support Darwinian (i.e. microbes-to-marineiguana) evolution.When evolutionists see adaptation taking place and call it ‘evolution’, they are guilty of equivocation. Small changes of this nature do not make ‘microbes-to-man’ a fact.Changes of behaviour, as a species learns to adapt to a new habitat, also is not Darwinian evolution. If such adaptation means an animal can no longer breed with its previous fellows, i.e. if speciationoccurs, this too is not Darwinian evolution, because this involves a sorting of existing information, not the acquisition of new genetic information.2 In fact, such adaptation and speciation among the original created kinds is an integral part of the young age worldview. See Q. & A. Speciation.Likewise, natural selection is not evolution, but a ‘culling’ process, ‘choosing’ from what is already there and exterminating unfavourable variations. Several authors wrote on this before Darwin; of these, creationist chemist and zoologist Edward Blyth (1810–1873) had three major articles published in The Magazine of Natural History from 1835 to 1837.3 Note too that Alfred Russel Wallace, the co-inventor of modern evolutionary theory, challenged Darwin re the latter’s misuse of the term. 4 And the finding of a new species does not prove that evolution has occurred; different species within a created kind has been part of the creation model since the time of Carl Linnaeus (1707–1778), and that is the only type of speciation that is observed. Galápagos tortoises living apart are not evidence for evolution Earth Observatory 8270 and NASA GSFC; Wikimedia commons/M.Minderhoud. Click to enlarge. Attenborough shows viewers the crater on the island of Isabela, where the razor-sharp lava has formed an impassable physical barrier for the giant tortoises, dividing their territory into two, and he says: “So two tortoise populations that were once one, must now live apart.” Then: “If there is any significant difference, now or in the future, between their two territories, the tortoises may eventually become two different species.” This has not yet occurred, but if it did, it would not be Darwinian evolution because, as explained above, such speciation as a result of adaptation to a new habitat involves a loss of genetic information or at most a sorting of existing information. ‘Darwin’s finches’ are not evidence for evolution Concerning the Galápagos finches, Attenborough tells viewers: “We now know that the ancestral Galápagos finches arrived in these islands about two million years ago.” To set the record straight: we know no such thing. According to the young age model, the Galápagos finches most likely were descendants of South American mainland finches, but these were descendants of those who srvived the Flood. So the finches came to the Galápagos some time after the Flood, not two million years ago. Charles Darwin visited four of these islands over a period of five weeks, when H.M.S. Beagle visited there in 1835. Concerning this, Attenborough says: It was his collection of these undramatic little birds, the finches, which provided him with the most substantial evidence for his great theory. … Darwin, when he returned to England, brought back with him a wide variety of specimens of all kinds, and he spent years studying his collections. He had a range of finches from several of the islands, and he noticed one particular way in which they differed. They had beaks of different sizes. Why? An idea grew in his mind … . To set the record straight: Darwin actually knew very little about the birds he collected on the four islands he visited. His biographers, Desmond and Moore, write: “He remained confused by the Galápagos finches, believing that they fed indiscriminately together, unaware of the importance of their different beaks. He still thought his collections contained finches, wrens, ‘Gross-beaks’, and ‘Icteruses’ (blackbird relatives).”5It was English ornithologist John Gould who realized that “Darwin’s mixed bag of birds was in fact a unique flock of finches.”6 Darwin had not labelled his finches by the island of collection, but others on the expedition had taken more care. From them he was able to establish that the species were unique to different islands. As to these birds and their beaks being evidence for evolution, Darwin did not mention these finches or their beaks even once in his major work on evolution, On the Origin of Species. So finches and their beaks were not the origin of the Origin.Darwin’s drawings of four finch beaks from his Journal of Researches 2nd ed., 1845, p. 379. Modern long-term research has established that the beak size within the species changes as the food supply changes.Desmond and Moore say that a single sentence in the 1845 2nd edition of his Journal of Researches, was “as much as he would ever say on finch evolution”. 7 In this work, under a picture of four different finch beaks and a brief description of them, Darwin wrote: “Seeing this gradation and diversity of structure in one small, intimately related group of birds, one might really fancy that from an original paucity of birds in this archipelago, one species had been taken and modified for different ends.”8The term ‘Darwin’s Finches’ was not used by anyone until it was thought up by Percy Lowe in 1936, and popularised by David Lack in 1947 in his book Darwin’s Finches.9Finch beak type (prevalence) on a particular island happened like this: birds with beaks that enable them to eat the type of food available on any island are the ones that will best survive and propagate on that island. This is an example of natural selection, a sorting process that gives no support to ‘evolution’—the birds (in this case finches) have not become
non-finches. Also, an 18-year study by Princeton zoology professor Peter Grant showed that a new species of finch could arise in only 200 years, which inadvertently supports the young age model of rapid speciation, seecreation.com/darwinsfinches. This means that a mere thousand years or so would be enough time to allow for all the observed speciation. Another problem with using these finches and their beaks as evidence for evolution is that the variation is cyclic. Evolutionist Jan Komdeur, Professor of Avian Evolutionary Ecology, Centre for Ecological and Evolutionary Studies, University of Groningen, speaking on the Darwin documentary film Darwin: The Voyage that Shook the World, says:The finches in the Galápagos change rapidly, but the species doesn’t change, it is the morphology [i.e. body form] that changes rapidly. So first of all we thought these were different species, but actually they’re the same species. The phenotype [i.e. observable characteristics] of the Darwin finches is cyclic. It stays within certain boundaries. So some years you have finches with big beaks depending on food environments, and the other years you have the same species of finches with thin beaks.Such built-in adaptability to changing food conditions is not evolution in action. Note too that this latter data is the result of observation over several years, and so would not have been seen by Darwin, as he was there for only five-weeks in 1835. Also see later re beak reversal due to the presence of humans. Giant Galápagos tortoises are not evidence for evolution Attenborough now resumes his discourse on the giant tortoises. He tells viewers that on Española island there is virtually no edible vegetation except for the fleshy leaves and flowers that grow at the top of the tall prickly pear cactus, Opuntia. And only those tortoises with peaked shells and long necks could reach them. And he says: So they were the ones that survived and produced young. Over many thousands of generations and millions of years, the shell shape of the Española tortoise became more and more exaggerated. Now, the peak at the front of the shell is shaped like a saddle. Such a change didn’t happen just on Española— different islands had their own versions. Eventually, there were 15 different species on the islands, all descended from a single founder. To set the record straight: no one knows how many tortoises reached the different Galápagos islands from South America in the four-and-a-half millennia since the Flood, let alone in the alleged millions of years claimed by Attenborough and his fellow evolutionists. But just suppose there was ‘a single founder’ (which would have had to have been a pregnant female), this one would have had all the genetic information for all the tortoises seen today. That is, the “11 types of giant tortoises left in the Galápagos, down from 15 when Darwin arrived.”10 Wikimedia commons/Avenue A dome-backed, short-necked, giant Galápagos tortoise. Concerning their shell shapes, the larger dome-backed, short-necked offspring could have survived in the humid highlands where there was plentiful vegetation. However, the smaller saddlebacked, longer-necked offspring probably survived better on the dryer grass-free islands because they could reach the tall cactus vegetation, whereas the dome-backed offspring would have starved.11 These are nice examples of natural selection in operation, just like the finches, but this sort of thing will not change a tortoise into a non-tortoise (a different kind of animal)—‘evolution’. As to Attenborough’s alleged “many thousands of generations and millions of years”, all the tortoises can hybridize (i.e. interbreed).12 CMI geneticist, Dr Rob Carter points out in our Darwin documentary film Darwin: The Voyage that Shook the World that, because the major Galápagos islands are only about 50 to 65 km (30 to 40 miles) apart, over millions of years you would expect species to migrate from island to island again and again and again and again, with all sorts of hybridization and blurring of the species lines. Why then, our film asks, do we still see such differences from island to island? The obvious answer speaks strongly against evolution’s ‘millions of years’. How did the Galápagos islands form? Attenborough asks: “Why should the environments of the islands be so different?” And he replies: In the 3 million odd years since this island emerged above the surface of the ocean, it has drifted in a south-easterly direction by about 60 miles (95 km). … A giant hotspot, rising from the earth’s molten core, began to build the Galápagos, four million years ago. But, as the island drifted away from it, other volcanoes replaced it, one after the other. … But then, as each moved away, eruptions ceased. So a group of islands appeared one after the other. This is what his fellow evolutionists generally believe, but no one saw it happen. It may well have been quite different. And indeed, the creationist explanation is that these islands would have formed after the Flood by volcanic action, within a moderate time frame, similar to the way Surtsey Island formed off the coast of Iceland from 1964 to 1967. This is explained in depth in our response to his first episode in this series, see creation.com/galapagos-origin. The behaviour of lava lizards is not evidence for evolution Male lava lizards do push-ups to establish their territory and attract females.Attenborough’s next claim for evolution is the change in the behaviour of animals, and he directs viewers’ attention to the small lava lizards that grow to a maximum size of 1 foot (30 cm). We are told that each island has its own distinct species, which differ “not so much in the way they look as the way they behave”. The males compete with one-another for territory and for females by doing pushups. These vary in the number, the intensity, and the speed at which the lizards do them, and how high they bob their heads. Attenborough says: “The responses vary from species to species. In other words, each species has its own language of gestures. … Now, because they have developed different gestures, they can’t interbreed, even if they meet. They’re separated by a language barrier.” To set the record straight: Tze Keong Chow of the University of Michigan writes: “‘Push-up’ displays are used to ward off intruders, as well as courtship communication. Change of skin color can communicate the mood of the lizard from fear to aggression.”13 As all seven sub-species do this, obviously all seven species know what the push-ups mean. In other words, they all do have ‘a similar language’! Whether the seven sub-species can interbreed does not appear from the literature to have been investigated to date. Be that as it may, they are all still lava lizards. They have not evolved into anything else, like birds, or even into the larger iguanas. Galápagos snail species are not evidence for evolution
Attenborough says: “New technology now enables students to investigate the workings of evolution in ways that Darwin could hardly have ever imagined.” He then shows viewers X-rays of several different tiny snail shells (about 1 cm long) and says that their shape is “different enough to define them as separate species”. These live in different habitats, such as black lava rocks, sandy beaches, dark caves, leafy forests, well watered areas, and dry areas. However, these X-rays show very little that Darwin could not have seen with a good magnifying glass (if he had looked). They do not even demonstrate that the sub-species arose on the Galápagos, as no evidence is offered as to how many species or how few arrived from South America, or whether there were some that preceded any of the others, and if so which. Nevertheless Attenborough makes the gratuitous claim: “In other parts of the world evolution usually proceeds in a slow gradual way. It can take millions of years for a new species to appear. But in Galápagos it’s been happening in the evolutionary blink of an eye.” This is a non-sequitur.14 In any case, formation of sub-species does not establish any form of Darwinian evolution, as against the recent Flood-migration model, which entails speciation, not just the formation of sub-species. Lack of large predators is not evidence for evolution Attenborough tells us: “Galápagos for its size has more unique species than anywhere else on Earth, and all have appeared in the islands’ comparatively short history.” And he asks: “Why did such a great number appear so quickly?” His answer is the absence of large predators, and he says that because of this: “Time that would be spent hiding from attackers can now be used to find food, find mates, and raise young and so produce more young, which hastens the progress of evolution.” However, this is a fallacy, even from an evolutionary point of view. There are lots of species that are at the top of the food chain in their habitats, and this doesn’t produce more speciation, which Attenborough continues to confuse as ‘evolutionary’ change. E.g. lions, rhinos, hippopotamuses, crocodiles, sharks, eagles, hawks, and so on. He continues: There is no more impressive example of that than Fernandina’s iguana colony. With no significant predators around, these herbivores produce lots of young; so many that their problem is not how to defend themselves, but how to find enough food to support their great numbers. So they ventured into the sea itself to graze seaweed on the sea floor. … The lack of big predators has had an effect on all the animals of the Galápagos. They reproduce freely, so populations increase rapidly. And so, consequently, does evolutionary change. Population increase due to lack of predators has had nothing to do with speciation, as claimed. Oops! Attenborough must have forgotten what he said in the second episode of this series, concerning the very first iguanas that arrived in the Galápagos. In that episode he said: “To survive, these iguanas had to eat the only kind of leaf that was available, seaweed … .” So the initial eating of seaweed had nothing to do with the numbers! And since then, population increase due to lack of predators has had nothing to do with speciation, as claimed. Have humans affected the course of evolution on Galápagos? We are told that “Scientists are now trying to analyse the impact of human beings on the course of evolution in the islands.” It is claimed that the medium ground finch in its natural setting has both small and large beaks, caused by the type of foods they eat, and “is on the verge of dividing into two separate species”. However, this has not happened, as Attenborough’s guest, biologist Andrew Hendry, explains: It is as if the two variants are here merging back into one. The presence of human beings has stopped this finch from evolving. They feed a lot on human food, ranging from rice to fruit to grains to potato chips. Feeding on those types of different foods, it doesn’t really seem to matter what your beak size is any more. … So it seems like humans have caused a speciation reversal; they’re fusing back together again as a result of human influences. Speciation reversal, yes. Evolution, no. A new pink iguana is not evidence for evolution Viewers are told: New species are still being discovered. One was found just 35 miles (55 km) north of Alcedo on the giant, little-visited volcano Wolf . … A completely new and unknown species of reptile. A pink iguana. … Genetic studies of the hundred or so individuals that make up this tiny population have shown that it diverged from its land iguana cousins more than five million years ago … but has remained unknown to science until now. How could it have diverged “more than five million years ago” on islands that supposedly didn’t begin to form until four million years ago? This is just one of many indications that the millions of years claimed by evolutionists for everything about the Galápagos is ‘just-so’ story-telling, a product of their imagination, and not ‘facts’. Conclusion Variation within created kinds has been seen on the Galápagos, but nothing that supports the view that all life on Earth came about by mutations and natural selection, with one kind of organism changing into an entirely different kind, over millions of years. Rather, the data from the Galápagos make excellent sense within the recent migration worldview.15 Galápagos with David Attenborough: Adaptation by Russell Grigg Published: 9 April 2013 (GMT+10) Galápagos with David Attenborough is the title of a 2013 three-part Sky 3D TV series that was shown in Australia with the revised title David Attenborough’s Galápagos. In this, the second episode,1 Sir David discusses the way animals have adapted to the varying conditions on the Galápagos islands. He labels various islands as ‘old’, ‘middle-aged’, and ‘young’, but the millions of years claimed by evolutionists for all this to have happened are not needed in the creationist model.Attenborough shows viewers the crescent-shaped island of Tortuga,2 which he says is the last fragment of an extinct volcano, and he goes on to say that each island: Is born on the bottom of the sea and rises up through the waters to emerge as a volcano. … But then after a million years of eruptions, volcanic activity ceases. Two million years after its first appearance, the island is approaching middle age, it has a moist climate, and is covered by forest. It begins to sink under its own weight of ash and lava. It’s battered by erosion and, after four million years, it’s near the end of its existence. Low lying and arid, with little rainfall, it’s surrounded by beaches of soft sand. The waves and rain [sic] continue to take their toll, until all that is left is a craggy outcrop of rock. Today there are islands in the Galápagos archipelago that illustrate every stage in this history.
Earth Observatory 8270 and NASA GSFC; Wikimedia commons/M.Minderhoud. Click to enlarge. In our response to his first program in this series, titled Origin, we showed how the recently formed volcanic island Surtsey (near Iceland) mimics most of the features of the Galápagos islands, but all within a few years after Surtsey rose from the sea in 1963. Note that Surtsey stopped erupting in 1967. There is no way that anyone can show that any island has experienced “a million years of eruptions”, as Attenborough claims above! In the last 50 years, there have formed on Surtsey wide sandy beaches, gravel banks, impressive cliffs, soft undulating land, faultscarps, gullies and channels, and “boulders worn by the surf, some of which were almost round, on an abrasion platform cut into the cliff.”3 Millions of years were not necessary for these features to form, either on Surtsey or on Galápagos. See: Surtsey, the young island that ‘looks old’
Surtsey still surprises Likewise, since Surtsey stopped erupting in 1967, erosion has caused the island to substantially diminish in size (see later). A large area on the south-east side has been eroded away completely, while a sand spit called Norðurtangi (north point) has grown on the north side of the island. Again, millions of years were not necessary for this erosion to take place, either on Surtsey or on any of the islands that make up the Galápagos. Wikimedia commons/D. Gordon E. Robertson Marine iguana on Santiago island. Marine iguanas are not evidence for evolution Attenborough introduces these reptiles by telling viewers that their ancestors almost certainly lived in the jungles of Central America, where they are vegetarians. Then he says that ‘a long time ago’ a few were swept by favourable currents out to the ocean and pitched up in the Galápagos. To survive, these iguanas had to eat the only kind of leaf that was available, seaweed, of which there was an endless supply under the water. So, he says: They had to swim. They even learned to dive. They acquired the ability to hold their breath for up to an hour. Their claws strengthened so they could cling to the rocks on the seabed. Their snouts became flatter to help them graze. Their teeth became sharper to grip the slippery seaweed. Such learned behaviour and variation within a species are not the result of biological evolution, which is about the changes in genes that would be required to turn microbes into marigolds, mice, and musicians; and prokaryotes into professors. However Attenborough does make one claim for evolution, he says that because these iguanas ate nothing but seaweed “they evolved a special gland in their nose [to] sneeze the excess salt from their blood.” The Galápagos land iguana Conolophus subcristatus also appears to possess salt glands, 4 as do (elsewhere) crocodiles, sea snakes, marine turtles and some seabirds. The salt disposal mechanisms in these animals are different, and this poses a huge problem for evolutionists in explaining how these salt disposal features evolved not just once but several different times in different creatures and in different locations.In addition to being the residence of the marine iguana, the Galápagos Islands are home to seven species of lava lizards (genus Tropidurus) and two species of land iguana (genus Conolophus).5 The iguanas have similar enough genetics to produce hybrids. This suggests that they thus all belong to the same original created kind.6According to the young age worldview, these animals were created complete with all the features within their bodies that He knew they would need to survive in their various habitats, and to adapt to their various circumstances (including salty diets). El Nino does not promote evolution Attenborough tells us that every three to seven years the extreme and irregular weather condition known as El Nino decimates the food supply of the Galápagos marine iguanas, and this causes as many as 90% of them to perish. He then claims: Iguanas have evolved a special ability that enables them to survive the famine. Their bodies shrink. The iguanas can actively reduce their skeletons over just a few months … by as much as 20%. They lose not just fat and muscle, but bone. … This amazing ability to reabsorb bone in times of hardship is unique to these reptiles. However, these marine iguanas have not evolved into non-iguanas. The ‘shorties’ are just as much marine iguanas as their starved-to-death parents were. In all vertebrates, bones are constantly being restructured to oppose stresses. This involves a fine balance of the activity of bone-depositing cells (osteoblasts) and bone resorbing cells (osteoclasts). There are natural
variations in the speed of these processes. In an environment exposed to famine, natural selection would select the individuals that had greater rates of bone resorption and depositing. See: Bone building: perfect protein Bridges and bones, girders and groans Symbiosis is not evolution Attenborough’s next example of ‘evolution’ is on Santa Cruz island when the climate changes and the eco-system is exposed to the equatorial heat. He says: Wikimedia commons/Haplochromis Scalesia trees on Santa Cruz island. Some trees, however, have evolved a way of protecting themselves. The [Scalesia tree shown] has developed a mutually beneficial relationship with the lichen that grows on it. The lichen shields the tree from the sun, preventing it from getting scorched. And the tree provides the lichen with moisture and nutrients. But if the weather gets really sunny, then the lichen shrivels and stops taking nutriment and moisture from the tree, but at the same time still prevents it from getting sunburnt. And when the moisture returns, the lichen can grow back. So plant and lichen make the best of the two extremes of climate. This is an excellent example of the biological phenomenon known as symbiosis (‘together-living’), but symbiosis is not evolution. No increase in information is involved. Real evolution would require changes that increase genetic information, while non-information-increasing changes such as the one shown are part of the creation model. 7 As Australia’s top scientist, Dr Raymond Jones says of the symbiotic relationship in cattle rumen: “The animal needs the microbes and the bugs need the animal. It’s a good example of design.” 8 So this evidence, claimed by Attenborough to support evolution, actually supports the creation model. Wikimedia commons/David Adam Kess One of the hundreds of lava tube tunnels on Santa Cruz island. Blind spiders are not evidence for evolution Subterranean animals live in the network of hundreds of tunnels on Santa Cruz island called lava tubes. Attenborough introduces these by saying: “Here the speciestransforming power of the Galápagos is as active as everywhere else.” And we are further told that there are species unknown to science. Viewers are shown an amblypygid—‘half scorpion, half spider’, a millipede that has lost all its colour, and we are told that: Spiders too haunt the lava tubes. And just like the tortoises and iguanas, these creatures have evolved into many different species. There are 90 of them, all unique to the Galápagos. The spiders don’t just differ from island to island. They do so dramatically even within a single lava tube. Some that have been here for a long time are blind and feel their way through the cave. A few have lost their eyes entirely. But living just centimeters from them are more recent colonist species that still retain their eyes. However, speciation is an important part of the creation model. Speciation and adaptation are not evolution in the bacteriato-barristers sense. SeeSpeciation Q & A and ‘Evolution in action’ or ‘Evolution inaction’. Furthermore, blind cave spiders are examples of ‘downhill’ or ‘information-losing’ mutations causing ‘devolution’, not evolution. Such a degenerative process could not generate seeing eyes in the first place .Consider a spider which, because of a mutation, acquires a defective gene for eye development. Such a defect would be passed on to all of its descendants. Above ground, such a mutation would very quickly be ‘selected against’, as any spider inheriting it would be less likely to find prey and evade predators. But in a totally dark environment, blind spiders are not at a disadvantage to their sighted fellows, because eyes are no longer an asset. They can easily be injured in darkness, e.g. by sharp rocks, allowing the entry of potentially lethal bacteria. On average, the eyeless spider will be more likely to survive and reproduce. It would not need many generations before all the spiders in that environment were of the ‘eyeless’ type.9 Atheists are fond of using blind troglobionts (cave-dwelling organisms) as evidence for evolution.. 10 In fact, as shown above, creationists would have no problem with arch-atheist Richard Dawkins’ explanation: Evolutionists on the other hand, need to come up with an explanation for the loss of eyes where they are no longer needed. … How does losing its eyes benefit an individual cave salamander so that it is more likely to survive and reproduce than a rival salamander that keeps a perfect pair of eyes, even though it never uses them?Well, eyes are almost certainly not cost free. Setting aside the arguably modest costs of making an eye, a moist eye socket, which has to be open to the world to accommodate the swivelling eyeball with its transparent surface, might be vulnerable to infection. So a cave salamander that sealed up its eyes behind tough body skin might survive better than a rival salamander that kept its eyes.But there is another way to answer this question … most mutations are disadvantageous, if only because they are random and there are many more ways of getting worse than getting better. Natural selection promptly penalizes the bad mutations. Individuals possessing them are more likely to die and less likely to reproduce, and this automatically removes the mutations from the gene pool. Every animal and plant is subject to a constant bombardment of deleterious mutations: a hailstorm of attrition. It is a bit like the moon’s surface, which becomes increasingly pitted with craters due to the steady bombardment of meteorites. With rare exceptions, every time a gene concerned with an eye, for example, is hit by a marauding mutation, the eye becomes a little less functional, a little less capable of seeing, a little less worthy of the name of eye. In an animal that lives in the light and uses the sense of sight, such deleterious mutations (the majority) are quickly removed from the gene pool by natural selection.But in total darkness the deleterious mutations that bombard the genes for making eyes are not penalized. Vision is impossible anyway. The eye of a cave salamander is like the moon, pitted with mutational craters that
are never removed. The eye of a daylight-dwelling salamander is like the earth, hit by mutations at the same rate as cavedwellers’ eyes, but with each deleterious mutation (crater) being removed by natural selection (erosion).11 Millions of years not needed to erode Galápagos islands We are told that the island of Española is “nearing four million years old”, and “its forests have gone”. Presumably we are meant to deduce that one statement is proof of the other. However, Attenborough offers no evidence that Española ever had forests. He continues: Millions of years of erosion have created beaches of soft sand, and they suit some animals very well. [Such as Galápagos sea lions, and nesting waved albatrosses shown.] The many habitats of Española and all aging Galápagos islands were created by the erosive power of sea and weather, but erosion can have only one final result. Destruction. So a Galápagos island worn down by the waves and the weather eventually reaches the last stage of its existence. After millions of years sustaining life, all that remains of it above water is a rocky curving cliff, like Tortuga.” [Shown.] Top: NOAA; Bottom: Wikimedia commons/Worldtraveller Top: Surtsey shortly after it began erupting in 1963. Bottom: Surtsey in 1999. Notice the many ‘old-looking’ features on this young island. By 2002, it had eroded and subsided to half it’s maximum size.However, millions of years are not needed to erode a volcanic island to water level. In the years following the eruption from the seabed of Surtsey, measurements revealed that the island was slumping vertically and, in the 24 years of observations from1967 to 1991,12 had lost 1 metre of its original height of 174 metres. (Española is currently 200 metres high.) By 2002, Surtsey had shrunk to 52% of its maximum size in 1967.13 Attenborough goes on to tell us that “The remains of Galápagos islands stretch for hundreds of miles across the Pacific seabed.” However, in the young age worldview, these erupted towards the end of the Flood, as the ocean basins were established. Conclusion Attenborough’s purpose in this episode appears to have been to inculcate a time frame of millions of years (he mentions this no less than eight times) for the Galápagos islands, and to present the animals and plants there as evidence for evolution. In this he is following the evolutionist, anti-creationist and liberal theologian Rev. Post-Flood mutation of the KIT gene and the rise of white coloration patterns by Jean K. Lightner Identifying mutations and patterns of their appearance and impact is important in furthering the young age model. Genes affecting coloration are relatively easy to identify and several have been well studied. Here, variation in a gene affecting the development and movement of pigment cells, KIT, is examined. This complex gene codes for a complex protein important in a number of pathways. Many mutations have been identified in each of the species studied. Interesting examples of epigenetic modification and reversions have been documented in mice. This gene has shown up in surprising places in cats and dogs. Some mutations result in pleiotropy, although this is variable depending on genetic background, type of mutation, and location of the mutation. Mutations also result in interesting variety including white animals and white spotting phenotypes. Horses with roan coats have white hairs evenly intermingled throughout any other color. It has been mapped to the KIT locus. Previously, creationist studies have pointed out the importance of evaluating genetic data to determine the types of mutations which have likely occurred throughout history. This will contribute to a deeper understanding of the role mutations play and better inform apologetic arguments as it further builds the young age model. We don’t have enough information to know the genetic variability that existed at creation. We are not told how many animals were created in each kind. However, we do have an idea of the genetic variability that could be expected after the genetic bottleneck at the Flood. Unclean animals, such as pigs, horses, and mice, survived the Flood as single breeding pairs. Thus, up to four alleles for any particular locus could have been present. For humans, a maximum of 10 alleles could have made it through unless the people carried mutations.Genes affecting coat color are relatively easy to discover and study since they obviously affect the appearance of the animal. So far, well over three hundred genes have been identified as affecting coat color in mammals.1 Some of these, such as the MC1R2 and ASIP3 genes, have been fairly well studied and useful information has been obtained by examining mutation patterns at these loci. Mutations in these genes affect proteins involved in the signaling pathway for pigment production and explain a large amount of the color variation in mammals. Other genes
affecting coloration are involved in pigment production or development (i.e. regulating the development and migration of pigment cells during embryogenesis). The KIT locus One locus important in embryogenesis, KIT, has been associated with white coat patterns in several mammalian species and piebaldism in humans. The white areas are depigmented due to the absence of melanocytes, the cell type which produces pigment.KIT has also gone by several other names including c-kit, v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog, stem cell factor receptor, mast cell growth factor receptor, and CD117.4 It encodes a receptor tyrosine kinase involved in the development and homeostasis of several cell lines including melanocytic (pigment), hematologic (blood), mast, and germ cells. 5 This explains why heritable loss-of-function mutations sometimes have pleiotropic effects, not only resulting in white color patterns, but also anemia and/or infertility. Some of the stronger mutations cause a dominant white phenotype which is lethal in the homozygous condition. Activating (gain-of-function) mutations, which are generally somatic and not heritable, have been associated with progression in certain cancers. 6The KIT gene is rather complex consisting of 21 exons in a 70 kb region. Most of the exons are relatively short (<300 bp). The exception is the final exon which not only codes the terminal portion of the receptor, but also includes a 2,147 bp non-coding sequence that follows. This complex organization of the gene reflects the complex nature of the protein receptor it produces.Extracellularly the receptor is made up of five immunoglobulin-like domains. Each is coded by one or two exons with the boundaries of the exons defining the boundaries of these domains. The receptor makes a single pass through the cell membrane and contains an intracellular kinase catalytic region divided by a hydrophilic insert. Most of the 10 exons coding the intracellular portion correspond to specific structural elements, such as α-helices or β-sheets. 7 Both mice and men express two isoforms of this membrane-bound receptor8 from alternative splicing; these isoforms differ somewhat in their signaling characteristics.9Expression of KIT and its ligand, sometimes referred to as stem cell factor, occur in waves during development and have intricate homeostatic patterns in the adult. Ligand binding induces activation of tyrosine kinase through dimerization of receptors.6 This subsequently influences a variety of pathways downstream. The pattern of downstream activation is dependent on numerous other cellular factors. Thus, the receptor does not behave as a simple on/off switch, but instead as an “inducible and malleable scaffold upon which multiple cellular regulatory mechanisms can be modulated.”10 Variability in the KIT locus Variability in the KIT locus will be examined with the following questions in mind. Is there evidence for mutation in this gene? If so, what type(s) of mutations occur and what effect do they have on phenotype? Are the mutations most likely pre- or post-Flood? Are there any particularly unusual patterns that exist in regard to these mutations (e.g. in type, timing and/or location)? Pigs (Sus scrofa) KIT resides on the short arm of chromosome 8 in the pig (SSC 8p12). At least eight different alleles have been identified (table 1).11 The wild type (i) was identified in the European wild boar and most colored domestic European breeds. The belted phenotype (IBe) of the Hampshire was mapped to this locus and is believed to be the result of a regulatory mutation. This dominant allele, which produces a white belt around the shoulders and front legs, is carried in the homozygous state with no apparent ill effects. Table 1. Summary of KIT mutations in pigs associated with white or partial white phenotypes ALLELE
PHENOTYPE
BREED
MUTATION(S)
INHERITANCE
i
wild type
European wild boar
NA
—
IBe
white belt
Hampshire
unknown
dominant
IP
patch
Pietrain
gene duplication
semidominant
I1
white
Large White
IP allele with splice mutation in one copy
dominant
I2
white
Large White
I1 allele with an additional duplication of the normal dominant gene
I3
white
Large White
I1 allele with an additional duplication of the copy dominant with a splice mutation
RC1
white
Chinese Rongchang
White V84M, R173K, V893A
recessive
RC2
white
Chinese Rongchang
White V84M, V893A
recessive
The patch allele (IP), a semidominant mutation resulting from a gene duplication, produces a phenotype of white and colored patches that are separated by sharp borders. There are three related dominant white alleles (I1, I2 and I3). The first was discovered to have the same gene duplication as the patch allele with one copy containing a splice mutation. The splice mutation is the result of a G to A substitution in the first nucleotide of intron 17 which leads to skipping exon 17. 12 The second and third alleles contain an additional duplication of the copy without and with the splice mutation, respectively.13 Despite the fact that dominant white alleles in other species can be lethal in the homozygote, these very popular white pigs are generally homozygous and show no ill effects.Two additional alleles have been identified in the Chinese White Rongchang. These lacked the gene duplication and differed from the sequence in European pigs by up to 10 nucleotide substitutions. Three amino acids are affected (V84M, R173K, and V893A) from exons 2, 3, and 19 respectively. The first was considered worthy of further investigation in potentially being associated with the recessive white phenotype in these Chinese pigs.14Since pigs are unclean, a maximum of four KIT alleles would have been carried by the pair on the Ark. The number of alleles in domestic pigs is at least twice this, indicating that new alleles have arisen post-Flood by mutation at this locus. Researchers identify mutations as a change in nucleotide sequence relative to the wild type, which in this case is
the European wild boar. In reality, the wild boar itself may carry mutations, but there are other details that can sometimes help to identify alleles carrying mutations. Alleles responsible for impaired migration of melanocytes, resulting in white coloration, can logically be inferred to carry mutations. This would include the mutations found in European domestic pig breeds, but not necessarily all polymorphisms in the Chinese White Rongchang. Most likely all of the mutations affecting coloration are post-Flood since these alleles don’t appear to be widely distributed in pigs. If the alleles were older and existed at the time of the population bottleneck, a much wider distribution would be predicted.There is an obvious bias toward gene duplications in European pigs. Four alleles contain gene duplications, suggesting at least three separate duplication events affecting the germ-line, thus making them heritable. It was suggested that the initial duplication acts as a dynamic mutation, increasing the chance of a subsequent event. Increased sequence homology resulting from the duplication is believed to increase the probability of additional rounds of gene conversion, unequal crossing-over, and subsequent rearrangement.15 Horses (Equus caballus) KIT resides on the long arm of chromosome 3 in the horse (ECA 3q). 16 There are over 15 alleles; 14 of which are associated with some degree of depigmentation (white or white spotted phenotype). 17 Roan horses are characterized by white hairs interspersed with pigmented hairs throughout much of the body. This dominant phenotype is assumed to be lethal in the homozygote. It has been mapped to the KIT locus, although the causative mutation has yet to be identified. Interestingly, some mRNA transcripts from a roan Belgian horse contained a 79 bp L1 element between exons 1 and 2. This resulted in a frame-shift and a non-functional protein. However, this L1 insertion was found in both roan and non-roan horses, although it was more common in the former.18The Tobiano color pattern typically consists of large white patches on the body and limbs which often extend across the dorsal midline. It is common among American Paint Horses and is found in other diverse breeds as well. Although no differences exist in the coding region of KIT, similarity was noted between this phenotype and several spotting patterns in mice that involved chromosomal rearrangements near this gene. Subsequently, a large paracentric chromosomal inversion was identified about 100 kb downstream from KIT which is suspected to disrupt regulatory sequences for the gene resulting in this dominant white spotting pattern. This allele was identified in Tobiano individuals from 12 different breeds, indicating an ancient origin. Homozygous individuals are phenotypically indistinguishable from heterozygotes; both are fully viable.19The Sabino white spotting pattern involves white patches on the face and legs which may extend up to the belly. Sometimes the belly and midsection have a more diffuse scattering of white hairs similar to the roan phenotype. One allele causing this phenotype was discovered with a T to A substitution in intron 16. This resulted in many transcripts missing exon 17. Homozygotes had more pronounced expression of the defective transcript and a white phenotype, but were fully viable. Also, heterozygotes that carried a second allele for a different spotting pattern, such as Tobiano, were white as well. 20There are eleven additional alleles that have been identified in horses with white or partial white phenotypes, all of which arose within the last 100 years. Three of these involve splice mutations in an intron, two involve a deletion in an exon resulting in a frameshift and premature stop codon, four involve non-synonymous substitutions which change the amino acid (missense mutation), and two involve non-synonymous substitutions which replace the amino acid with a stop codon (nonsense mutation). Some of these are associated with a dominant white phenotype which is believed to be lethal in the homozygous state. While none of the mutations were found in the homozygous state, not all resulted in a dominant white phenotype. Furthermore, in four cases only one white horse, presumably the founder animal, was tested. It remains to be seen which of these alleles may allow for viable homozygotes.17Considerably more than four KIT alleles are present in horses, indicating an increase in alleles due to postFlood mutation. Of the 14 alleles associated with depigmentation, and thus most likely the result of mutation, the origin of 11 were documented in the last 100 years. The other three appear to be older as they have a wider distribution in domestic horses. Still, it is likely that they are post-Flood since they do not appear to be present extensively in the equine baramin (which includes donkeys and zebras). Mice (Mus musculus) In laboratory mice Kit21 is on chromosome 5 (MMU 5). There are 97 alleles, 66 of which arose via spontaneous mutation.22 These alleles, only some of which have had the underlying mutation identified, show a variety of phenotypes and pleiotropic effects. Only a few will be discussed here.The dominant white spotting allele (W) in heterozygous mice results in fully viable and fertile adults with a white belly spot, white feet and tail tip. It was noted that in the early post-natal period these mice have unusual blood values. This allele in the homozygous condition is usually lethal due to severe macrocytic anemia. Few homozygotes are born alive, and those normally die within a day or two. The very few that survive to adulthood are black-eyed, white, severely anemic, and sterile. The difference in viability of homozygotes has been attributed to the different genetic backgrounds in which it occurs.23 The allele is attributed to a G to A substitution at a splice donor site in intron 10 which results in exon skipping in the transmembrane region. 24,7A viable dominant white spotting allele exists (Wv) where a white belly spot, white feet and tail tip are also seen along with significant dilution of the remaining coat pigment. Heterozygous mice are usually viable and fertile, but slightly anemic. In the homozygote the lifespan is near normal; they are black-eyed, white, less anemic than dominant white (W/W) mice, and may be semi-fertile. 23 This allele carries a single missense (T660M) mutation.25 A number of other alleles were found that result in a similar phenotype to W (Wa, Wj, Wx) or Wv (Wb, We).23Initially it appeared that mutations in mice had a similar effect on all three tissue types: melanocytic, hematologic and germ. However, mutations appeared that soon showed this was not always the case. For example, the fertile white mutation (Wf) appears to be the result of a missense (R816W) mutation in this gene. It is associated with anemia and pigment defects, but mice are fertile even in the homozygote (if it survives; there is an increased postnatal fatality rate).26 In contrast, an induced mutation (Y719F), which alters the binding site for the p85 subunit of PI 3-kinase, has a negative effect on spermatogenesis and oogenesis, yet no observable pigment or hematopoietic defects.27Several alleles have been identified where the mutations involve major rearrangements in the 5' regulatory region of this gene. W57 carries an 80 kb deletion in the 5' region; homozygotes have an irregular white band on the trunk, a white head spot, very mild anemia, and normal fertility. The white banded (Wbd)28 and sash (Wsh)29 alleles arose separately by spontaneous mutation involving a large 5' inversion affecting the orientation of numerous upstream genes. Heterozygotes carry a white band or sash on the trunk; homozygotes exhibit black eyes, white fur with possible residual ear and snout pigment, with normal fertility and red blood cell parameters. All three alleles are associated with mast cell deficiency from a lack of KIT expression. Interestingly, the Wsh allele is associated with increased Kit expression in dermatomal cells during embryonic development which is believed to cause the pigmentation defects.30 This is in contrast to W57 where KIT expression is down regulated in early trunk melanoblasts.28 Several tissue specific control elements have been identified in this upstream region. 30A cryptic promoter has been identified in exon 16 which is active in post-meiotic germ cells in the testes of mice. This cell specific promoter is only active during a short temporal window during spermatogenesis and results in a third gene product: a truncated protein which lacks the extracellular, transmembrane and first tyrosine kinase domains. 31 This truncated protein is suspected to play a role in fertilization since it has been observed to trigger parthenogenetic completion of meiosis II and pronuclear formation when microinjected into mouse eggs.32Reverse mutations are considered to be rare in mammals, but
12 mutations affecting pigmentation in mice show unusual phenotypic instabilities. One of these, the viable yellow at the Agouti locus, has been examined in previous creationist literature. 3 Seven of these mutations are at the KIT locus (Wa, WJ2, W37, W42, Wei, Wv = W55, Wrio). Mice heterozygous for the Wrio mutation are mostly white with some scattered pigmented hairs. In a French study, 3.6% of the heterozygotes exhibited strongly pigmented spots on a typical mutant background nearly devoid of pigment cells. Melanocyte cell lines were established from six independent reversion spots. Three of these appear to have undergone somatic reversion via mitotic recombination. One showed an increase in KIT expression and response to KIT ligand despite retaining a Wrio/+ genotype. The remaining two failed to respond to Kit ligand. While the underlying mechanism for phenotypic reversion was not demonstrated in the last three cell lines, the authors suggest that enhanced KIT expression, compensatory mutation, and/or another receptor tyrosine kinase in a similar pathway could compensate for KIT mutations on some genetic backgrounds.33There is evidence that epigenetic inheritance can occur at this locus. Unlike the epigenetic inheritance described at the Agouti locus,3 this does not appear to be associated with DNA methylation. It occurs in offspring of mice heterozygous for a targeted gene mutation (KITtm1Alf), which contains a lacZ insertion in the first exon. The homozygous wild type offspring retain, to a variable extent, the mutant phenotype of white feet and tail tip from a marked decrease in mature mRNA. Additionally, continued expression of full length KIT mRNA and increased expression of the truncated KIT mRNA during the post meiotic phase of sperm formation were observed in mice heterozygous for the mutant gene and in paramutated mice. These gene products were detected in mature sperm as well. Suspecting that the presence of this RNA might induce the mutant phenotype, researchers microinjected total RNA from heterozygotes into fertilized eggs which induced the mutant phenotype about half the time.34 Humans In humans KIT resides on chromosome 4 (4q12). Loss-of-function mutations at this locus are associated with a condition known as piebaldism, a dominant disorder characterized by patches of white skin on the forehead, abdomen, and/or limbs. Thus far, nearly 50 different alleles have been identified in people exhibiting piebaldism including: 28 missense mutations, 5 splice mutations, 9 small deletions, 4 large deletions, and two small insertions. 35 The extent of depigmentation tends to correlate with the region where the mutation occurs. Generally, mutations affecting the extracellular region of KIT are milder while those affecting the intracellular region are more severe. 36 The explanation for this is that mutations in the intracellular region generally prevent the receptor from transmitting the signal while retaining the extracellular site used to bind its ligand and induce dimerization.37 In other words, these mutant receptors can tie up normal receptors because they can still form dimers with them; this results in a dominant negative effect. Mutations affecting the extracellular region appear to prevent the mutant receptor from forming dimers and only haploinsufficency results. Unlike similar mutations in the mouse, anemia and fertility problems are not associated with piebaldism in humans. 38Gain-of-function mutations have also been identified in KIT. Many of these are somatic mutations associated with sporadic gastrointestinal stromal tumors (GISTs). Most of these mutations occur in exon 11 which codes the juxtamembrane domain of KIT. This intracellular region precedes the first tyrosine kinase domain and is believed to be important in dimerization. Less commonly, specific mutations in exons 9, 13 and 17 have been identified. These regions code for portions of the extracellular region, first tyrosine kinase (TK) domain, and second TK domain, respectively.Germline gain-of-function KIT mutations have been identified in a dozen families and are associated with multiple GISTs. Mutation in the juxtamembrane domain is present in eight of these families. Among the remaining families mutations have been identified affecting the extracellular region, the first TK domain, and the second TK domain. Patients in some families also exhibit hyperpigmentation in certain regions of the body and/or mast cell tumors. 39 A maximum of 10 alleles would be expected to make it through the Flood in humans. Considering both gain- and loss-offunction heritable mutations, more than 60 alleles have been identified to date. All are rare and would be post-Flood. While the data in mice tended to emphasize the importance of genetic background on the severity of the phenotype for any particular mutation, the human data highlights the importance of the location of the mutation in understanding its influence on phenotype. Other interesting patterns KIT has a propensity to show up in unusual places. For example, an acute transforming feline retrovirus, Hardy-Zuckerman 4 feline sarcoma virus, was identified with the oncogene v-kit in its genome. This virus induces multicentric fibrosarcomas in the domestic cat. Compared to the cellular form (often called c-kit) there are some deletions at either end of the gene as well as a few point mutations.40KIT has also been identified on the B chromosomes in the fox and raccoon dog. B chromosomes are supernumerary chromosomes, often rich in repetitive DNA, present in the karyotypes of some species. This was the first instance of a coding gene identified on a B chromosome. It is possible this gene could be transcribed as it includes a significant 5' region where transcription regulatory sequences would be expected to reside.41 Conclusion KIT is an amazingly complex gene important in a number of critical pathways. Clearly there has been an increase in the alleles at this locus for the species examined here. The vast majority of these alleles are clearly the result of mutation given how they affect the function of the receptor. There is considerable diversity in the types of mutations found at this locus. Unlike the previously studied receptor involved in coloration, the MC1R, KIT mutations are more likely to have pleiotropic effects. Pleiotropy is affected by genetic background and the location and type of mutation.Pleiotropy was best documented in mice. There may be several reasons for this. First, laboratory mice are often highly inbred. Possibly some lines carry other mutations impairing their ability to compensate for the loss of KIT. Rodents in general seem to have a propensity for rather rapid genetic change, and this may come at a cost of being less able to compensate for future mutations. Second, mice are relatively easy to study in detail and some of the documented pleiotropy could be from increased scrutiny of these laboratory animals. It was interesting that pleiotropy was virtually absent in pigs, where gene duplication involving KIT was identified in many alleles.Interestingly, the number of human KIT alleles identified is comparable to the number documented for human MC1R alleles.42 Many of these alleles are quite rare, but were identified because of color differences. While there are suspected advantages to some mutant MC1R alleles in certain environments, no similar situation has been proposed for KIT alleles in humans.43 The lack of documented pleiotropy for most humanKIT mutations suggests that other factors are able to compensate for the loss of KIT. It is also possible that mild pleitropy associated with loss-of-function KIT alleles may be identified with further scrutiny.One final observation about KIT mutations is their association with interesting variety. White horses have been admired throughout history and are important in the model. White sows are very popular because of their high productivity and good mothering ability. White coloration in animals and a white forelock in humans certainly add to the variety and beauty found in natre. The paradoxical urinary concentrating mechanism by Charles Soper Mammals and some birds concentrate urine (and thus conserve water) by a compact mechanism composed of several necessary and interdependent properties. It is an excellent example of ‘irreducible complexity’, a system which fails if only one component is removed. Its genesis poses a serious problem for gradualists. This is well illustrated by the 8-year
resistance to adopting the current model of urine concentration by the leading renal physiologist of the time. He was a celebrated evolutionist, and opposed the model chiefly on the grounds that it violated gradualist principles. *
Items with an asterisk are defined in the glossary at the end of this article.
Figure 1. Countercurrent exchanger. Passive heat flow in an arm or a leg preserves core temperature and a sharp temperature gradient from core to periphery. Our current understanding of how the kidney concentrates urine is founded on the countercurrent hypothesis proposed by Hargitay, Kuhn and Wirz in 1951. 1 However, the hypothesis was by no means readily accepted at first. On the contrary, the great renal physiologist Homer Smith, was opposed to the idea until eight years later, when, in the face of accumulating evidence, he conceded defeat. Darwinian evolution was of special interest to him, and he believed it to be foundational to explaining renal function.2 As he recounts, it was his adherence to strict gradualism which led to his considerable resistance to the new theory.3 Curiously, an examination of the evolution of renal function, marking the centenary of Homer Smith’s birthday, bypasses this.4 Darwin’s challenge Darwin’s theory of evolution requires each modification of structure or function to be slight, and for each change to be justified by an advantage for survival. He adhered strictly to Carolus Linnaeus’s maxim “Natura non facit saltum” (nature doesn’t make leaps).“If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down.” 5He carefully qualifies this statement with three conditions under which relatively abrupt modifications might be observed. These are: firstly, the specialization of an organ possessing two functions into one function only (citing Hydra’s ability to respire and digest from the same surface); second, the modification of one of two organs both performing an identical function to a separate function (e.g. the simultaneous respiration of oxygen from water via the gills, or from air via the swimbladder, the latter putative converting to primitive lungs); and finally, the acceleration or retardation of the period of sexual reproduction in relation to ordinary maturation. Richard Dawkins restates this basic claim as the holy grail of Neo-Darwinian orthodoxy. 6 On this basis of gradual steps, he even aspires to account for the evolution of the eye. The countercurrent* concentrating mechanism Reptiles and amphibians are able to excrete nitrogen-based waste products via their kidneys, but are unable to concentrate urine. Concentration is the unique property of mammals and some birds by virtue of an extraordinary concentrating system. Its mechanism is counterintuitive and complex. Before examining its simplified essence, we review a more familiar, related device, the countercurrent exchanger. Consider, for example, the system of heat exchange in an arm or a leg on an icy day (fig. 1). Blood coursing from the heart into the arteries is at core temperature, but as it passes down the arm, it cools rapidly. By the time it reaches a gloveless hand, it may reach temperatures similar to the environment. As the blood passes back through the veins, it warms again rapidly, and by the time of its arrival at the shoulder, while still less than core temperature, it is much warmer than the air around. This conservation of valuable core heat is facilitated by an intimate relationship between the arteries and the vein network. Heat is exchanged from the arteries (leaving the heart) to the veins (as they return). The result is a sharp gradient in temperature down the arm. There is a hairpin loop, with flow running into, and out of it, and an exchange of energy between its two limbs. In this situation, all the transfer is passive, or ‘downhill’. Figure 2. Countercurrent concentrator, showing transport and permeability characteristics. Countercurrent exchangers* of a different kind form a vital part of the kidney’s concentrating mechanism, but its driving force is a countercurrent concentrator*(originally, but less helpfully, described as a multiplier). Unlike an exchanger, whichpreserves an existing gradient by passive transport, the concentrator generates a gradient by active transport. The transport that concerns us in the kidney is not of heat, but of salt and water. The lining of the tubules of the kidneys is equipped with a remarkably varied array of ion pumps and channels, each with a specific function and location, some of which are still being discovered and defined.7 The arrangement of these pumps and channels is complex, as are their interdependent functions, but to understand the countercurrent model, it is only necessary to grasp some fundamental principles. The transport characteristics are set out in figure 2. The descending limb of the loop is permeable to water and salt, which for our purposes means the electrolytes sodium and chloride. The lining of the ascending limb is largely impermeable to salt and water. However, it possesses a system of pumps which result in the active removal of salt from the tubule.It is difficult at first to see how active salt transport out of an impermeable tube should lead ultimately to a higher concentration gradient. After all, what takes place within the lumen of the ascending tube is dilution, which is why this part of the nephron* is often called the diluting segment. However, the looped arrangement enables salt pumped from the ascending limb to pass into the permeable descending limb, which leads to an incremental increase in salt gradient as the fluid in the loop reaches the tip. To help picture this mentally, consider a loop with these characteristics filled with, and surrounded by, saline at a particular concentration. As the fluid is driven through the loop, the gradients slowly change, first in the ascending limb in response to the pumps and then in the descending limb in response to local increases in salt concentration. This series of events is illustrated in figure 3. In life, the
two microscopic limbs of the loop are long and intimately intertwined; therefore the length of the axis of the loop is vastly greater than distance between its two limbs.
Figure 3. Progressing axial concentration gradient with countercurrent flow and active transport The driving force for the concentrator, or ‘single effect’ as the original paper describes it, is the energetic pumping of sodium and chloride from the ascending limb of the loop. In the figure, a hypothetical maximum gradient of 200 mmol/l is generated between the lumen of the loop and the surrounding fluid. As filtrate runs through the loop, the first event is a progressing dilution of fluid as it rises up the ascending limb. Progressively, salt pumped from the ascending limb accumulates in fluid around it and then by passive diffusion in the descending limb. Salt is passively concentrated in the fluid descending in the loop. Then as it flows past the hairpin bend, it, too, is progressively diluted inside the loop by the salt pumps in the ascending limb. This accumulation of salt in the interstitium* and in the descending limb gives rise to an axial salt gradient from the base to the tip of the loop. Eventually, as salt diffusion dissipating this gradient matches the pumping mechanism which generates it, a steady state is reached.The loop is also coupled with the final pathway of urine (the collecting duct *) before it is excreted (fig. 4). By varying the water permeability of the wall of the collecting ducts, fluid running inside it, up the concentration gradient generated by the loop, can be concentrated. This water permeability is controlled by the action of a hormone called vasopressin (VP). If VP is present, permeability is switched on and water is drawn out of the duct by the concentration gradient generated by the adjacent loop. If VP is absent, permeability is not activated, water remains in the duct and dilute urine is excreted. An obstacle for gradualism Figure 4. The coupling of the collecting duct with the nephron loop enables removal of water from urine before excretion. The concentration gradient generated by the loop is denoted by shading. Water permeability in the collecting duct is under the control of the hormone vasopressin (VP). It seems impossible to account for the urinary concentrating mechanism by “numerous, successive, slight modifications”, even after taking each of Darwin’s qualifications into account. Urine concentration requires the simultaneous presence of several contrasting properties in different parts of the nephron loop. Can anything other than a large and precise leap be conceived to account for its existence? Four major contrasting properties, each essential to any utility of the whole, are evident: its biologically eccentric hairpin loop structure, a salt- and water-permeable descending limb, a salt- and water-impermeable ascending limb, combined with ‘uphill’ active salt pumping, which is confined to the ascending limb.How could a structure derived from straight reptilian nephrons gradually progress towards a long, hairpin-looped configuration, after a small-stepped Darwinian manner, unless there was an adaptive advantage in doing so? What use could this be if not to concentrate urine? Could urine even begin to be concentrated until this process had progressed to very near similarity of shape to a mammalian nephron? How could the descending and ascending limbs progressively acquire contrasting water permeability characteristics, despite the fact that such properties would be of no adaptive advantage until an axial concentration gradient had been established? What selection benefit is there if the ascending limb of the loop, as distinct from other portions of the nephron, progressively accumulated considerable potential for ionic transport until all the rest of the concentrating mechanism was in place? If the descending limb also shared this marked active ionic transport, then the necessity for a clear distinction between the two for both water and sodium permeability is only heightened. However, multiple nephron loops with all the other necessary
properties but insubstantial active salt transport in the ascending limb would be completely futile for urine concentration. Nephrons with little difference in water permeability between the two limbs, despite every other necessary property, would again serve no purpose, particularly to the loop, other than to dissipate energy and thereby become a liability. A nephron of reptilian configuration with all the appropriate transport and characteristics, both active and passive, would achieve nothing other than generate valueless, transient ion fluxes, at the cost of its possessor.The real difficulty is that none of these quite different and necessary properties appear to confer any distinguishing selective value unless all are found together simultaneously, and found to be substantially present; substantially enough, that is, to begin to subserve the concentration of urine, thus providing a selection advantage to its possessor. A slight tendency towards the demonstration of any, or all, of these properties by a reptilian nephron will not generate any axial gradient, until a discrete state of quite advanced similarity in all four aspects to the mammalian nephron is attained. If one aspect lacks, urine concentration will utterly fail.Such a commitment to gradualism undergirded Homer Smith’s considerable reluctance to adopt Kuhn and Hargitay’s model. As he puts it: “I still do not like it: it seems extravagant and physiologically complicated—though so is the whole glomerular filtrationtubular reabsorption pattern … . Least of all however, do I like to see the squamous epithelium of the thin segment freely permeable to water (if not to sodium also) in the descending limb, only to acquire water impermeability and active sodium transport at the tip of the loop for no better reason, apparently, than the circumstance that it has turned a corner.”2 This comment begs the question, is evolution such a valuable key to understanding nature, as we so often hear, or has it become a blinker, blinding even the brightest of minds from perceiving the intricacies of the Designer’s handiwork? Has it become a presupposition to be defended in spite of the evidence?Nor do these four principle characteristics constitute the only foundation of the mechanism. The coupling of the loop with the collecting duct is also essential to concentrating urine prior to its excretion, with its variable water permeability under the control of VP. Without this control mechanism, urine concentration would lack regulation, water balance regulation would become impossible, and the device would become a dangerous liability. Similarly, maintenance of the concentration gradient in the loop requires that the blood supply matches and follows the course of the loop exactly. The capillary network around the loop in this way acts as a countercurrent exchanger, similar to the arrangements of the blood supply in the arm for preserving core heat. This enables the capillary contents to match the osmolarity of the loop, in some desert rodents reaching levels of up to 35 times plasma levels. These arrangements in some species realize remarkable intricacy.8,9 These blood vessel exchangers must also be sufficiently configured to allow for reasonable efficacy, right from the outset. Otherwise, any axial gradient would immediately disperse by downhill transport from isosmotic* blood.10 Gradualistic counterexamples examined To defend the possibility that the looped nephron might have evolved gradually from mammals, two examples are sometimes cited. The first is the looped tubules found in the kidneys of two species of lamprey, Lampetra fluviatilis and Petromyzon marinus,11,12 which have been claimed as evidence of a vertebrate antecedent for the loop of Henle. The claim is dubious. Briefly, micropuncture studies in the former showed no change in electrolyte concentration in the ascending limb of the loop, and although tubular fluid osmolarity falls by 13%, this appears mainly due to non-electrolytic osmolar transport,13 more characteristic of an earlier portion of the nephron than the loop of Henle*. The ascending limb, in contrast to its descending partner, reabsorbs water, which destroys the possibility of generating a concentration gradient.13 The length of the loop, at 1.1 mm seems too short compared even to simple avian nephrons 14 and the renal perfusion rate too slow to enable countercurrent concentration.15 Therefore, these loops, and other looping structures akin to them, such as those found in the dogfish, Triakis scyllia, do not serve as a useful functional paradigm for Henle’s loop, 16 and are not observed widely in kinds closer to birds and mammals.The second example is the smooth transition of forms between the reptilian (straight) and mammalian (looped) nephrons found in the kidney of Gambel’s quail, Lophortyx gambii.14 This might be used to indicate that “however the avian nephron did attain an advanced state, it most likely did so by small, discrete alterations”. Yet even its modest concentrating ability, at 2 to 3 times plasma osmolarity, is dependent not on the transitional nephrons, but on the longest-looped ‘mammalian’ nephrons (still short by mammalian standards). The situation has an analogy in mammals, in which nephron length varies considerably in the same kidney. Short-looped nephrons depend on, and augment, the concentrating work of longer-looped nephrons.8 Without denying a contribution from intermediate ‘reptile/mammal’ nephrons in the quail, their small assistance is wholly dependent on a pre-existent osmotic* gradient, generated and maintained by the longer, ‘more-advanced’ nephrons. A kidney entirely composed of intermediate nephrons of an attainable kind would not concentrate, despite considerable energy expenditure. It is therefore no basis upon which to assert the gradual modification of structure, when adaptive utility to the whole organ, or rather whole creature, is obligated for every new investment. Evolutionary gradualism appears far too thrifty for this. It is too short-sighted a workman to justify its reputation as a ‘watchmaker’, a visionary engineer capable of crafting improbable marvels. Conclusion Can any distinctive purpose for which Henle’s loop exists be proposed, other than urinary concentration, which might obviate these difficulties? If not, here is another argument as to why the presuppositions of neo-Darwinism require profound revision. Glossary Collecting duct:
The final common pathway for filtered fluid before it’s excreted as urine.
Countercurrent:
A looped system in which two flows run side-by-side in opposite directions as they flow through the loop.
Countercurrent concentrator:
A device which generates a solute concentration or energy gradient along the axis of a countercurrent loop, by a combination of loop properties, including active transport in the limb that exits the loop.
Countercurrent exchanger:
A device which preserves an existing gradient by passive (‘downhill’) energy or mass exchange across the two limbs of the loop.
Interstitium:
The extracellular tissue and space surrounding the loop.
Isosmotic:
An equivalent solute concentration to mammalian plasma (about 280 mOsm).
Loop of Henle:
The mammalian nephron loop, named after its first describer.
Nephron:
A unit composed of the structures which filter and modify urine. A human kidney contains about one million of them.
Osmotic:
The property of a solute concentrate arising from the tendency of solutes to flow down their concentration gradient. Osmosis is capable of generating considerable hydraulic pressure across a semipermeable membrane. ‘Vampire moth’ discovered by David Catchpoole
According to National Geographic News, “entomologists may have caught evolution in the act”.1 They have reportedly found a “previously undocumented population of vampire moths” in far-eastern Russia. The moths look just like a fruit-eating moth species,Calyptra thalictri, which lives in central and southern Europe.2 But the Russian population of moths sucks blood! Entomologists say it looks like the bloodsucking moths have evolved from purely fruit-eating ones.Film footage1 shows researchers offering their hands to the moths, which the moths accepted, drilling their hook-and-barb-lined tongues under the skin. One researcher can be heard saying “It’s starting to hurt” as a moth began sucking her blood. The bloodsucking can go on for several minutes—in fact, the researchers reported that some moths sucked for more than 20 minutes!Entomologists say that this discovery suggests that the Russian population of moths “could be on an ‘evolutionary trajectory’ away from other Calyptra thalictri populations”.1 However, contrary to the researchers’ claim, this is most certainly not “evolution at work”.1 Behaviour modification is not evolution! The moths are still moths. The “vampire moth” is more aptly viewed as yet another example of how a creature that is normally herbivorous can turn to non-plant food sources when it suits, as has happened with many creatures.3–8 Lizards moving from eggs to live birth: evolution in action? by Shaun Doyle Published: 18 November 2010(GMT+10) The lizards Saiphos equalis, Lacerta vivipara (pictured) and Lerista bougainvillii are the only three lizard species known that have the capacity for both oviparity and viviparity. Lizards reproduce in an amazing variety of ways. Some lay eggs (oviparity) and some bear live young (viviparity). Most species rely mostly on egg yolk for nutrition during embryonic development; a few have next to no yolk and rely completely on a placental connection to the mother. Some lizard placentas even compare with the complexity of mammalian placentas. Some species can vary the timing of birth. There are a rare few species that even have variety in their reproductive mode.National Geographic recently reported on one of these rare few species that have differing reproductive modes between populations—one of only three in the world—the yellow-bellied three-toed skink Saiphos equalis.1,2S. equalis is a small skink located mainly from the mountains to the coastline of New South Wales, Australia. Smoke and mirrors National Geographic portrayed these skinks as evolving from egg-laying to live birth: “Evolution has been caught in the act, according to scientists who are decoding how a species of Australian lizard is abandoning egg-laying in favour of live birth.” 1This is mere smoke and mirrors; there’s no evidence S. equalis is abandoning oviparity. No oviparous populations of S. equalis are showing signs of changing reproductive mode. There is a difference in reproductive mode between populations that appears to be related to differences in climate, but individual skinks are stable; they don’t change reproductive mode throughout their lifetimes even when climates change.3 Even if some populations of S. equalis were genuinely making a transition from one reproductive mode to another, the species as a whole is not moving in that direction; only certain populations. All your eggs in one basket? Evolutionists believe this is a transition from oviparity to viviparity because of the way they interpret observations about lizard paleontology and biology. Oviparous organisms appear lower in the stratigraphic column than viviparous organisms, and evolutionists interpret this ‘geologic column’ as a time sequence of millions of years of evolution, so they believe oviparity came before viviparity. They believe the current variation in birthing practice in lizards is related to a general trend to move from oviparity to viviparity. As a result, evolutionists state that viviparity has evolved independently in reptiles nearly 100 times, and that squamates (lizards and snakes) account for the vast majority of such events. 1,4 S. equalis becomes a prime example because both reproductive modes exist within the one species, and oviparity in S. equalisis somewhat intermediate in form between ‘normal’ lizard oviparity and viviparity.There is however a another option: many types of lizard (including S. equalis) originally had the capacity for both reproductive modes, but due to natural selection most subsequently lost the ability for one or the other. This is consistent with the post-Flood dispersion of the kinds. Evolutionists don’t generally consider this possibility because it’s a process of information segmentation and loss, which gives no support to microbes-to-microbiologists evolution, and also gives no chronological priority to oviparity.From this, we would expect to see much variation in the mode of birth/placental complexity in lizards because they originally had the information for numerous modes of reproduction. As described above, there is a multitude of reproductive methods among lizards.5
We would also expect most species to have only one reproductive mode because as the lizards spread from the ark after the Flood, genetic bottlenecks would have given rise to rapid diversification under natural selection. We find that most lizard species around the world are eitheroviparous or viviparous, but not both.2,6We may, however, expect to see a few species that retain the diversity, but not many, since we would expect most to have specialized after the genetic bottleneck of the Flood. Since there are only three known species of lizard that retain diversity in reproductive mode (S. equalis,2,7 Lerista bougainvillii,8 and Lacerta vivipara9), this is also consistent with the young age model. Is it an intermediate form? Viviparous populations of S. equalis retain eggs to the later stages of embryonic development, whereas most oviparous lizards lay their eggs much earlier.5 Therefore, evolutionists have a point that S. equalis is significant for understanding mechanisms of reproductive variation among lizards because it represents an intermediate form on the oviparity–viviparity spectrum of lizards. However, this does not necessarily mean that since S. equalis is an intermediate form that it is evidence for the evolution of viviparity de novo. This intermediate form can also be interpreted as a parallel of an ancestral form in (at least some) lizards that had the potential for both oviparity and viviparity. Polarization between reproductive modes occurred, as Smith and Shine pointed out, because the intermediate form is not reproductively stable long-term. 5 But this favours natural selection from an ancestrally large gene pool rather than the repeatedde novo creation of viviparity because specialization and information loss is the norm in biology—it is commonly observed.The only ‘transition’ that may possibly arise is if the skink populations are on the whole ‘transitioning’ from the warmer coastal climates to the colder mountain climates. The skinks from within contiguous populations don’t show variety in birthing practice with changing climate. Natural selection likely weeded out the variety in birthing method in individual populations, though the individual populations are still not yet reproductively isolated from one another.Natural selection involves only a sorting (often involving a loss) of genetic information, which adds nothing new. As a population becomes more specialized via natural selection, it is less capable of adapting to changing conditions in the future. The problem is that evolution requires vast amounts of new information to be constantly added to the biosphere.Moreover, de novo creation of viviparity requires the production of new regulatory systems which could only evolve via many information-adding random mutations. However, experimental science is hardpressed to find examples of random mutations that produce new information, where neo-Darwinism requires many. 10 We also see an inexorable trend of genetic deterioration caused by near-neutral mutations that will eventually lead to the extinction of all multi-cellular life.11,12 Molecules-to-man evolution expects the exact opposite of what we see happening in biology, so the de novo creation of viviparity via evolution is highly unlikely. Conclusions Despite what evolutionists think they are seeing, they’re really just seeing one more example of natural selection, which is not microbes-to-man evolution. The evolution of the horse by Mats Molén The horse series has long been a showcase of evolution. But in reality, this series is the best argument that can be presented against evolution from the fossil record. 1 Creationists have various opinions on whether the horse series is in fact made up of different created kinds. This article addresses some of the current problems, and concludes that the horse series probably comprise three different created kinds, not including all animals that have been labeled Hyracotherium. Hyracotherium itself appears to contain several different created kinds such as animals similar to tapirs. Horse fossils have been found in sedimentary strata at the beginning of the Tertiary period during a time-span called the Eocene (approximately 50 million years ago, according to uniformitarian dating). They are usually labeled2Eohippus or Hyracotherium (see figure 1). Illustration by Jan Nord Figure 1. Evolutionary tree of the horse constructed by George Gaylord Simpson in 1951. The tree was later simplified5, but has recently become even more branched and confusing with the addition of more members as a result of new fossil finds (see ref. 2). Possible evolutionary gaps are here marked with a question mark. Equus = modern horse. View larger imageAccording to the theory of evolution, it is possible to follow horse evolution through millions of years: how the horse slowly became larger and stronger (figure 1), lost many of its toes (figure 2), and how its toothstructure changed when it moved from a diet of broadleaved plants, shrubs and trees (browsing) to eating hard, dry grass (grazing) (figure 3).3,4Horse evolution is believed to have been driven by a cooling and drying climate. Early horses supposedly lived in humid forests full of plants rich in foliage. Their toes, four at the front and three at the rear, sprawled out at different angles which helped them from sinking in the marshy ground. As the climate became drier, foliage plants disappeared and huge grass fields formed. This forced grazers to become better runners to be able to escape their predators.All horses resemble each other so much that they have been classified in the same family—Equidae. Because of this close similarity it can therefore often be difficult to discern any differences through the study of fossil skeletons alone. Another caution in identifying vertebrate fossils is that the variation in structures even within a genus of living animals can often be so great that it overlaps with the variation in other groups; e.g. there is much analogy in the tooth structure between different carnivores, even when the animals are not
classified in the same genus (or sometimes not even the same family). The most important diagnostic differences between different groups of animals are often in the construction of the soft parts. Many findings of fossil horses furthermore only consist of teeth or parts of jaws. Groups of horses In the horse series, it is possible to discern certain animals that could represent created kinds, even though we only have access to fossil skeletons. The following facts seem to support such an interpretation. In the horse series there are at least two evolutionary gaps a) The first gap occurs at Epihippus8 Only sparse fossil pieces have been found of this animal, and they resemble those of the earlierOrohippus, Eohippus and other formerly-identified hyracotherid species.9 b) The second gap occurs in or just after the group Parahippus 10 The early Parahippus species are supposed to resemble Miohippus and Mesohippus while the latter ones are supposed to look like Merychippus; this is only partly supported by the fossil findings.11Furthermore, the fossil material for Parahippus is incomplete.12 It would probably be possible to classify the different parts of Parahippusas belonging to two different animals—Miohippus (figure 4) and Merychippus.13 This latter result can also be inferred by the work of Cavanaugh et al.,14 as Parahippus showed similarities to 14 of 18 species of horses. Therefore, the “Parahippus” step in the horse series appears to be a mixed up group of unrelated fossils. Illustration by Jan NordFigure 2. The legs of horses, which are taken as support for evolution. The left leg in each pair in the picture is from the front, and the right leg is from the rear.6 Since 1989, the monophyly of Hyracotherium have been challenged 9 In 1992, the genus Hyracotherium was reclassified as five animals belonging to different families of which only one group was regarded as having anything to do with horses.15 More recent research has reclassified these animals into ten different genera and at least three families, of which many are not supposed to have anything to do with the horse series but are similar to e.g. tapirs (family Tapiromorpha). 9 One Hyracotherium species (angustidens) has been renamedEohippus, and all the other Hyracotherium species except one, have been given new genus names. The single animal still retaining the nameHyracotherium (leporinum) is no longer in the horse series but is regarded as belonging next to the Palaeotheriidae, which resemble tapirs and rhinoceros. “Early” horses have been preserved in strata from the same evolutionary age as several “later” horses Hyracotherium/Eohippus and Orohippus do for instance appear in the fossil record at the same time as Epihippus. Mesohippus and Miohippus appear together with Merychippus and Parahippus. Almost all other horses (with a possible exception of one or two)—Parahippus, Merychippus, Pliohippus, Equusand possibly also Miohippus—are represented at the same time during much of the period when they have been found as fossils. 16 (But especially in the newer evolutionary schemes, different names have been given to very similar animals, giving the appearence of evolution as well as providing fame to their discoverers; see examples in Froehlich 2002 9 and MacFadden 20054). Fossils ofHyracotherium (sic) have also been found very high up in the strata (Pliocene), but these findings have been rejected as reworked (i.e. eroded and deposited at a later strata) in spite of the fact that the geological observations do not show any signs of disturbance.17 Thus, the fact that most of the horses lived almost at the same time undermines their proposed evolution. “Transitional” forms between horses with teeth designed for browsing (Parahippus) and those with teeth for grazing (Merychippus) are rare13 Illustration by Jan Nord Figure 3. Tooth construction in leaf-eating (the two on the left) and grass-eating horses (the two on the right).7 Teeth on browsing (leaf eating) horses have closed, very narrow roots with small holes for their blood supply and nerves; i.e. these are teeth that wear down as the animal gets older. Teeth on grazing (grass eating) horses have an open root with many blood vessels which supply the teeth with lots of nutrients so they can keep growing during the entire life of the animal; this is termed hypsodonty, meaning high-crowned teeth. This change of tooth structure from bunodont (low-crowned with rounded cusps) to hypsodont (high-crowned) is not just supposed “microevolution”, but a complete change in design, even though it may not seem to be much of a new thing for those not acquainted with tooth construction.18 There is no evidence for any change of one tooth structure to another, even though it has been suggested by some authors.19 Some animals ate both grass and foliage,3,4 but this does not help to explain the transformation of one kind of teeth to the other.
Three completely different animals The animals that have been interpreted as different horses are therefore, with the above facts at hand, easily identified as belonging to three completely different animal kinds, instead of various horse intermediates which supposedly evolved from one and the same original ancestor. The created kinds, not counting all Hyracotherium members that have been removed to new families, should therefore more or less correspond to the following three groups (note that not all the newly named horses and not all members of the side groups are mentioned below):Eohippus (and many fossils that were formerly labeled Hyracotherium, but are classified into the family Equidae with new genus names9), Orohippus and Epihippus.Mesohipp us, Miohippus, certain Parahippus and probably most of the horses branching out from these three groups. (The horse series has been rearranged and many new genera have been added; e.g. Neohipparion, Nannippus and the Hipparion clades have been moved close to Parahippus and away from Merychippus,4 in contrast to figure 1, so we can not be sure if the classification/grouping of all the fossils is correct. But the horses branching out from Merychippus in figure 1 are still classified in the subfamily Equinae, and are therefore combined in group three, below. But all these details cannot be dealt with in this article). Figure 4. Two ‘horses’, Neohipparion (right) and Miohippus (left) from the Museum of Natural History in Los Angeles. Merychippus and those horses branching out from this group, includingPliohippus and all later horses (including the Hipparion clades). (Note that in the recent revisions of horse evolution there are two different genera with the name Merychippus: I and II. Merychippus is therefore thought to be polyphyletic, i.e. it is believed to have evolved twice. These two genera have been placed on different evolutionary lines. Genus I is in the original place leading to Equus, as seen in most horse evolution diagrams. Genus II has been moved away from the line leading to Equus—it is contemporaneous with Parahippus during most of its extension in time—and it is believed to be ancestor to the Hipparion clades as described by MacFadden 2005.4)The animals in group 3 are all classified in the same subfamily— Equinae.20Although, Cavanaugh et al.10 discovered that the fossil animals could be sorted into subfamilies, they disregarded this finding and instead constructed their own horse evolution tree. It would not be difficult to create a similar tree by simply arranging any number of unrelated living animals in a series from small to large (figure 5). No horse evolution The Cavanaugh, Wood and Wise hypothesis, 14 that the horse series (including the genus Hyracotherium) shows real (postFlood) “microevolution” (or linear/progressive variation) is, based on the above results, untenable as there is no progression in horse evolution (except maybe locally) and the data show a mixture of various horse-like animals. Moreover, the Cavanaugh et al. paper14 was based mainly on statistical data from one 1989 source (and some discussions from more recent creationist journals), and it did not qualify the differentHyracotherium finds. Also, the Froehlich paper9, which reclassified all the Hyracotherium species, was published in February 2002, about a year before the deadline of the Cavanaugh 2003 et al. ICC paper.14 This lack of clarity regarding the Hyracotherium finds has also not been addressed in an article by Wood in 2008,21 even though Wood referred to a 1992 book by MacFadden 22 who stated that Hyracotherium was not one single animal but instead several genera belonging to different families. Whitmore and Wise in 2008 even use Hyracotherium to establish an early post-Flood date, and this non-horse animal is mentioned as the first member in the horse series.23 Illustration by Jonathan Chong Figure 5. From left to right, Eland, Gnu, Bushbuck, Gazelle and Dik-dik. Even animals alive today can be arranged into a hypothetical evolutionary series, since variations in the skeleton within one group of animals often overlap with the variation in other groups within the same family. This does not prove, however, that any individual animal has evolved into another.Froehlich,9 who completely renamed most Hyracotherium species and placed them in different genera and families, used statistics, but also provided criticism to the way statistics can be misused in this case. But, at any rate, one cannot use statistics on design or on a limited amount of data (which in these cases are mostly teeth and jaws) to find out how evolution supposedly occurred, as the above authors have done. 9,14 Statistical analysis in this case does not take into consideration function or completed/designed living entities, but can only compare small differences (see also more critical points in Froehlich9). In this case, most of the statistical analysis has been carried out on the small differences in tooth enamel/structure and jaws, and very little work has been done on other parts of the body. This does skew the interpretation of the data in a similar way as if, for example, we would conduct statistics on 75 differences on the outside appearance of the eyes of octopuses and humans—the analysis would probably show that we evolved from octopuses.Although it is easy to discuss and criticize single finds, or a single place where fossils have been found, according to all the available data there appears to be three groups of animals that closely correspond to the subfamily groups of Equidae, and only the subfamily Equinae appears to represent horses. The discussion about post-Flood and Flood criteria, based on horse evolution by e.g. Cavanaugh et al. 200314and Wood 200821, must therefore rest upon criteria other than the purported post-Flood “microevolution” of the horse resulting from a changing environment, as proposed by the common evolutionary story (see other criteria for Flood boundaries in Oard 2007 24). There were also no real environments where these animals could have lived, only large deserts—most fossils are found in sedimentary deposits which show evidence of being from the Flood, but there is no evidence of a plant cover which could feed large herds of animals, and no proper soil. 25 There is also no support for changes in environment, as evolutionists and Cavanaugh et al.14 and Wood21 insist on based on speculative
interpretations.In the case of the horse, it could be body size that governed how quickly the animals sank, were transported and buried, and then sometimes eroded and redeposited, during the Flood or in the close aftermath of the Flood. This would have been before the continental environment had become habitable again and living animals repopulated it. Small animals with similar construction commonly disintegrate and sink quicker than large animals, and smaller bones are also more easily transported by currents after having reached the bottom. Also, during post-Flood catastrophes, living animals could have been buried together with reworked, dead, unfossilized or partially fossilized animal remains buried during the Flood. Conclusion A study of fossil horses reveals at least three groups of animals within the horse family Equidae, in addition to some unrelated animals such as tapirs. The three equid groups correspond closely to different subfamilies of Equidae, and could be considered three separate created kinds. Most of these different kinds lived (or actually, were buried!) nearly at the same time and do not show much progressive change as far as horse evolution is concerned, just a general increase in size. No one has explained how new, specialized kinds of teeth could have supposedly evolved, and it appears rather to be a case of intelligent design instead of “microevolution” (variation within a kind, as suggested by various creationists) or “macroevolution” (new kinds of organisms, as suggested by evolutionists). The Cavanaugh et al. (2003)14 hypothesis of intrabaraminic variation of all animals that belong to Equidae (or animals that they did put into Equidae, even if the evolutionists put some of them in different families) is not well supported by the available evidence and ought therefore to be abandoned. Addendum According to Julian Huxley (arguably one of the most prominent evolutionists of the last century) at least one million positive mutations were required for the modern horse to evolve. He believed that there is a maximum of one positive mutation in a total of 1,000 mutations. With the help of these values Huxley calculated the probability for the horse to have evolved from one single unicellular organism was 1 in 10 3,000,000. He believed, however, that natural selection would be able to solve this problem.26 But this faith did not help him in the end, and will not help any other evolutionist either, as this calculation is based on the origin of positive mutations, even before natural selection would start to work. If all electrons in the universe (about 1080) would have participated in 1012 reactions every second, during the 30 billion years which evolutionists have put as the upper age limit of the universe, there would still not have been more than c. 10 110 possibly interactions—still a long way from the Huxley calculation.1 Karyotypic and allelic diversity within the canid baramin (Canidae) by Jean K. Lightner Previous studies suggest that all dog-like creatures (canids, family Canidae) belong to a single created kind. As unclean animals, all modern canids are descendants of two canids preserved on the Ark during the Flood. This pair of canids would have carried a limited amount of genetic diversity. They would be expected to have had a fairly uniform arrangement of chromosomes (low karyotypic diversity) and up to four different versions of any particular gene (allelic diversity). Today there is considerably more karyotypic and allelic diversity within the canids. The patterns imply that more than random mutation and natural selection are involved; instead, certain genetic components appear designed to change and numerous designed mechanisms may be involved in driving many of these changes. This suggests that animals were designed to be able to undergo certain genetic mutations which would enable them to adapt to a wide range of environmental challenges while minimizing risk.
Table 1. List of canid species and their normal diploid (2n) number which were included in a phylogenomic analysis by Graphodatsky et al.7 There is a need to more fully describe intrabaraminic (within kind) variation on a genetic level for understanding the basis for the variety we see within baramins today. It has been pointed out that the majority of mutations are near neutral. 1 Yet intuitively, I would expect random (chance) ‘errors’ in such a complex system to be more consistently disastrous unless the system was designed to change.2 If genetic systems were designed to allow for such changes, then mutations (changes in the nucleotide sequence of DNA) are not necessarily just ‘errors’ or ‘accidents’. On the contrary, some mutations may be directed to allow animals to adapt in the present fallen world. By examining intrabaraminic genetic diversity, we should be able to discover a clearer picture regarding the role of mutations in the development of the diversity found in animals today.Previous baraminic studies have identified all canids (family Canidae) as belonging to a single baramin. 3Since they are unclean animals, all living canids would have descended from a single breeding pair preserved on the Ark about 4,500 years ago.4,5 This historical information is important because it suggests there was a limited amount of diversity present in canids at that time. Today, this family is represented by 34 species that are widely distributed around the world. 6 There are considerable data available on the karyotypic and allelic diversity in protein coding genes for several of these species. A brief overview of the data is presented here. Karyotype The family Canidae exhibits the most highly rearranged karyotypes* of any family within the order Carnivora. Normal diploid numbers vary from 34 for the red fox (Vulpes vulpes) to 78 for the domestic dog (Canis familiaris) and dhole (aka Asiatic Wild Dog; Cuon alpinus) (table 1). The Arctic fox (Alopex lagopus) is polymorphic for a centric fusion; diploid numbers of 49
and 48 are found in individuals carrying one or two copies respectively of this fusion. Phylogenomic analysis suggests that 82 may have been the ancestral karyotype. Within the 10 species that have been studied in detail it appears that approximately 80 rearrangements have occurred. This includes numerous fusions, both centric and tandem, fissions, pericentric inversions and/or centromere transpositions.7 Several paracentric inversions, and even whole arm (telomere to centromere) inversions, have been implicated based on the differences in loci order among species (figure 1).8,9 Figure 1. Diagrams depicting some of the chromosomal rearrangements reported within the canid baramin. Such rearrangements often result in the loss of relatively small portions of DNA. Fusions (top row) involve combining two distinct chromosomes to form one; to become stable, one centromere must then be silenced. Inversions (bottom row) involve reorienting a portion of DNA within an existing chromosome. There also is evidence that the amount of heterochromatin can be adjusted. These types of rearrangements are too complex to be the result of ‘purely chance events’. While rearrangements do involve some risk, they probably also have purpose, such as adaptation in a fallen world.Evidence of similar rearrangements is present within other baramins and even within some species.10–12 Detailed studies of rearrangements in ruminants strongly suggest that numerous designed mechanisms operate to repair breaks, silence an extra centromere, adjust amounts of heterochromatin and possibly alter the position of the centromere. 13 The fact that such rearrangements often become fixed within a species suggests that they may be beneficial under certain circumstances. However, fixing these rearrangements also likely required a small population, since it is difficult to fix even beneficial mutations in a large population. 14 Thus, rearrangements should not be viewed as a major genetic accident from which animals occasionally may recover. Instead, the presence of multiple designed mechanisms enabling translocations to occur while maintaining viability of the animal suggests that such rearrangements are likely helpful for adaptation in the present fallen world. This is not to say that such rearrangements are without risk. For example, many heterozygous carriers experience some decline in fertility. Occasionally there are more serious results with infertility and/or serious chromosomal aberrations in the offspring. 13 Furthermore, these types of rearrangements certainly don’t explain the origin of chromosomes.The red fox and both subspecies of raccoon dog carry B chromosomes as part of their normal karyotype. 7These small, supernumerary chromosomes can vary in number both within as well as among individuals. Generally their numbers are low, with three to five being typical for the red fox. 15 They usually contain significant amounts of repetitive sequences and, until recently, it was thought that they did not contain any protein coding genes. However, the canid B chromosomes have been found to contain the KIT gene, which encodes a transmembrane tyrosine kinase receptor involved in the proliferation, migration and differentiation of hematopoietic, melanoblast, and primordial germ cells. Adjacent sequences were detected, including the RPL23A pseudogene and, in the raccoon dog only, a portion of the more distal KDRgene. This suggests that the B chromosomes were derived from an autosome in a common ancestor and have been lost in other lineages descending from this ancestor. Further studies need to be done to determine if the KIT gene of B chromosomes is actually transcribed.16 Major histocompatibility complex genes The major histocompatibility complex (MHC) consists of a number of genes involved in immune function and which are known for high allelic diversity. Several dog leukocyte antigen (DLA) genes have been evaluated for polymorphisms. As of 2006, there were 90 alleles recognized for DLA-DRB1, 22 for DLA-DQA1 and 54 for DLA-DQB1, with more expected to be discovered.17 High levels of polymorphism are generally considered a sign of a healthy population, although some dog breeds and wild mammals have low MHC diversity with no apparent ill effects. The DLA genes are on dog chromosome (CFA) 12.18 Some DLA haplotypes are associated with various canine autoimmune diseases such as primary immune mediated hemolytic anemia, polyarthritis, hypothyroidism and diabetes. 19 However, it is important to recognize that these haplotypes do not cause disease directly; instead, they may be risk factors that affect the likelihood of disease development. As suggested previously, there is risk in maintaining sufficient variability to adapt in the present fallen world. Dopamine receptor D4 gene There are two portions of the dopamine receptor D4 (DRD4) gene that are variable in dogs. The first is in exon 1 where the two known alleles differ by a 24-base pair (bp) indel. 20 Interestingly, humans also are polymorphic in this region with a 12-bp duplication and a 13-bp deletion having been identified.21 The latter is particularly intriguing as it is found in 2% of the human population and is not associated with any known disease; yet the frameshift is predicted to result in a truncated, nonfunctional protein.22 Figure 2. A representation of the variable number tandem repeat (VNTR) patterns in exon 3 of the dopamine receptor D4 (DRD4) gene for seven dog alleles (after Hejjas et al.23). The nonrandom pattern of mutation suggests designed mechanisms are involved in this mutation. The variability in this region appears to have some influence on personality and behaviour.The second polymorphic region is found in exon 3. There are eight alleles that have been identified in dogs.20 A number of these have been identified in wolves. The alleles differ by variable number tandem repeats (VNTRs) of 12-and 39-bp (figure 2). A similar pattern has been observed in humans, where a 48-bp segment is repeated from 2 to 10 times. These variations are believed to influence behaviour because certain alleles have been shown to be associated with the novelty-seeking personality trait in humans, primates and dogs.23 VNTRs have been identified in exon 3 of the DRD4 gene of nearly all mammals examined except rodents. The length of the repeated segments varies among taxa, but is consistently a multiple of three.24This bias of indels, particularly VNTRs, in base pairs that are multiples of three does not appear to be explicable by natural selection. If essentially random, approximately one-third of
indels should be multiples of three unless a frameshift, which often results in a premature stop codon and a nonfunctional protein, is lethal or significantly detrimental. It does not appear that frameshifts in DRD4 would be subject to such selection pressure, since a frameshift mutation is carried by a number of normal humans and knock-out mice. 20,22 Furthermore, variability in this gene appears to contribute to variability in personality. The number of alleles in canids (greater than eight, as the raccoon dog has a separate allele identified 25) is greater than the maximum of four alleles expected in the pair of canids on the Ark. Humans also carry more alleles than can be attributed to the first man and woman. This suggests that this gene was designed to vary in a rather unusual way to enhance variability in personality and perhaps other traits as well. Olfactory genes Olfactory (smell) receptor (OR) genes are seven transmembrane receptors. While 1,094 OR genes have been identified in the dog,26 the canine repertoire of odorant molecules is significantly greater than this. This appears to be from a complex combinatorial code. Odorant molecules can bind 20 or more ORs depending on their concentration. ORs can bind more than one odorant molecule. Through interpretation of the complex signalling patterns, dogs are able to detect an incredibly wide array of individual odorants and a large number of mixtures. 27In one study, 16 OR genes were examined in 95 dogs from 20 different breeds. All genes were polymorphic ranging from two to 11 alleles per gene. There was an average of one change per 920 sequenced nucleotides, which is much higher than most coding sequences and a random sampling of noncoding sequences. Of the 98 single nucleotide polymorphisms (SNPs) identified, 55 resulted in an amino acid change and 30 of these involved changes to a different amino acid group. These changes were found throughout the protein (figure 3), mostly in variable or highly variable regions within OR genes. However, two come from highly conserved regions, one in transmembrane (TM) 3 and the other in TM7. 28Five of the 16 genes had an allele with a disrupted open reading frame. These were from one of the four indels identified or an SNP introducing a stop codon. Pseudogenization of OR genes is fairly common. In poodles, 18% of ORs are pseudogenes while 20.3% (or 222/1094) are in the boxer. Interestingly, 17 of the OR pseudogenes in the poodle were not found in the boxer, and 22 of those found in the boxer were not found in the poodle.28It may be premature to assume there is no purpose in mutation or pseudogenization within OR genes. 29There is a tremendous amount of redundancy in OR genes which may have been designed to allow for future specialization. For example, a study involving Drosophila sechellia, a highly specialized vinegar fly that feeds solely on fruit from Morinda citrifolia, a shrub which strongly repels related species of flies, suggests that pseudogenization of ORs and gustatory (taste) receptors has occurred nearly 10 times faster than in the closely related species D. simulans. For those genes which remained intact, D. sechelliaappears to have fixed non-synonymous substitutions at a consistently higher rate than synonymous substitutions compared to the same genes in D. simulans.30 Therefore, the ability of OR genes to be modified or pseudogenized may be an important design element introduced by a intelligent designer. Conclusion Figure 3. Two-dimensional diagram of an olfactory receptor (OR) indicating positions of 55 non-synonymous single nucleotide polymorphisms (SNPs) and their allele frequencies in dogs, as identified by Tacher et al.28 ‘*’ indicates the SNPs found in highly conserved regions of the OR genes. There are 1,094 OR genes that have been identified in dogs.The two canids preserved on the Ark would be expected to have carried a fairly uniform karyotype and up to four alleles for non-duplicated genes. This brief examination of present-day karyotypes and several groups of genes indicates that significant diversity has arisen since the Flood. Several different lines of evidence suggest that many of these mutations may have some benefit to the animal. For example, intrabaraminic chromosomal comparisons have implicated numerous designed mechanisms which control chromosomal changes in a way that maintains viability of the animal. The fact that such mechanisms appear to be operating suggests there is purpose to chromosomal rearrangements. The fact that different karyotypes often are fixed in different species within a baramin seems to support this concept as well. The various genes examined here appear to handle mutations very well. In fact, it is generally believed that the high allelic diversity in the MHC genes is important for a healthy population. The redundancy in ORs and the pattern of mutation and pseudogenization in these genes suggests that these genes were designed to vary so that animals can adapt to different environments. Finally, the striking non-random pattern of VNTR mutations, all in lengths divisible by three, when there is no known selection that could produce this non-random pattern, strongly suggests that in some instances there are designed mechanisms driving mutations. The patterns seen here suggest that animals were designed to be able to undergo genetic mutations which would enable them to adapt to a wide range of environmental challenges while minimizing risk. Climbing Mt Improbable “evo devo” style by David White Evolutionary champion Richard Dawkins provides an intriguing analogy for how the evolutionary process works—he likens it to climbing a mountain, Mount Improbable.1 Many structures in living things are so complex, he concedes, that the likelihood they could arise by chance is absurd (like scaling a mountain in a single leap).2 But, according to Dawkins, if we climb the mountain in incremental steps (of gene mutation filtered by natural selection) we can reach the summit without any need to invoke a creator. This evolutionary mechanism is known as neo-Darwinism. And even though it has been enthusiastically taught for many years, numerous evolutionary biologists now concede that neo-Darwinism is not sufficient to climb Mount Improbable. This doesn’t mean they are accepting defeat. As we shall see, evolutionary biology is itself evolving. A new paradigm in evolutionary biology: “evo devo”
About three decades ago I was only a single cell (a fertilized egg), but now I’m a “galaxy” of cells (over 100 trillion) typing this article. As I developed in utero, different cells took on different tasks. Some started forming eyes, other cells became cardiac muscle, and so on. But how did the different cells “know” how to carry out this highly orchestrated task? This mystery of embryonic development has puzzled scientists for centuries. But it wasn’t until biologists discovered a set of developmental genes (known as Hox genes) in 1983, that the black box of embryonic development finally began to be opened.Hox genes are developmental genes that guide overall body architecture. A single mutation in a Hox gene can dramatically change an organism. For instance, consider the mutant fruit fly that has legs in the place of its antennae! Although this condition obviously disadvantages the fly, these types of changes have excited many evolutionists, because they think they might provide clues as to how radical new body designs could evolve.As more developmental genes have been discovered, a whole new field of inquiry has “sprouted” that attempts to merge developmental and evolutionary biology. The result is Evolutionary Developmental Biology (“Evo Devo”). The basic principle driving Evo Devo is that if embryonic development is “re-programmed”, “improbable” structures like limbs, wings and new body designs might arise. Diverse organisms, similar genes Hox genes are part of a broader group of developmental genes that have many varied roles. Some of them mark out the geography of the embryo’s body. Others play key roles in the development of structures like limbs, eyes and hearts. But the most astonishing thing about Hox and other developmental genes is that they are shared across the animal kingdom. Organisms as diverse as leeches and lawyers are “built” using the same developmental genes! This discovery has come as such a shock that one of the world’s most eminent biologists, Sean Carroll3, confessed: “no biologist had even the foggiest notion that such similarities could exist between genes of such different animals.”4But why are evolutionists so surprised? Well, it’s simply because creatures that supposedly diverged millions of years ago shouldn’t share the startling similarity in developmental genes that they do. For example, evolutionists allege that humans once shared a common ancestor with fruit flies. However, since we diverged so long ago, any similar genes we shared should’ve been scrambled beyond recognition by almost countless generations of mutations. This is why Ernst Mayr, a man once described as “the world’s greatest living evolutionary biologist” stated, “the search for homologous [similar] genes is quite futile except in very close relatives”. 5 But this is wrong. Not only do we share similar developmental genes with fruit flies, but also with almost every other creature on the planet!So how has this changed the way scientists view evolution? Well, since very different animals are made using similar genes, Evo Devo proponents contend that the driving force of evolution is not changes in (protein coding) genes, but changes in regulatory DNA (genetic switches) that control the genes. 6 In other words, “ … the evolution of form is not so much about what genes you have, but about how you use them.”7 Yet this contradicts what neo-Darwinists have long told us —“According to the modern theory (called neo-Darwinism), changes occur in organisms by mutations of genes”8 [emphasis mine]. Building a “baby” Many of the shared developmental genes are part of genetic switches that regulate other genes. 9 During embryonic development these genetic switches initiate the cascade of gene expression that builds various structures. For example, the Pax-6 developmental gene is part of a genetic switch that induces eye development. When Pax-6 from a mouse was inserted into a fruit fly’s genome, fruit fly eye structures were formed. The mouse gene was so similar to its fly equivalent (even though these creatures supposedly diverged over 500 million years ago) that it induced the fly program for eye development! Likewise, the Distal-less gene forms part of a master switch for limb development and theTinman gene (named after Tin Man in The Wizard of Oz) is part of a master switch for heart development. So embryonic development involves a vast array of master genetic switches that turn on the right program in the right place. Evolution of genetic switches? Since changes in genetic switches are now being hailed as the key to evolution, Evo Devo proponents have been keen to highlight adaptations caused by such changes. Probably the most cited example involves stickleback fish. Normally, these fish have long spines projecting from their body. On the lake bottom, these are a disadvantage because dragonfly larvae latch onto them. However, some varieties have adapted to their environment. Due to a mutated genetic switch, they don’t develop pelvic spines, so they are much better at evading the grasp of predators. 10 However, these sorts of changes are really devolution, not evolution, because a genetic switch has been corrupted, preventing the expression of a key spinebuilding gene (Pitx1) in the pelvic region. This showcase example of “evolution via genetic switches” hasn’t inspired prominent evolutionists like Jerry Coyne (University of Chicago), either: “these examples represent the loss of traits, rather than the origin of evolutionary novelties”.11,12
Furthermore, Jerry Coyne remains unconvinced that changes in genetic switches are the key to evolution: “the evidence for this critical hypothesis, however, rests more on inference than on observation or experiment”. 11 But despite his Evo Devo skepticism, Dr Coyne’s belief in evolution shows no sign of wavering. “Urbilateria”—your long lost relative? Since common developmental genes are shared across the animal kingdom, evolutionists think they must have originated before the different animal groups embarked on their separate evolutionary pathways. So the last common ancestor of people and snails must have possessed them. This hypothetical creature, which evolutionists tell us lived over half a billion years ago, has been dubbed “Urbilateria” (i.e. the ancestor of all animals with two-fold symmetry). 13Urbilateria was certainly “ahead of its time”. It supposedly possessed many key developmental genes for complex “improbable” structures like limbs, eyes and hearts—but it allegedly lived long before evolution had “invented” limbs, eyes or hearts! No wonder Sean Carroll muses, “it is intriguing to ponder just what so many genes were doing in Urbilateria”. 14 Remarkably, these evolutionists now insist that much of the genetic program for building complex animals existed long before the animals did! “The genetic potential was in place for at least 50 million years, and probably a fair bit longer, before large, complex forms emerged”.15 Statements like this inadvertently give the impression that evolution has foresight! But Dawkins himself insists that “nature, unlike humans with brains, has no foresight”. 16 And if genomes are supposedly “shaped” by the demands of their environment over time, why should “nature” write a complex genetic program 50 million years before it is needed?Thus, the discovery that the animal kingdom is built using the same developmental genes does not support the notion that all life has descended from a common ancestor (although this is how it is commonly reported). 17 Ironically, though, the data fits nicely with the proposal that a single designer used a common “blueprint” to “build” the animal kingdom, rather than there being many creators. Indeed, in most cultures, a designer using the same underlying design in a variety of applications would bring him great honour, showing his mastery over his designs.18A recent New Scientist article cautioned its readers: “If you want to know how all living things are related, don’t bother looking in any textbook that’s more than a few years old. Chances are that the tree of life you find there will be wrong”. 19 As we have seen, it doesn’t seem to matter what sort of problems the data raises for evolutionists (or how much it offends past predictions) the idea that all living things have descended from a common ancestor is not negotiable. Even questioning this idea is regarded as scientific heresy.20 Facilitated variation: a new paradigm emerges in biology by Alex Williams Facilitated variation is the first comprehensive theory of how life works at the molecular level, published in 2005 by systems biologists Marc Kirschner and John Gerhart in their book The Plausibility of Life: Resolving Darwin’s Dilemma. It is a very powerful theory, is supported by a great deal of evidence, and the authors have made it easy to understand. It identifies two basic components of heredity: (a) conserved core processes of cellular structure, function and body plan organization; and (b) modular regulatory mechanisms that are built in special ways that allow them to be easily rearranged (like ® Lego blocks) into new combinations to generate variable offspring. Evolvability is thus built-in, and the pre-existing molecular machinery facilitates the incorporation of new DNA sequence changes that occur via recombinations and mutations. The question of origin becomes especially acute under this new theory because the conserved core processes and the modular regulatory mechanisms have to already be in place before any evolution can occur. The new molecular evidence shows virtually all the main components of neoDarwinian theory are wrong. Figure 1. The Distal-less gene is generally used in insect embryo, leg and wing development and has a switch for each of these functions (e.g. the fly, top panel). In butterflies (bottom panel), it has an extra switch that turns it ON to produce wing spots. Gene switches are easily disabled by mutation so this rules out a mutational origin for new
switches.Scientific literature is currently drowning in information about the molecular mechanisms of life, but most people are unable to appreciate what it all means—so vast is the amount, so highly specialized in each reported study, and so obscured by the necessary but incomprehensible jargon. The publication in 2005 of the first comprehensive and easily readable theory of how it all works—Marc Kirschner and John Gerhart’s The Plausibility of Life: Resolving Darwin’s Dilemma1—thus marks a great milestone in the history of biology. Kirschner is Professor of Systems Biology at Harvard Medical School and Gerhart is Professor of Systems Biology at UC Berkley Medical School.2In this article, I shall show how Kirschner and Gerhart’s theory signals the emergence of a new paradigm in biology by contrasting it with origin-of-life experiments and neo-Darwinian theory, and will augment it with some more recent research findings. Life and non-life To appreciate what life looks like at the molecular level we need some background understanding of the gap between life and non-life, and how originating events may have filled that gap. According to neo-Darwinian theory, life evolves in small steps. Genes produce organisms, and mutations in genes produce changes in organisms. Those changes that survive the ‘sieve’ of natural selection provide the required small steps that turn one kind of life into another. Population biology experiments are claimed to have validated this theory for many different kinds of genetic traits.Extrapolating this theory backwards, life must have also arisen in small steps via natural chemical events in the environment. Nobel Prize winning biochemist Christian de Duve has clearly summarized most of the necessary events in his book, Singularities: Landmarks on the Pathways of Life.3 There is, yet, no experimental evidence for a stepwise neo-Darwinian originating mechanism, so de Duve’s singularities are what we might colloquially call ‘brick walls’.Living organisms have two main components: (a) enzyme-mediated biochemistry and (b) information-based regulatory processes. Which came first? De Duve favours an ‘enzymes first’ model because the information-based systems are so optimal and specialized that he believes some process of selection was needed to separate out the spectacularly clean (100% purity) components from the ‘dirty gemisch’ (impure mixture) of the environment.However, physicist Hubert Yockey has studied information in biology for 50 years and persuasively argues that because life has no reverse code for transferring information from proteins to RNA or DNA then it is impossible for life to have arisen in a ‘proteins first’ scenario. The information must have come first. The simplest code would have been a binary (two-letter) alphabet but all life works upon a more complex four-letter alphabet, so Yockey concludes that the question of origin is undecidable.4 This is not a necessary conclusion however, and appears to be no more than a ruse to avoid the uncomfortable conclusion that life may have been intelligently designed. Life in molecular detail: the new paradigm Against this background, we can now look to the summary model of how life works as given by Kirschner and Gerhart (I shall refer to it as the KG model). They identify two major components: conserved core processes of cell structure, function, and body plans; core processes are regulated in modular ways (like ® Lego blocks) that can be easily rearranged into new combinations, to be used in new times, places and amounts to generate variable offspring. Evolvability is thus built-in. The existing modular structure and its regulatory systems facilitates the incorporation of changes in DNA sequences (produced by recombinations and mutations) into functionally viable offspring that can adapt to new environments. KG theory is claimed to be a largely complete molecular explanation for how natural variation and natural selection produce all the variety of life on Earth—Darwin’s theory, according to the authors, is now a validated whole. A new view of heredity Neo-Darwinists view heredity as being all about genetics. For example, the official journal of the Genetics Society is called Heredity. But genetics is all about change and we have discovered so many ways in which organisms can change that we are now faced with a huge unanswered question: how do they manage to stay (approximately) the same, generation after generation? As the late Stephen Jay Gould maintained throughout his career in paleontology—stasis, not change, is the major feature of natural history.5Neo-Darwinism has no answer to this challenge for two reasons: (a) genes and chromosomes can be mutated at any and every position so there is no limit to the potential for change, and (b) the agents of change (mutations and environment) are beyond the organism’s control.But KG theory does give us an answer—the conserved core processes remain the same during reproduction. When a mother passes on an egg cell to its offspring, that cell contains everything required by the offspring in its architecture and machinery. The DNA sequences provide for the manufacture of more raw materials for the embryo to go through its development process, but the actual architecture and machinery itself is provided by the mother. The new outer membrane of the embryo is just that of the mother’s cell extended with more of the same material. The new cytoskeleton is just the mother’s cytoskeleton extended with new material. The new organelles are the mother’s organelles that replicate independently of the chromosomes. The new membranes are the mother’s membranes extended with more of the same material.During the early stages of embryogenesis, the new chromosome set is entirely shut down and all the groundwork of the embryo is laid by thousands of different RNA types supplied by the mother. Only after this groundwork is laid does the new chromosome set become active and the mother’s RNAs are degraded and recycled.The variability that is built-in to this heredity process is the modular gene regulation and signaling networks. A suitable analogy might be a house and its network of power, plumbing and communications channels and interfaces. The wiring and piping are built into the house structure, but there are numerous interface points to which a wide variety of household appliances can be attached, detached and rearranged. It is the combination of devices plugged into this network that provides the variation, and the house with its plumbing and wiring system that provides the stasis. To what extent the ‘house’ itself can be varied is yet to be determined. Conserved core processes Chapter 7 of Kirschner and Gerhart’s book summarizes this subject so I will simply quote selectively from it. My additions or summaries are in square brackets: ‘Conserved core processes [typically consist of] several protein components [on average about 5, maximum probably about 300], conserved in their [amino acid] sequence. Their function is to generate the phenotype from the genotype. These processes arose historically in a few intermittent waves of innovation. ‘On the lineage towards humans, these innovations include: the processes in the first bacteria [all the machinery in a bacterial cell], [the processes in] the first eukaryotes [all the machinery in a eukaryote cell], [the processes in] the first multi-cellular organisms [cooperation between cells, specialization of structure and function of different cells, and integration of specialized cell complexes into functional organs and organisms], [the processes in] large bilateral body plans in metazoans (including chordates and vertebrates), [the processes in] neural crest cells in vertebrates [which allow diversification of the head region], [the processes in] limbs in the first land animals, [the processes in] the neocortex [the key region of brain development].
‘Most evolutionary change in the metazoa [multi-celled animals] since the Cambrian has come not from changes of the core processes themselves or from new processes, but from regulatory changes affecting the deployment of the core processes. These regulatory changes alter the time, place, circumstance and amount of gene expression … ‘The core processes are built in special ways to allow them to be easily linked together in new combinations … these special properties include: (a) Weak linkage, a property particularly of signal transduction [detection and response] and transcription [copying]. … the response is maximally prepared and ready to be triggered [by a GO or STOP signal]. (b) Exploratory behavior, a property of [cellular processes and populations of organisms] … the capacity to generate an unlimited number of outcome states [which are] built to be receptive to the [selective] agent [that will serve] as a stabilizing force, selecting one state among the large number of states generated. (c) Compartmentation, a property of embryonic spatial organization and cell type control. [Compartmentation has] facilitated a large increase in the complexity of anatomy and physiology without a corresponding increase in the complexity of the conserved core processes. ‘Generation of variation is facilitated principally by: reducing the lethality of mutations, reducing the number of mutations needed to produce novelty, and increasing the genetic diversity in the population by suppressing lethality [and thus allowing the mutations to be stored and inherited].‘Robustness [is] at the centre of our theory … the conserved core processes are built [robustly] to give sufficient outputs despite altered conditions and inputs. [The properties] of robustness, flexibility and versatility are [needed] to enable the core processes to work together … the organism as a whole is … a poised response system … It responds to mutation by making changes it is largely prepared in advance to make. … Genetic variation or mutation does not have to be creative; it only needs to trigger the creativity built into the conserved mechanisms.‘All the special properties of the conserved core processes had to evolve before regulatory evolution could escalate, for if the components of different processes were to interfere with one another in the new combinations, such expression would afford no benefit.‘Facilitated variation assumes the availability of [the conserved core processes]. The evolution of these processes and properties would seem to be the primary events of evolution, requiring high novelty. … Once the conserved processes were available, though, the possibility of variation by regulatory shuffling and gating of these processes was unleashed, and shuffling and gating were much simpler than inventing the processes.‘The main accomplishment of the theory of facilitated variation is to see the organism as playing a central role in determining the nature and degree of variation … We think the organism is so constituted that its own random genetic variation can evoke complex phenotypic change.’Further relevant comments from Chapter 8 include: ‘ … evolvability … is the greatest adaptation of all … Variation is facilitated largely because so much novelty is available in what is already possessed by the organism’ (pp. 252, 273).‘The theory of facilitated variation opens up a new set of questions about the origins of the conserved core processes … [they] may have emerged together as a suite, for we know of no organism today that lacks any part of the suite. … The most obscure origination of a core process is the creation of the first prokaryotic cell. The novelty and complexity of the cell is so far beyond anything inanimate in the world of today that we are left baffled by how it was achieved’ (pp. 253, 256). Invisible anatomy Kirschner and Gerhart coined the term ‘invisible anatomy’ to describe the regulatory circuits that produce the visible anatomy. To construct an adult from a zygote, the zygote must first build a phylotypic embryo—a mass of cells with highly conserved form, which is the same right across its phylum. This philotypic stage is divided into numerous, largely independent, 3-dimensional compartments within which different gene switching networks are wired up in different ways appropriate for the unique developmental cascade that will subsequently occur in each compartment.But the signal network is not instructive, it is permissive—it does not tell the circuits what to do, it merely releases or represses the already built-in abilities of cells to do whatever needs to be done. Humans have about 300 compartments in their phylotypic embryo. That means there must be least 300 different circuits—developmental programs for body segments—that can be activated or repressed in every cell. Switching networks
Figure 2. Gene switches are extremely complex devices, comparable in their complexity and precision to a Global Positioning System (GPS) satellite navigation device. Part (a)shows the essential parts in the switch, which begin with the signal inputs A and B, and end with the gene product in the form of protein. Part (b) shows some (not all) of the signal systems involved in programmed cell death (apoptosis). Just as the GPS device integrates the information from many different satellites, so the gene switch must integrate the information from many different signal cascades. (Part (b) from Bell25). The main difference between neo-Darwinian and KG theory is that the former views genes as having a continual effect on organisms, whereas the molecular reality is that genes only work when they are switched ON. This is a profound difference. Everything in KG theory flows from this fact. Evolution occurs not primarily by changing DNA sequences, as neo-Darwinists assume, but by rearrangement of switching circuits. Gene switches are sections of DNA on the chromosome usually near to where the gene is situated (figure 1). One gene may be involved in ten or more stages in development and it will have a separate switch for each stage. Sean Carroll, a leading researcher in this field, says, ‘animal bodies [are] built—piece by piece, stripe by stripe, bone by bone—by constellations of switches distributed all over the genome [emphasis added].’6Evolution occurs primarily by adding or deleting switches, for this is the only way to change the organism while leaving the gene itself undamaged by mutation so that it can continue to function normally in its many other roles. Carroll considers this concept to be ‘perhaps the most important, most fundamental insight from evolutionary developmental biology.’ 7 Figure 1 illustrates evolution-by-switch-addition by showing how butterfly wing spots are produced by adding a new wingspot switch to an existing gene Distal-less that is already involved in development of the insect embryo, leg and wing. 8Gene switches are very complex devices. Carroll compares them to a Global Positioning System (GPS) satellite-navigating device that integrates information from many different satellites to calculate the correct output in a given situation. Gene switches likewise give ‘exquisite geographic specificity [from the built-in logic] … the makeup of every switch is different [and] the physical integrity of switches is very important to normal development. If a switch is disrupted or broken by mutation, then the proper inputs are not integrated.’ 9The reason why genes only work by being either fully ON or OFF is very easy to understand—because a part-formed transcript would become useless junk in a crowded cell. Only fully formed transcripts are useable, and when they are not wanted, the gene needs to be turned OFF so that it will not clog up the heavily crowded cell with unwanted transcripts.Figure 2 outlines the components of a gene switch that uses negative feedback as its control mechanism. The molecules involved in switches are called ‘transcription factors’ and can be activators (that send a GO message) or repressors (that send a STOP message). If a repressor is repressed then STOP STOP = GO. Uri Alon at the Weizmann Institute has researched switches and signal networks and found two main types:10 Switches associated with signal reception and response, which act over metabolic time scales of seconds. These include: single factor regulation, negative autoregulation, positive autoregulation, feed-forward loops (FFL) of both positive
and negative kind, multi-output FFLs that regulate numerous genes simultaneously, single-input modules, and dense overlapping regulons that can regulate one or hundreds of output genes, and they can have one or hundreds of inputs from various sources.Switches associated with development over the lifetime of the organism. These include: positive feedback loops, negative feedback loops, diamond networks, multi-layer diamond networks, and feed-forward loops that combine into large networks.Switches are readily disabled by mutation, so Alon addressed the question of whether systems such as FFLs evolved from duplication of an ancestral FFL. The answer appears to be no, because apparently homologous genes are usually regulated by transcription factors that are so different that they are classed into completely different families. Evolution must have converged independently on the same regulation circuits over and over again. This is perhaps explained by the fact that ‘ … transcription networks seem to rewire rapidly: it takes only a few mutations to remove the binding site of a regulator in a given promoter, and thereby lose an arrow in a network. Hence, even closely related organisms often have different network motifs to regulate a given gene, provided that they live in different environments … One hypothesis is that the network[s] are selected according to the computations that are required in the environment of each species.’ 10This latter finding seems to agree with KG theory, that switching circuit modularity provides the major source of natural variation. Another important confirmation of the concept is the Savageau demand rule. This experimentally observed rule is that frequently needed genes tend to be regulated by activators, while rarely needed genes tend to be regulated by repressors. It has been shown that a strategy in which errors are minimized leads to the Savageau demand rule. 11 That is, errors (mutations and imprecise biochemical reactions) are minimized in the search for useful circuit combinations. Embryonic switching patterns We are now in a position to illustrate embryogenesis, in broad outline, as a series of switching events. The ‘geography’ or ground-plan for each organism is established during the early divisions of the zygote. Important geographical factors include: Inside (endoderm and mesoderm) and outside (ectoderm) Head (mouth and brain end) and tail (anal end) Left and right (in bilateral animals) Front and back (in bilateral animals). These geographical circuits are positive feedback loops that shunt irreversibly into, for example, ‘tail OFF and head ON’ mode. The comparable circuit in the tail end shunts irreversibly into the ‘tail ON and head OFF’ state. In all descendents of these cells, later instructions will pass through these circuits so that, for example, when the instruction is given to build a limb, the state of the geographical circuits will ensure that a forelimb is produced at the head end and a hind limb is produced at the tail end.Within our group of bilaterians, the vertebrates, further circuitry is linked up within this threedimensional ground-plan so that by the ‘phylotypic stage’ all the embryos look remarkably similar (drawings of which Haeckel infamously fudged to make look even more similar than they really are). The similarity is no coincidence, however, because all vertebrate embryos are patterned by exactly the same set of genes, as shown in figure 3. All the genes up to hox6 regulate brain and head development, and those from hox7 to cad regulate spinal cord and body development.By this stage, the vertebrate embryos consist of about 300 largely independent compartments, and further development occurs according to a separate switching cascade in each compartment. The body-patterning genes shown in figure 3 create these compartments via single-input circuits that have multiple thresholds of interaction with the ground-plan circuits (insideoutside, head-tail, left-right, front-back) and the body differentiating genes (those that produce limbs, ears, ribs, etc.). Autopoietic control Life is controlled by coded information. The overall purpose of that information appears to be survival, and in particular, survival via variable reproduction. KG theory says that organisms are built to vary, and it could not be any other way because brittle life, like Paley’s metal watch, would malfunction under the first impact of either internal or external impediment. Rather ‘the organism as a whole is a … poised response system [ready to make] changes it is largely prepared in advance to make’ (KG, p. 226). Figure 3. At the ‘phylotypic’ stage, embryos of all vertebrates are organized into independent developmental segments by the same set of conserved core genes, operating in the same sequence from head to tail. The names of the genes are listed in order for the fish, frog, bird and mouse embryos. Human embryos are organized in the same way. (Redrawn from information in Kirschner and Gerhart, p. 268). But protein-coding information of DNA is clearly not the only information operating in cells. A gene only gives the linear sequence of amino acids in a protein, yet its key function is the result of its 3-dimensional shape, not its linear sequence. Many different amino acids could substitute into the linear sequence without reducing its functionality, but the 3-D shape is very tightly constrained, yet cannot be predicted from its linear sequence. Proteins can fold in numerous different ways, so there must be extra information somewhere else that guides the folding process. Special molecules called chaperones guide the folding process, so there must be folding information built-in to the chaperones. They can also detect and correct mis-folded proteins, and they can detect when a protein is mis-folded beyond repair and have it marked for degradation and recycling.Autopoietic decision making during embryogenesis is of the ‘if … then … ’ kind familiar to computer programmers. Embryonic cells make decisions based upon three kinds of information: (a) instructions from the mother (mRNAs in the egg cytoplasm), (b) conditions within the cell itself, and (c) information from its immediate neighbours. Thus, if a cell has all its specialization circuits in OFF mode, and it has its polarity circuit in an ON state, and it has only one neighbouring cell, then it concludes that it is in the two-cell state of embryogenesis so it will divide and switch ON its bilateral circuits but keep all its specialization circuits in OFF mode.
At a later stage, if there are no longer any instructions from the mother, and the cell’s specialized liver circuit is ON and all its neighbours are liver cells, and the embryogenesis circuitry is OFF and the fetal circuitry is ON, then the cell will divide and reproduce an identical copy of itself to allow the liver to grow in size until birth stage.In later life, the autopoietic system will ensure that maintenance and repairs are carried out to keep the cell functioning properly. But when the telomere ‘clock’ says that time has run out, it will trigger a release of cytochrome c from the mitochondria into the cytoplasm which will set the apoptosome into action to dismantle the cell and recycle its contents.12 Evidence supporting the theory Figure 4. In neo-Darwinian theory, genes produce organisms, and mutations in genes produce new kinds of organisms. In facilitated variation theory, genes are used by cells to construct organisms, and mutations in genes are used by cells to produce variations in progeny. The crucial difference between the the theories is the central role of the cell, rather than the genes, in producing the organism.The primary difference between neoDarwinism and KG theory is that the former puts genes in control of heredity and thus evolution, while the latter puts the cell in control. Figure 4 illustrates this crucial difference.The molecular evidence is clearly in favour of cell control. A recent intensive study of transcription activity in a 1% sample of the human genome found an astonishing amount of unexpected activity. Virtually the whole genome is transcribed, in both directions (both strands of the DNA double helix), in multiple copies (on average 5 in gene regions and 7 in non-gene regions) that overlap by an average 10 to 50 times the size of a typical gene. The best predictor of where and when this transcription takes place is just one factor—chromatin structure. 13Chromatin is the complex of DNA and protein that super-coils the long thin DNA into short fat chromosomes, and it must be uncoiled in order for transcription to occur.The same conclusion—that chromatin structure lies at the heart of transcription activity—was arrived at via study of the relationship between chromatin and nuclear pores.14 In eukaryotes, chromosomes are housed in the nucleus, and access to and from the nucleus is very closely controlled via special structures called the nuclear pore complex (NPC). Transcription only occurs at the inner opening of these NPCs. The relevant chromosome must be brought to a pore and the transcription site correctly aligned. The DNA is unwound from its scaffold proteins, then the histone coils are twisted around to expose the copy region, the double-helix is unzipped, and the transcription machinery produces an RNA copy of the DNA. The transcript is checked for accuracy and corrected if necessary (or degraded if faulty beyond repair) then the RNA is tagged for export out through the NPC and to its destination in the cell. The DNA is then silenced again by being zipped up and rewound onto its histone and scaffold protein chromatin structures. So DNA is normally in a form analogous to a closed book. When the cell wants some information it opens the book, copies the relevant section, and then closes the book again. DNA does not control this process—it is kept in storage until it is needed. The cell is clearly in control.The second major difference between KG theory and neo-Darwinism is in the way genes act upon organisms. In the classic case of Darwin’s Galápagos finches, neo-Darwinian theory explains the variation in finch beak size and shape via mutations and natural selection acting repeatedly over a long period of time. Many small changes must occur independently in the upper and lower beaks, in the adjacent skull, and in the head muscles, to coordinate and order them all into the necessarily viable intermediate beaks of the birds that need to survive throughout the period of divergence.In contrast, recent experimental work suggests that just two regulatory changes are involved. The bone morphology protein BMP4 when expressed earlier or later in embryogenesis causes broad or narrow beak development,15 and more or less of the calcium regulator proteincalmodulin produces long or short beaks, respectively.16 Gerhart and Kirschner17 cite this as experimental validation of their theory. The whole craniofacial developmental process is compartmented and coordinated by a modular regulatory system that can be easily rewired ‘with a few regulatory mutations’ (KG, p. 236) to produce new features that are readily integrated into the already-prepared, robust, conserved-core-process-based system. Field observations confirm that such changes take place rapidly across just a few generations.18 More neo-Darwinian errors The neo-Darwinian genetic theory of heredity assumed that characteristics of organisms are coded on genes with roughly a ‘one-gene-to-one-character’ correspondence. As organisms evolved to greater complexity, more genes were added via gene duplication and subsequent independent mutation of the extra copy into useful new characters. 19 More complex organisms were thus expected to carry more genes than less complex ones. Furthermore, lineages that diverged early in the history of life would have mutated at virtually every locus, making them quite unlike at the genetic level. This led Ernst Mayr to state in his 1963 book Animal Species and Evolution ‘the search for homologous genes [derived from the same ancestor] is quite futile except in very close relatives.’20 These predictions have all been dramatic falsified by molecular discoveries: There is no one-to-one correspondence between genes and characters. Most genes are pleiotropic—they affect many different parts and stages of life. And all but the most trivial characters are determined by large numbers of genes—50% to 80% of the entire genome is required for many bodily functions in vertebrates. 21Genetic information structures are not linear, but interleaved, producing multiple overlapping transcripts. Moreover, the exons (DNA segments that directly code for protein segments) in a gene are not specific to that gene but can participate in modular fashion with up to 33 different genes on as many as 14 different chromosomes.22There is no correlation between organism complexity and gene number. Rice and crayfish carry more genes than humans.Homologous genes occur right across the spectrum of life. About 20% of the human genome is homologous with bacteria, about 50% is homologous with eukaryotes (fungi, plants, animals), about 80% is homologous across the animal kingdom, and about 99% is homologous across all the vertebrates, leaving only about 1% that is uniquely human.23 About 500 genes are ‘immortal’ and have not changed at all in their key functional sequences across the whole history of life. 24One of the most serious errors—that will need a lot of undoing—is the vast amount of molecular taxonomy that has been based upon the idea that ‘junk DNA’ provides us with a record of past mutations and thus acts as a ‘molecular clock.’ We now know that non-protein-coding DNA ismore active in the cell than genes. According to KG theory, molecular taxonomy can only work correctly by comparing ‘hidden anatomies’ across taxa, not DNA sequences. To understand hidden anatomy we will have to find the regulatory code. New aspects of gene regulation are being reported daily, but so far, no one has been able to put together the complete code for a whole organism. Conclusion
Let’s stand back consider the big picture of how life works at the molecular level.Life consists of conserved core processes and modular regulatory circuits. All the special properties of the conserved processes had to be in place before regulatory evolution could take place. Where did they come from? ‘They may have emerged together as a suite, for we know of no organism today that lacks any part of the suite.’‘The novelty and complexity of the cell [the most important conserved core processes that has modular regulatory circuitry built-in] is so far beyond anything inanimate in the world of today that we are left baffled by how it was achieved.’A living organism is ‘a poised response system [that] responds to mutation by making changes it is largely prepared in advance to make.’ ‘Genetic variation or mutation does not have to be creative; it only needs to trigger the creativity built into the conserved mechanisms.’ It could not be otherwise, because invariable life would soon become extinct. Creative frogamandering by David Catchpoole Frogs like to hop, salamanders like to walk. But what did this creature do? The above illustration is how the general public saw the ‘frogamander’ confidently portrayed in news and popular science reports.4,6,7But is that how the creature dubbed Gerobatrachus hottoni really appeared?Are frogs and salamanders of the same originally created ‘kind’, or different? As far as I’m aware, creationists have not definitively addressed this question, not having had any particular need to do so.1For evolutionists, however, it’s a very different story. Evolution ascribes common ancestry to all living things, so evolutionists have a pressing need to find fossil examples of ‘intermediates’ to be the common ancestors of various organisms, ultimately leading back to the mooted single-celled ancestor(s?2 ) of all life. But the needed ‘intermediates’ have proved, for 150 years now, to be elusive3—which is why, for example, even just the supposed evolutionary origin of amphibians alone (Lissamphibia: frogs, salamanders and caecilians) has been a matter of ‘longstanding debate’4 and ‘one of the most controversial questions in vertebrate evolution’.5So it’s hardly surprising that the discovery of a fossil said to have a mixture of frog and salamander features, and claimed to have ‘set to rest one of the greatest current controversies in vertebrate evolution’,6 has been enthusiastically embraced by proponents of evolution. (E.g. well-known Australian science populariser Dr Karl Kruszelnicki.)The new fossil has been named Gerobatrachus hottoni (‘elderly frog’). ‘It’s a perfect little frogamander,’ said lead researcher Assistant Professor Jason Anderson of the University of Calgary. He told National Geographic: ‘It had an overall amphibian gestalt. … You know, kind of a froggy salamander-y sort of look.’ 7And that’s just how the illustration that featured in various media outlets 4,6,7 portrayed it (figure 1). But didGerobatrachus hottoni really look (and walk) like that?‘The fossil itself is almost perfectly complete,’ one news outlet 4 reported Anderson as saying. But National Geographic News7 was more circumspect, warning that John Bolt, curator for fossil amphibians and reptiles at The Field Museum in Chicago had urged caution in interpreting the fossil specimen. (Note that John Bolt is an evolutionist himself.) Bolt said that it is difficult to say for sure whether this creature was a common ancestor of frogs and salamanders, ‘given that there is only one known specimen of Gerobatrachus, and an incomplete one at that’. 7Going back to the original paper in Nature to resolve this apparent contradiction—i.e. whether the fossil is ‘almost perfectly complete’4 or ‘an incomplete one’7—reveals that the research team’s original wording was:‘The 110-mm-long specimen (Fig. 1) is preserved fully articulated in ventral [bottom] view, and is missing only the stylopods, zeugopods, and ventral portions of the skull and pectoral girdle.’5Note that their ‘Fig. 1’ in the Nature paper is not the illustration that appeared in the popular media (reproduced in our figure 1 above). No, that ‘frogamander’ illustration does not appear anywhere in that research paper. Instead, their ‘Fig. 1’ shows a photograph of the fossil in the rock, along with an adjacent interpretive outline drawing of the bones evident in the fossil. There’s a curious lack of any legs in the fossil evidence (apart from portions of two feet at one end of the fossil). You might wonder what the missing ‘stylopods’ and ‘zeugopods’ might be in this otherwise ‘almost perfectly complete’ fossil. Prominent evolutionists Neil Shubin, Clif Tabin and Sean Carroll define them thus:The tetrapod limb consists of three distinct compartments: a, the stylopod (upper arm and thigh); b, zeugopod (lower arm and calf); andc, autopod (hand and foot).8Thus, the Gerobatrachus hottoni fossil missing its ‘stylopods’ and ‘zeugopods’ is actually missing its legs! One wonders if the likes ofScienceDaily, National Geographic and other science news outlets actually realized that? Perhaps they would not quite so readily have published the confident-looking artists image of the perambulating ‘frogamander’ if they’d known that the legs—not to mention the pectoral girdle—were missing. Hence no-one can tell from the fossil remains of Gerobatrachus hottoni how, or even if, it might have walked (hopped?). So no-one can say for sure what sort of amphibian it might be.John Bolt, the aforementioned evolutionist who urged caution in interpreting the fossil made a couple of other interesting comments, too. The fossil is said to be 290 million years old, and Bolt observed that it is ‘remarkably like the modern amphibians’. 7 Of course, ‘evolutionary stasis’ does catch evolutionists by surprise, and Bolt added:‘The most astonishing thing to me about this study is that this animal is far more froglike than I would ever have expected from its age.‘Nothing this nonprimitive has ever been described from this age. It’s just amazing.’ 7It’s not at all amazing when one realizes that millions-of-years ages don’t stack up with closer inspection of sedimentary strata and the fossils within. Colourful creature coats by Jean Lightner Animals display a wide variety of coat colours. These colours result from a pigment called melanin. There are two types of melanin: one that results in a yellow-to-red colour (pheomelanin) and another that results in a brown-to-black colour (eumelanin). Most animals can produce both, and a number of different genes (instructions found in DNA) regulate the relative amounts of these two forms of melanin and their distribution.
Sometimes genes can be changed by a process known as a mutation. A mutation is basically a mistake in copying a gene and results in a new allele (variant form of the gene). How it affects the animal depends on where it occurs. Mutations that occur in one specific gene have interesting effects on animal coat colour. 1 This gene codes for a protein that works like a switch.2 Normally, a hormone3 switches it ‘on’ to produce more of the darker eumelanin, while another protein4switches it ‘off’ so more pheomelanin is produced.One type of mutation messes up the switch. In this case the animal cannot produce eumelanin, even when it is signalled to do so. The yellow/red colour of Golden Retrievers, Yellow Labradors, and Irish Setters results from one such mutation.5 A different mutation with a similar effect causes the chestnut colour in horses. A number of other animals have this type of mutation as well. These are called loss-offunction mutations because the animals lose the ability to produce eumelanin. They are usually recessive, meaning that if the other of the pair of alleles is the normal type, the mutant allele has no effect; it is hidden. This means that animals with light coat colour must have a gene pair of two mutant alleles, one being inherited from each parent. If one of the alleles is the normal form, the colour will be normal, not light.A second type of mutation in this same gene results in pigment production that is always switched on. In this case the production of eumelanin is ongoing, regardless of the signals being received. This type of mutation has been found in cattle, sheep, mice, and chickens. 6 It is sometimes called a ‘gain-of-function’ mutation7 because the animal produces more eumelanin than it would normally, resulting in very dark / black colouring. However, this term is misleading because the animal has lost its ability to control eumelanin production. These mutations are typically ‘dominant’; only one mutant allele is necessary for the animal to be affected. Since this gene affects only the colour of an animal, mutations in it are well tolerated,8 meaning that it does not affect the animal’s ability to survive. Therefore, it is no surprise to find that dozens of different alleles have been found for this gene.9 These mutations are all downward changes, where a complex pathway has been disrupted. None are examples of onward, upward change that evolutionists imagine have occurred throughout history. What we see fits the young age history where an universal designer made everything very good and these downward changes in the well-designed biochemical pathways of living things began after mankind rebelled against him.While the mutations discussed here may be well tolerated, thousands of others result in disease. They remind us of the fallenness of the creation, where everything is now ‘in bondage to decay’.
MIGRATION Migration after the Flood How did plants and animals spread around the world so quickly? by Dominic Statham Published: 12 March 2013 (GMT+10)
The young age model provides a better explanation for the observed patterns of biogeography than evolution. This article is about biogeography—the study of where on the earth we find the different kinds of plants and animals. It is also about two competing views of Earth history: the secular, evolutionary ancient Earth view the young age Earth view. The secular, evolutionary, ancient Earth view According to this, the earth is billions of years old, and natural processes have been slowly changing the earth’s continents and slowly changing life on Earth over many millions of years. If we go back a couple of hundred million years, so we’re told, the earth looked like this. All the continents were together in one great continent they call Pangaea. And the world we see today, we’re told, formed as this single land mass split up, as the continents we know today slowly drifted apart. (See repeating animation below.) Credit: Ron Blakey, NAU Geology
The separation of the continents As this was happening we’re told—as the continents were slowly drifting apart over millions of years—dinosaurs went extinct, reptiles evolved into birds and mammals, non-flowering plants evolved into flowering plants and, of course, apes evolved into people. So the evolutionists tell us, when we study biogeography we discover lots of evidence supporting this view. Indeed, there’s a mountain of evidence they say, from biogeography, showing that evolution is true; and a mountain of evidence confirming that the continents split apart millions of years ago, separating the various plants and animals that lived on the earth around that time.When we go to Africa, we find leopards, rhinoceroses, giraffes and gorillas. In America, we
don’t find any of these. Instead, we find raccoons, jaguars, armadillos and opossums. When we go to Australia we find marsupials like kangaroos. (See here.) Evolutionists claim that the reason we find these different animals on these different continents is that they evolved in the different parts of the world. So, they say, gorillas are found in Africa and not America, because they evolved in Africa and not in America. Armadillos are found in America, because they evolved there and not anywhere else.Evolutionists also claim that strong evidence for evolution can be found from studying the biogeography of islands. For example evolutionists make much of the different species of finches found on the Galapagos Islands. One of the prominent features of the Galapagos finches is their different beak shapes, and of particular significance is that the finches have beaks best suited to the kind of food found on the islands where they live. Some have strong stubby beaks for crushing hard seeds; others have thinner beaks for probing flowers or fishing insects from the crevices in trees. And so the story goes —and there’s much to be said for it—one original species flew to these islands from the mainland and, over time, diversified into all the different species. This is often termed ‘speciation’—where a number of different species come from one original species.Actually, much more impressive examples of speciation can be found on the Hawaiian Islands, right out in the middle of the Pacific. Around 500 unique species of fruit fly can be found here. Also, Hawaii is home to more than 1,000 different species of snails and slugs, species that, again, are found nowhere else in the world. Evolutionists claim that what we see on the Galapagos and Hawaiian islands provides absolutely ‘irrefutable’ evidence supporting their theory of evolution.Within mammals, there are two main groups: the placentals and the marsupials. 1 Placental mammals, such as humans, complete their embryonic development in the womb, joined to the mother by a placenta. Marsupial mammals, such as kangaroos, have a very different reproductive system, where the mother carries and suckles her young in a pouch at the front of her body. (See here.) We can see here a few more placentals on the left and a few more marsupials on the right. There are around 140 species of marsupial in Australia, most of which are not found anywhere else; according to evolutionists, there’s a very straightforward explanation for this. You’ve guessed it—these marsupials evolved in Australia! According to Professor Richard Dawkins, “The pattern of geographical distribution [of plants and animals] is just what you would expect if evolution had happened”2 and Jerry Coyne, who is Professor of Biology at the University of Chicago, had this to say: “The biogeographic evidence for evolution is now so powerful that I have never seen a creationist book, article or lecture that has tried to refute it. Creationists simply pretend that the evidence doesn’t exist.”3 The young age Earth view Many creationists believe that there was, originally, one great continent—.There would have been much geological activity, volcanism and ground movements. Probably a majority of creationist scientists—not all, but probably a majority—would agree that the continents we see today did split apart from the one original land mass. And they would say that this happened at the time of the Flood, when all this geological activity was going on. Of course, they wouldn’t say this happened slowly, over millions of years, but rapidly—not by ‘continental drift’, but ‘continental sprint’. And it’s important to note that, according to this view, the movements of the continents would have occurred beneath the flood waters. So we wouldn’t have had living populations of plants and animals being split by this continental separation.During the Flood, the whole of the preflood world was destroyed. So the world we see today grew up after this global catastrophe, and over the last 4,500 years or so. Plants left floating on the surface of the waters would have recolonised the areas where they finally settled, after the flood waters receded, and the animals would have migrated to the places they now inhabit. Which view best fits the data? The question we might ask is this: “Which view is best supported by the scientific evidence, the data? The secular evolutionary ancient Earth view, or the young age Earth view?”Firstly, the finches on the Galapagos and the many fruit flies and snails on the Hawaiian islands are not a problem for creationists. We believe that animals were designed with the capacity to vary within their kinds, and with the capacity to change and adapt to different environments; and when we study this carefully, we actually find a problem for the evolutionists. This is because there is growing evidence that this kind of adaptation occurs quickly—it doesn’t require hundreds of thousands or millions of years. 4There’s lots of evidence that plants and animals can change. Finches can become other species of finch, fruit flies can become other species of fruit fly, snails can become other species of snail and so on. But this is hardly scientific evidence that an amphibian can become a reptile or that a reptile can become a bird. Nor is it scientific evidence that an ape can evolve into a man. Have the continents really been separated for millions of years? Now the evolutionary view is that we have different animals on different continents because they evolved in different parts of the world.According to this view, jaguars and lions descended from a common evolutionary ancestor that lived around three million years ago. And after three million years of evolution, they say, we got jaguars in South America and lions in Africa. But it’s possible to mate a jaguar and a lion and get a hybrid, a jaglion. If these two species, jaguars and lions, were really separated by three million years of evolution, it is most unlikely that their mutated DNA would allow them to hybridise.Evolutionists face an even bigger problem trying to explain hybrids between jaguars and leopards. This is because the female of this kind of hybrid is fertile. Think about it. Three million years of separate evolution—half the time it allegedly took for ape-like creatures to become people—and the hybrid is still fertile. This seems very unlikely. But the ability of these big cats to hybridise fits the young age account of history very well. If jaguars, lions, leopards and tigers all descended from a pair of cats around 4,500 years ago, it is not surprising that they can mate and produce offspring.Arguably, evolutionists face an even greater problem with the iguanas of the Galapagos Islands. The land and marine iguanas supposedly separated from their common evolutionary ancestor around 10 million years ago. But, as we pointed out in our Darwin documentary, land iguanas can mate with marine iguanas and produce offspring. This amazed evolutionists when they saw it. Were the continents really joined for millions of years? In the evolutionary view, South America and Africa were joined for millions of years (see here). Why then are more seed plants common to South America and Asia than to South America and Africa? Of around 200 seed plant families native to Eastern South America, only 156 are common to Eastern South America and Western Africa, but 174 are common to Eastern South America and Eastern Asia.5 (See here.) If South America and Africa had really been joined for millions of years, we would expect to see exactly the opposite. We would expect there to be more plants common to S. America and Africa than to S. America and Asia.According to Dr Simon Mayo, of the Royal Botanic Gardens, Kew (near London), “The overall similarity of the floras [plants] of the two continents is surprisingly low given such a clear geophysical background.”6 Dr Mayo expresses surprise that there are so few plants found in both South America and Africa. Why is he so surprised? Well, be believes these two continents were joined for millions of years. The actual locations of plants, however, doesn’t support this view.Some biogeographers have found this kind of data so puzzling that they have argued against the idea of a super continent, Pangaea, where South America and Africa were joined, and proposed a different arrangement—they have suggested instead that there was a super continent they call Pacifica, where South America and Asia were joined.7If the ancient earth view were correct, we would expect the data and the models of ancient earth geologists to fit with the data and models of ancient earth biogeographers. We would expect them to be harmonious, but they’re not; often they’re inconsistent and contradictory.
New World monkeys We find monkeys in South America, Africa and Asia. For example, we find the Spider Monkey in South America, the Olive Baboon in Africa, the Langur in India and Macaques in Japan. (See here.) Now evolutionists tell us that monkeys evolved in Africa. Well, it’s not difficult to see how they might have migrated to Asia. But how did they get to South America? According to evolutionary theory, South America split off from Africa millions of years before monkeys had evolved. Evolutionists have the same problems explaining why rodents and some flowering plants are found on these two continents, because, again, they are said to have evolved after South America split from Africa.8 Beringian fossils Currently, the western tip of Alaska is very close to the eastern tip of Asia. They’re separated only by the narrow Bering Strait. In fact, many people believe that in the recent past, the two were connected. But, according to evolutionists, and their theory of slow continental drift, Asia and Alaska have only been close to one another for ten million years or so; not for very long in their thinking.Prior to this, in the supercontinent Pangaea, Alaska and Asia are understood to have been separated by thousands of miles of ocean—by all the water on the far side of the globe. (See here.) However, we find plant fossils of the same species in rocks either side of the Bering Strait; and these rocks were laid down in what evolutionists would call the Jurassic period.9 But the Jurassic period, we’re told, ended around 150 million years ago. So according to this thinking, these identical plant fossils were buried at least 150 million years ago.Do you see the problem here for the ancient earthers? In their thinking if we go back over 150 million years, Eastern Asia and Alaska weren’t close to one another as we see in this slide. They were separated by thousands of miles of ocean. Why, then, do we find plant fossils of the same species buried in Jurassic rocks in these two very distant regions? This is yet another example of the kinds of conflicts that arise between ancient earth geology and ancient earth biogeography. Millions of years of evolution? There are many similar plants and animals found in eastern Asia and eastern North America, but not in the regions between them.10,11 (Seehere.) Now evolutionists try and explain this by saying that millions of years ago the northern regions were warmer and these two areas of Asia and America were part of one continuous plant and animal distribution—like this. And a few million years ago, they say, the climate then cooled and the plant and animal life was separated into the two zones. But, again, their millions of years’ scenario hits a problem. And it’s a big problem, because many of the plants in these two regions are regarded as being the same or virtually the same species. 12 How, then, could they have been separated for millions of years? If all these plants had really been separated for millions of years, they would not be expected to have retained their similarities to the point that they would still be considered to be the same or virtually the same species. Creationists would expect them to change because plants and animals appear to be designed to vary within their kind; and evolutionists would expect them to change because of genetic mutations and their understanding of the evolutionary process.In evolutionary thinking it took only six million years for ape-like creatures to evolve into people. Make no mistake, there are considerable differences between apes and people. But to the evolutionist this is easily explained: the evolutionary process, they say, is so powerful it can bring about these kinds of remarkable changes in just a few million years. Why then did all these plants and animals in Asia and America not evolve too and change significantly over the same period?From a creationist point of view, though, it would seem perfectly reasonable to understand that there was a continuous plant and animal distribution linking these two parts of the world—but not of course millions of years ago, but in fairly recent history. More biogeographic puzzles for evolutionists Many plants and animals are found only in the northern regions and southern regions and not in between. Crowberries are one example. It certainly can’t be said of these that they are found where they are because that’s where they evolved. There are so many plants and animals found only in the northern and southern regions that some biogeographers have made the astonishing suggestion that these parts of the world were once in contact with each other. They have seriously suggested, based on biogeographic data, that the arrangement of the continents in the past was such that the northern regions were adjacent to the southern regions.13 So, again, we see the thinking and views of ancient earth biogegraphers conflicting with the views of ancient earth geologists. Few of the latter would have much time for the idea that the northern regions were once adjacent to the southern regions. So how might we explain biogeography within the framework of the young Earth history? One process by which plants and animals could have spread around the world after the Flood is rafting—that is, on log mats driven by ocean currents. Actually, a growing number of evolutionists are proposing rafting as an explanation for how some plants and animals dispersed from one island to another, and even from one continent to another. 14When Mt St Helens erupted in 1980, a tsunami was generated in the nearby Spirit Lake, and this caused around a million trees to be uprooted from the surrounding hillside. These eventually settled on the lake as an enormous log mat. Following the great earthquake off the coast of Japan in 2011 and the resulting tsunami, a trail of debris formed in the Pacific ocean, around 70 miles (100 km) long and covering an area of over 2 million square feet (186,000 square metres).Now the effects of the Mt St Helens and Japanese tsunamis were nothing as compared with the destruction that would have been wrought by a global flood. The flood would have resulted in billions of trees floating on the surface of the oceans. These log mats would have been like enormous floating islands and, regularly watered by rainfall, they could have easily transported plants and small animals great distances. Some creationists believe that the pre-Flood world included great floating forests, a bit like the quaking bogs we know today.15 Perhaps these were broken up during the Flood and became rafts too.The ability of ocean currents to distribute floating objects around the world was seen recently, when thousands of bathtub rubber ducks were lost off a container ship in the North Pacific. Within just a few months, these had floated to Indonesia, Australia and South America, and subsequently into the Arctic and Atlantic oceans.16,17,18 (See here.) Often we find plants distributed along coastlines and islands. The distribution of the Sago palm can be seen here. It’s found in East Africa, Madagascar, the tip of Indian and parts of Indonesia and Australasia.Pelargonium is another example. It’s found right out in the Atlantic, in South Africa, Madagascar, east Africa, India, Sri Lanka, southern Australia and New Zealand. Another example is a type of fern plant, Strangeriaceae. It’s found in South Africa and along the eastern coast of Australia. This shows the distribution of a plant called Hook and Arn, a member of the carrot family. Based on the routes taken by the rubber ducks, it seems very reasonable to believe that rafting explains this. We can see how the rubber ducks floated to North and South America. Tracks of dispersal A prominent feature of biogeography is ‘tracks of dispersal’. This is an example. It shows how Oreobolus plants dispersed throughout Indonesia and Australasia and across the Pacific ocean. And what’s so significant about this is that many other plants (and small animals) have followed a similar route.Note, too, that all the plants and animals following this track are found either side of the Pacific Ocean. Now, when the habitats of particular plants or animals are broken or split by land or water, it’s called a disjunction. So we might say that all these plants and animals are disjunct (or split) across the Pacific Ocean. Areas of endemism
Text books typically show the main biogeographic regions like this. This is the map for animals, showing six main faunal (or animal) regions—regions where we tend to find the same sort of animals. But these kinds of diagrams are really over simplifications. A more realistic picture is like this, where we find many different plants and animals concentrated in small regions known as ‘Areas of Endemism’. 19,20 Now, endemic means native or restricted to a particular area, and an area of endemism is one where there are a high number of endemic species—where many different species are found in the same small distinct region. And here, each colour represents one of these regions.Interestingly, areas of high plant endemism often coincide with areas of high animal endemism.21,22 So, these areas where we find lots of different plant species concentrated together tend to be the same as the areas where we find lots of different animal species concentrated together. Many areas of endemism are coastal regions and islands.For example, the tropical Andes, shown here enclosed in red on the left, is the richest and most diverse plant region on Earth. It contains around 15% of the all the world’s plant life in less than 1% of the world’s land area. Around 20,000 of its 40,000 plant species are endemic. The area of Sundaland, enclosed in green to the right, contains 15,000 endemic plant species and the island of Madagascar, enclosed in blue, has over 9,000 endemic plant species.We also find many similarities between these regions—where the same plants and animals are distributed around or either side of an ocean. There are numerous patterns of disjunction like this, where, again and again, we find the same plants and animals in the same widely separated areas. 23 In the last century, a man called Leon Croizat plotted many tracks like these showing dispersal routes across the world (see here). Each of these lines is known as a ‘generalized track’, where many different plants follow the same route. 24 Croizat’s work made clear that many tracks of dispersal either cross oceans or follow coastlines. A good case can be made for the biogeographic regions being oceans rather than continents! Christopher Humphries of the Natural History Museum in London and Lynne Parenti of the Smithsonian Institution wrote,“Characteristically, many disjunct patterns span ocean bottoms, to the point that the oceans have been characterized as the natural biogeographic regions and the continents represent the land areas around the periphery.”25To me, this is very strong evidence supporting the rafting hypothesis—that transport across oceans explains much of the biogeography of the world. I believe that many plants and small animals were transported on great log mats left over from the Flood and that the areas of endemism we see today correspond to the landing places of these rafts. Interestingly, researchers from Bryan College, Tennessee, showed that the intersections of ocean currents with the continents tend to coincide with these areas of endemism.26 (See here.) Migration across land bridges Another way animals could have spread around the world is through migration across land bridges that are now below sea level.We believe that soon after the Flood, there was an Ice Age. We don’t believe in many ice ages, but just one. Conditions would have been ideal for an Ice Age at the end the Flood. The oceans would have been warm, due to hot underground water being added to them at the beginning of the Flood, and this warming of the oceans would have caused much water to evaporate into the atmosphere. At the same time, volcanoes erupting during and after the Flood would have thrown lots of dust into the air and this would have blocked some of the sun’s heat, keeping the continents cool. So the large amounts of water vapour in the atmosphere would then have fallen as snow, building up significant amounts of ice on the land. Sea levels would then have fallen as the oceans’ water evaporated and was trapped as ice sheets on the continents. And land bridges would have appeared as the sea level dropped.There was likely a land bridge across what is now the Bering Strait and a number of land bridges linking parts of Indonesia and perhaps even Australasia. Of course, we don’t see these land bridges today, because much of the ice has now melted and sea levels have risen again. Also, due to continued geological activity after the Flood, ground movements could have caused other land bridges to fall below sea level. So it’s not difficult to imagine how animals could have migrated from Ararat to many places throughout the world. Also, some plants and animals, especially those useful for farming, may have been transported by man, particularly during the dispersal from Babel.I think, too, there was probably some rafting of animals to Australia and South America. In fact, North and South America may not have been connected until sometime after the end of the Flood. 27 You can see on this diagram that I’ve shown South America detached from North America. Marsupial distributions Living marsupials are found in Australia, New Guinea and parts of America—see here. Most marsupials, however, are found in Australia and New Guinea and many of these are found nowhere else. So how can we explain this within the framework of the young Earth history? Well, I don’t have any firm answers, but I can outline one possibility that I think makes sense.Now, you remember we’re dealing here with two types of mammal—placentals and marsupials. And there’s some evidence to suggest that placentals tend to outcompete marsupials when they share the same habitats. From a creation point of view, this does seem plausible. Marsupials alongside the placentals must have lived around the Middle East and the surrounding continents. Yet only placentals live in these places today. It seems significant, too, that North America has only one marsupial—the Virginia opossum. Marsupials have become well established in Australia but largely in the absence of placentals.Perhaps competition from placentals drove marsupials to migrate away ahead of placentals. Marsupials then gained an early foothold in Australia and South America and, without competition from placentals, they thrived in those places. And perhaps, as the log rafts broke up and sea levels rose and covered the land bridges, Australia and South America became almost completely isolated before very many placentals had made their way to those continents. So, driven by competition from placentals, marsupials could have migrated to Australia and South America and then been protected from placental competition as these continents were cut off from the rest of the world. Fossils of marsupials are found on every continent.28 So, in evolutionary thinking, marsupials died out in all the continents except the ones where we see them today. Why can’t creationists simply argue the same?There are some interesting twists in the evolutionary story about marsupials. If, in evolutionary thinking, we go back to the late Cretaceous rocks, supposedly around 65 to 80 million years ago, we don’t find any marsupial fossils in Australia and South America. They are found only in Europe, Asia and North America. An article in Science journal said this:“Living marsupials are restricted to Australia and South America … In contrast, metatherian [marsupial] fossils from the Late Cretaceous are exclusively from Eurasia and North America … This geographical switch remains unexplained.”29So, again, according to evolutionists, 65 million years ago marsupials lived in Europe, Asia and North America, but they then died out in those areas and now live in Australia and South America. If evolutionists can have marsupials dying out in Europe, Asia and North America, why can’t creationists?Another problem for evolutionists is the ‘Little Mountain Monkey’ of South America. DNA comparisons suggests that this little South American marsupial is more similar to the Australian marsupials than to other American ones. How did it end up in America? It seems very difficult to argue that it evolved there. Summary The main evidence for evolution from biogeography is speciation—a fact of biology that is better explained by the creation model.The distribution of plants does not support the belief the continents were joined for millions of years.Fertile hybrids between animals on different continents indicate that they have not been separated by millions of years.Plants and animals are concentrated in small regions of high biodiversity along coastlines and islands. While these correspond, to some degree, with areas of high rainfall, this does not explain why there are many patterns of disjunction where the same plants and
animals are found in the same widely separated areas of endemism.Such biogeographic observations, however, appear to be well explained by transport across oceans.Log rafts left over from the Flood could have provided the means of rafting. Migration across land bridges may explain other biogeographic distributions. Conclusion As with other branches of science, the data appear to fit the young account of Earth history very well. ABiogeography* by Dominic Statham Evolutionists claim that the biogeographic distribution of organisms provides strong evidence for evolution. Although studies of biogeography provide strong support for the process of speciation, they do not fit the wider predictions of evolutionary theory, and are inconsistent with the ancient earth geologists’ model of slow continental drift. Evolutionary theory has difficulty explaining areas of endemism and the disjunct distributions seen in both the fossil record and the living world. The data can be seen to fit the young age account of recolonisation following the Flood, and particularly the hypothesis that the observed patterns arose from global dispersal on natural rafts. Figure 1. Placental mammals (left) and their marsupial counterparts (right). Biogeography is the study of the distribution of plants and animals throughout the world. From this, it is known that each of the continents has its own distinctive fauna and flora. In Africa, for example, we find rhinoceroses, hippopotamuses, lions, hyenas, giraffes, zebras, chimpanzees and gorillas. South America has none of these. Instead, it is home to pumas, jaguars, raccoons, opossums and armadillos. Marsupials are found in Australia and South America, but not in Europe. Such observations have led biogeographers to divide the world into six main faunal regions. Similarly, six main floral regions have been identified. Evolutionists claim that the most reasonable explanation for these biogeographic distributions is that the different animals and plants evolved separately, from ancestors that colonized different areas of the world thousands or millions of years ago. Further evidence for this is argued from the study of island biogeography. For example, of the 1,500 known species of fruit flies (Drosophila), nearly one third of them live only on the Hawaiian Islands. These islands are also home to more than 1,000 species of snails and other land molluscs that are not found anywhere else.Here, again, it is necessary to differentiate between speciation within a kind (which is accepted as fact by both creationists and evolutionists) and evolution between kinds. Biogeography does indeed provide evidence in support of the former, and the fruit flies, snails and other molluscs found on the Hawaiian Islands arguably provide some of the strongest evidence we have of this. Similarly, clear biogeographic evidence exists for the speciation of finches around the Galápagos archipelago, where similar but different species are found on the different islands.1 Almost certainly, this arose because the islands are close enough to enable a few birds to fly to a neighbouring island, but far enough away for the new colony to be isolated from the original group and less likely to interbreed with it. But how well does evolutionary theory explain the more general observations of biogeography?In fact, some biogeographic observations are extremely difficult to explain within an evolutionary framework. According to the theory of evolution, mammals developed from small, shrew-like creatures around 100 million years ago. These creatures are argued to have evolved into, among others, the marsupials found in Australia and theplacentals found in Europe and other parts of the world. What is so remarkable about these two groups is that, while their reproductive systems are fundamentally different, in other ways they are very similar (figure 1). For example, the skeletal structures of some European placental dogs are almost identical to those of Australian marsupial dogs. This is particularly evident when the skulls of the Tasmanian marsupial wolf (Thylacinus cynocephalus) and the European placental timber wolf (Canis lupus) are compared. Other placentals and marsupials, which supposedly evolved independently from one another, also show similar characteristics. Is it really credible that random mutations and environmental conditions on separatecontinents could have given rise to such similarities? Areas of endemism Since evolution is argued as being a global phenomenon, it would be expected that new species would originate in many places throughout each continent. Hence, evolutionary theory would predict that centres of plant and animal dispersal would be randomly distributed, rather than concentrated in a few areas.2 It has been known for many years, however, that this is not the case. As far back as 1820, Augustin de Candolle realized that the global pattern of plant distribution is closer to that of “areas of endemism”, where
many different plants are confined to the same distinct and often small regions (see figure 4 below). 3 Subsequently, de Candolle’s areas of high plant endemism were found also to correspond to areas of high animal endemism.4 Disjunct distributions Figure 2. Distribution of the plant genus Clethra (from Thorne, ref. 9). Another problem for evolutionary explanations of biogeography arises because similar plants and animals are found not only across adjacent regions of land or neighbouring islands, but also on different continents, separated by large stretches of land or ocean. These are called disjunct distributions. Evolutionists sometimes explain these by arguing that continental drift separated similar groups that once lived in close proximity and therefore shared common ancestors. This is the explanation given, for example, as to why chironomid midges are found in Antarctica, Southern Australia, South America, New Zealand and South Africa.5 However, according to evolutionists’ own theories, many species that are disjunct across previously joined continents evolved after their separation.6For example, South America and Africa allegedly separated around 100 million years ago, but species of cactus, which supposedly evolved in South America around thirty million years ago, are also found in Africa. Similarly, the evolutionary accounts of the emergence of rodents found in South America and Africa do not fit the generally accepted timing of continent drift.7 Many other puzzling disjunctions across these continents are known.8 Moreover, disjunct species are frequently found on continents that never bordered one another. For example, many plants and insects are known to be disjunct across the Pacific Ocean.9 The distribution of the plant genusClethra, for example, is shown in figure 2. Interestingly, the opossum Dromiciops, found in Chile, is much closer to Australian marsupials than to other South American marsupials. 10There is an abundance of other biogeographic anomalies that do not fit the expected evolutionary pattern. For example, the fauna of central and southern Africa is closer to that of southern Asia than that of northern Africa,11 and flora found in Madagascar is remarkably similar to that of Indonesia.12 Crowberries (Empetrum) are found only in the more northern regions of the northern hemisphere and in the most southern regions of the southern hemisphere. Many closely related plants are found only in eastern North America and eastern Asia. A study conducted by the Illinois State Museum showed that 627 seed plant genera are common to eastern Asia and eastern North America, 151 of which are not found in western North America. 13 Significantly, some of the plants (and fungi) found in eastern Asia and eastern North America are identical at the species level, indicating that the disjunctions occurred very recently (that is, within the last few thousand years). If these disjunctions had occurred millions of years ago, as evolutionists believe, it is most unlikely that so many species would have remained the same in the two areas. This is because plants and animals are known to change rapidly in response to changes in their environments. Fossils The fossil record also presents problems for evolutionary explanations of biogeography. For example, there are many similar plant fossils in western North America and eastern Asia, but, according to the account of continental drift preferred by geologists, these rocks were laid down when Alaska and Russia were separated by thousands of kilometres of ocean.14 While living marsupials are very largely restricted to Australia and South America, their fossils from the period evolutionists call the “Late Cretaceous” (allegedly between 85 and 65 million years ago) are found exclusively in Eurasia and North America. As noted by Richard Cifelli, an Associate Professor in the Department of Zoology at Oklahoma University, “this geographical switch remains unexplained”.15 Interestingly, fossil marsupials have now been found on every continent.16 According to evolutionary theory, placentals evolved in the northern hemisphere and did not appear in Australia until around five million years ago. However, a recent discovery of what appears to be a placental fossil in Australia, in rocks supposedly 120 million years old, has caused evolutionists to suggest that placentals might have evolved first in the southern hemisphere, migrated north, and then become extinct in the southern continents! 17 Lions are known to have lived in Israel, but fossils of lions have not been found there. Similarly, millions of bison once roamed the USA, but very few bison fossils are found there. To argue that a particular animal must have evolved in a particular place, simply because evidence that it lived anywhere else has not (yet) been found, is not necessarily scientific.For these reasons, it is clear that the observed distributions of organisms cannot be explained simply by arguing that they evolved in the places they are now found. Consequently, evolutionists have supplemented their models of biogeography with alternative theories, such as migration across previously existing intercontinental land bridges, bird and wind transport, and transoceanic dispersal of plants and animals on floating vegetation mats.18 In some cases, it is argued that distributions that are now disjunct were once continuous, and that plants or animals of these groups became extinct in the connecting land areas. Another theory proposed to explain puzzling biogeographic observations is “convergent evolution”. According to this, different organisms evolved similar forms in different parts of the world as a result of having to adapt to similar environments. This is the explanation provided by evolutionists for the similarities between the placentals and marsupials, for example. 19In any discussion of patterns of biogeography it should be recognized that many of the theories are inevitably data-poor and, consequently, imagination-rich. The events in question all occurred many years outside of living memory and much of the evidence that might have supported any particular view may have disappeared long ago. It is perhaps significant that, in the nineteenth century, the case for an evolutionary interpretation of biogeography was based on a belief in separate, fixed continents, whereas now it is argued that the observed patterns of life support an evolutionary interpretation of biogeography based on continental drift. Perhaps the truth is closer to the view expressed by Drs Gareth Nelson and Norman Platnick of the American Museum of Natural History, who maintain, “biogeography (or geographical distribution of organisms) has not been shown to be evidence for or against evolution in any sense.”20 According to this, a recolonization of the world began immediately after the Flood, when the waters subsided .The animals, and floating vegetation, carrying seeds, insects and freshwater fish, would have settled on the emerging land. The young age models concentrate on four main processes which are understood to have influenced post-flood biogeography: transoceanic transport on vegetation mats transport by man migration and partial extinction speciation. Transoceanic transport on vegetation mats The potential for dispersal of plants and animals across large stretches of water by natural rafts has been accepted by evolutionists and creationists for many years. Professor Paul Moody of the University of Vermont argued,“In times of flood, large masses of earth and entwining vegetation, including trees, may be torn loose from the banks of rivers and swept out to sea. Sometimes such masses are encountered floating in the ocean out of sight of land, still lush and green, with palms, twenty to thirty feet [7 to 10 m] tall. It is entirely probable that land animals may be transported long distances in this manner. Mayr records that many tropical ocean currents have a speed of at least two knots; this would amount to fifty miles [80 km] a day, 1000 miles [1,600 km] in three weeks.”21
Figure 3. Oreobolus track (from the Buffalo Museum of Science New York, USA).More recently, the rafting idea has been advanced by evolutionists to explain the presence of the Bear Cuscus (Ailurops ursinus) and the Dwarf Cuscus (Strigocuscus celebensis) on the island of Sulawesi22 and of lemurs on the island of Madagascar.23 In 1995, fisherman witnessed the colonization of the island of Anguilla in the West Indies by iguanas. These were washed up on one of the island’s eastern beaches, having floated there on a mat of logs and uprooted trees, a few weeks after two hurricanes hit the islands of the Lesser Antilles. Scientists believed that the iguanas had rafted 320 km from Guadeloupe.24Significantly, biogeographers sometimes refer to oceans rather than continents as the main biogeographic regions. This is because, very often, patterns of disjunction are seen where many terrestrial organisms are distributed around the land bordering an ocean. So clear was this to the twentieth-century biogeographer Léon Croizat that he spent much time drawing “tracks” to chart repetitious occurrences of these patterns.25 Where a particular track reoccurs in respect of different organisms, in group after group, it is often referred to as a “generalized track”. The track forOreobolus plants, for example, is shown in figure 3 and is one that is shared with a multitude of other plants and animals.26 From these generalized tracks, Croizat identified five biogeographic “nodes” or “gates” of plant and animal dispersal across the world (figure 4).27
Figure 4. Correspondence of currents, gates and areas of endemism. The twenty areas of endemism identified by de Candolle are indicated by the numbers 1 to 20. The five biogeographic “gates” identified by Croizat are indicated by the letters A to E. (From Wise and Croxton, ref. 30). The destructive power of large volumes of fast-flowing water is enormous and, in the early stages of the Flood, would have been sufficient to rip up large amounts of woodland. Although some of this would have been buried in sediments, many billions of trees would have been left floating on the surface of the waters, as enormous “log mats”. 28 These islands of vegetation, regularly watered by rainfall, could have easily supported plant and animal life over significant periods of time. Ocean currents would have moved these massive “rafts” around the globe, sometimes washing them up beside land, where animals and insects might “embark” or “disembark”, and then transporting them back out to sea. The ability of ocean currents to distribute floating objects around the world was seen recently, when thousands of bathtub rubber ducks were lost off a container ship in the North Pacific in 1992. In fewer than twenty years, these had floated to Australia and South America, and subsequently into the Arctic and Atlantic oceans. 29 In support of the rafting theory, Professor Kurt Wise and Matthew Croxton point out that the intersections of ocean currents with land masses appear to correspond with de Candolle’s areas of endemism and Croizat’s biogeographic gates (figure 4). 30 It is not suggested here that land animals survived the Flood on rafts, but that rafts would have facilitated their dispersal after the Flood, as they multiplied and migrated away . Transport by man
The human race spread out over the whole of the earth.31Remarkable supporting evidence for this is found from archaeology, similarities in languages spoken by people in Europe and the Far East, and anatomical and DNA analyses. 32 It is reasonable to believe that many of these people, travelling to diverse regions, would have taken animals with them, as food for the journey and for subsequent farming on arrival at their destination.33 Migration and partial extinction Many creationists believe that an Ice Age 34 followed soon after the Flood. 35 This would have lowered sea levels, as water accumulated as ice sheets, and could have created land bridges across which animals could migrate. Most evolutionists believe that a land bridge once existed across the Bering Strait, linking Asia with America. 36 Many geologists believe that there were major tectonic upheavals following the separation of the continents,37 and land bridges that once existed in other parts of the world may have subsequently fallen below sea level. Animals could have migrated from one continent to another via these bridges, as they multiplied and spread outthe world, perhaps over hundreds of years. The speed at which animals can spread by this process is demonstrated by the rabbits of Australia. Prior to the arrival of Europeans, rabbits were unknown on this continent, but, in 1859, a colony was introduced in Southern Victoria, in the south-east. Within fifty years, this had spread all the way to the west coast. 38It is clear that major changes in climate have taken place on various continents. Mammoths, rhinoceroses, bison, horses and antelopes, for example, once lived in large numbers in Northern Siberia. The deserts of Egypt were once rich savannahs.39 Groups of animals that once thrived in certain areas could have become extinct in these places, and only those that migrated to other continents would have survived. Indeed, climate change and competition from other animals could well have driven migration. Alternatively, the absence of particular groups on particular continents can be understood to be because they never migrated or were never transported to these places and survived. Speciation Contrary to statements often made by those seeking to refute creationism, most creationists do not argue that species are fixed and cannot change. Rather, they argue strongly in support of the process of speciation. Apart from the strong scientific evidence in support of speciation, it is an essential component of the creationist explanation for the diversity of life now seen on the earth.However, that creationists do not believe that speciation can cross kinds, so a reptile would never “speciate” into a mammal, for example, nor an ape into a man.Accepting that animals and plants were made with the capacity to adapt to new environments, creationists argue that the presence of similar species or genera, in closely connected areas, can sometimes be explained by biological change. Conclusion While observations of biogeography provide strong evidence for the process of speciation, they do not support the more general predictions of evolutionary theory or the ancient-earth geologists’ model of slow, continental drift. The data, however, can be seen to fit the young age account of recolonization and diversification following the Flood. How did animals get to places such as Australia? • After the Flood, did kangaroos hop all the way to Australia? • What did koalas eat on the way? Animal distribution after the Flood There are severe limitations on our attempts to understand the hows and whys of something that happened once, was not recorded in detail, and cannot be repeated. We cannot go back in a time machine to check what happened, and our reconstructions of what the world was like immediately after the Flood will inevitably be deficient. In spite of these limitations, a yong age framework of thinking seems to make better sense of the evidence than an evolutionary model, which ignores the young age model. Clues from modern times Krakatoa, in the Indonesian archipelago, erupted in 1883 rendering the island remnant apparently lifeless. However, people visiting the island soon noted that it was being recolonized by a ‘surprising’ variety of creatures, including not only insects and earthworms, but birds, lizards, snakes, and even a few mammals. One might not have expected such an array of creatures to have crossed the ocean, but they obviously did. Even though these were mostly smaller than some of the creatures we will discuss here, it illustrates the limits of our imaginings on such things. Land bridges Evolutionists acknowledge that men and animals could once freely cross the Bering Strait, which separates Asia and the Americas.2 Before the idea of continental drift became popular, evolutionists depended entirely upon a lowering of the sea level during an ice age (which locked up water in the ice) to create land bridges, enabling dry-land passage from Europemost of the way to Australasia, for example. The existence of some deep-water stretches along the route to Australia is still consistent with this explanation. Evolutionist geologists themselves believe there have been major tectonic upheavals, accompanied by substantial rising and falling of sea-floors, in the time-period with which they associate an ice age. For instance, parts of California are believed to have been raised many thousands of feet from what was the sea floor during this ice age period, which they call ‘Pleistocene’ (one of the most recent of the supposed geological periods). Creationist geologists generally regard Pleistocene sediments as post- Flood, the period in which these major migrations took place. In the same way, other dry-land areas, including parts of these land bridges, subsided to become submerged at around the same time.3 There is a widespread, but mistaken, belief that marsupials are found only in Australia, thus supporting the idea that they ‘must have evolved there’. However, living marsupials are found also in Indonesia (the cuscus in Sulawesi), and in North and South America (opossums), and fossil marsupials have been found on every continent. Likewise, monotremes were once thought to be unique to Australia, but the discovery in 1991 of a fossil platypus tooth in South America stunned the scientific community.4 Therefore, since evolutionists believe all organisms came from a common ancestor, migration between Australia and other areas must be conceded as possible by all scientists, whether evolutionist or creationist. Creationists generally believe there was only one Ice Age after, and as a consequence of, the Flood.5 The lowered sea level at this time made it possible for animals to migrate over land bridges for centuries. Did the kangaroo hop all the way to Australia?
How did animals make the long journey from the Ararat region? Even though there have been isolated reports of individual land animalsmaking startling journeys of thousands of kilometres, such abilities are not even necessary. Early settlers released a very small number of rabbits in Australia. Wild rabbits are now found at the very opposite corner (in fact, every corner) of this vast island continent. Does that mean that an individual rabbit had to be capable of crossing the whole of Australia? Of course not. Creation speakers are sometimes asked mockingly, ‘Did the kangaroo hop all the way to Australia?’ We see by the rabbit example that this is a foolish question. Populations of animals may have had centuries to migrate, relatively slowly, over many generations. We lack information as to how animals were distributed before the Flood. Kangaroos (as is true for any other creature) may not have been on an isolated landmass. It may be asked, if creatures were migrating to Australia over a long time (a journey which would have included such places as Indonesia, presumably), then why do we not find their fossils en route in such countries? Fossilization is a rare event, requiring, as a rule, sudden burial (as in the Flood) to prevent decomposition. Lions lived in Israel until relatively recently. We don’t find lion fossils in Israel, yet this doesn’t prevent us believing the many historical reports of their former presence there. The millions of bison that once roamed the United States of America have left virtually no fossils. So why it should be a surprise that small populations, presumably under migration pressure from competitors and/or predators, and thus living in any one area for a few generations at most, should leave no fossils recording their migration? Unique organisms Another issue is why certain animals (and plants) are found in only one place. Why is species x found only in Madagascar and species y only in the Seychelles? Many times, questions on this are phrased to indicate that the questioner believes that this means species y headed only in that one direction, and never migrated anywhere else. While that is possible, it is not necessarily the case at all. All that the present situation indicates is that these are now the only places where x or y still survive. The ancestors of present-day kangaroos may have established daughter populations in several parts of the world, but most of these populations subsequently became extinct. Perhaps those marsupials only survived in Australia because they migrated there ahead of the placental mammals (we are not suggesting anything other than ‘random’ processes in choice of destination). Then after the sea level rose, the marsupials became isolated from the placentals and so were protected from competition and predation. The ability of marsupials to carry their young in pouches would facilitate faster migration than placentals that have their young at foot. Palm Valley in central Australia is host to a unique species ofpalm, Livingstonia mariae, found nowhere else in the world. Does this necessarily mean that the seeds for this species floated only to this one little spot? Not at all. Current models of post-Flood climate indicate that the world is much drier now than it was in the early post-Flood centuries. Evolutionists themselves agree that in recent times (by evolutionary standards) the Sahara was lush and green, and that central Australia had a moist, tropical climate. For all we know, the Livingstonia mariae palm may have been widespread across Australia, perhaps even in other places that are now dry, such as parts of Africa. The palm has survived in Palm Valley because there it happens to be protected from the drying out which affected the rest of its vast central Australian surrounds. Everywhere else, it died out. Incidentally, this concept of changing vegetation with changing climate should be kept in mind when considering post-Flood animal migration—especially because of the objections (and caricatures) which may be presented. For instance, how could creatures that today need a rainforest environment trudge across thousands of kilometres of parched desert on the way to where they now live? The answer is that it wasn’t desert then! The koala and other specialized types
Some problems might seem to be more challenging. For instance, there are creatures that require special conditions or a very specialized diet, such as the giant panda of China and Australia’s koala. We don’t know, of course, that bamboo shoots or blue gum leaves6 were not then flourishing all along their eventual respective migratory paths. In fact, this could have influenced the direction they took. But, in any case, there is another possibility. A need for unique or special conditions to survive may be a result of specialization, a down-hill change in some populations. That is, it may result from a loss in genetic information, from thinning out of the gene pool or by degenerative mutation. A good example is the many modern breeds of dog, selected by man (although natural conditions can do likewise), which are much less hardy in the wild than their ‘mongrel’ ancestors. For example, the St Bernard carries a mutational defect, an overactive thyroid, which means it needs to live in a cold environment to avoid overheating. This suggests that the ancestors of such creatures, were not as specialized. Thus they were hardier than their descendants, which carry only a portion of that original gene pool of information.7 In other words, the koala’s ancestors may have been able to survive on a much greater range of vegetation. Such an explanation has been made possible only with modern biological insights. Perhaps as knowledge increases other apparent difficulties will also be resolved. Such changes do not require a long time for animals under migratory pressure. The first small population that formed would tend to break up rapidly into daughter populations, going in different directions, each carrying only a portion of the gene pool of the original pair. Sometimes all of a population will eventually become extinct; sometimes all but one specialized type. Where all the sub-types survive and proliferate, we find some of the tremendous diversity seen among some groups of creatures which are apparently derived from one created kind. This explains why some very obviously related species are found far apart from each other. The sloth, a very slowmoving creature, may seem to require much more time than the model allows to make the journey from “the mountains of Ararat” to its present home. Perhaps its present condition is also explicable by a similar devolutionary process. However, to account for today’s animal distribution, evolutionists themselves have had to propose that certain primates have travelled across hundreds of miles of open ocean on huge rafts of matted vegetation torn off in storms.8 Indeed, iguanas have recently been documented travelling hundreds of kilometres in this manner between islands in the Caribbean.9 Evolutionists have even proposed that blind snakes, which they say evolved in Madagascar and India, crossed oceans by rafting to Australia, South America, and the Caribbean islands. They propose “several oceanic dispersal events, including a westward transatlantic one, unexpected for burrowing animals.”10 The model suggests a pattern of post-Flooddispersal of animals and humans that accounts for fossil distributionsof apes and humans, for example. In post-Flood deposits in Africa, ape fossils tend to be found below human fossils. Evolutionists claim that this arose because humans evolved from the apes, but there is another explanation. Animals, including apes, would have begun spreading out over the earth straight after the Flood.Human dispersal did not start until Babel, about a hundred years after the Flood. Such a delay would have meant that some ape fossils would be found consistently below human fossils, since people would have arrived in Africa after the apes.11 We may never know the exact answer to all such questions, but certainly the problems are far less formidable than they may at first appear.12 Coupled with all the, geological, and anthropological evidence for the Flood, one is justified in regarding the young age account of the animals’ dispersing from a central point as perfectly reasonable.13 Not only that, but the young age model provides an excellent framework for the scientific study of these questions. Indeed, very valuable work has been done on the distribution of plants and animals from a creation perspective.14,15 Many of the distributions are not consistent with expectations based on a deeptime evolutionary model, contrary to the claims of some high-profile popularizers of evolutionary ideas, but readily fit a post-Flood dispersal model. Natural rafts carried animals around the globe by Dominic Statham Various theories have been put forward to explain how this could have happened, some of which seem quite plausible, such as migration across land bridges, which have now fallen below sea level, and transportation by humans.Another explanation which is gaining increasing support is the rafting hypothesis.Interestingly, the potential for dispersal of plants and animals across large stretches of water by natural rafts has been accepted by evolutionists for many years. Professor Paul Moody of the University of Vermont argued, Steve Murray Iguanas colonised Anguilla in the West Indies on rafts. “In times of flood, large masses of earth and entwining vegetation, including trees, may be torn loose from the banks of rivers and swept out to sea. Sometimes such masses are encountered floating in the ocean out of sight of land, still lush and green, with palms, twenty to thirty feet [7 to 10 m] tall. It is entirely probable that land animals may be transported long distances in this manner. Mayr records that many tropical ocean currents have a speed of at least two knots; this would amount to fifty miles [80 km] a day, 1000 miles [1600 km] in three weeks.”1 More recently, the rafting idea has been advanced by evolutionists to explain the presence of the Bear Cuscus (Ailurops ursinus) and the Dwarf Cuscus (Strigocuscus celebensis) on the island of Sulawesi 2and of lemurs on the island of Madagascar.3 In 1995, fishermen witnessed the colonisation of the island of Anguilla in the West Indies by iguanas. These were
washed up on one of the island’s eastern beaches, having floated there on a mat of logs and uprooted trees, a few weeks after two hurricanes hit the islands of the Lesser Antilles. Scientists believed that the iguanas had rafted 320 km from Guadeloupe.4,5Significantly, biogeographers sometimes refer to oceans rather than continents as the main biogeographic regions. This is because, very often, patterns are seen, where many terrestrial organisms are distributed around the land bordering an ocean. So clear was this to the twentieth century biogeographer, Léon Croizat, that he spent much time drawing “tracks” to chart repetitious occurrences of these patterns. 6,7 The track for Oreobolus plants, for example, is shown in fig. 1, and it is one that is shared with a multitude of other plants and animals.8,9
Fig 1. Tracks showing occurrence of Oreobolus plants around Pacific Ocean. The destructive power of large volumes of fast-flowing water is enormous and, in the early stages of the Flood, would have been sufficient to rip-up large amounts of woodland. Although some of this would have been buried in sediments, many billions of trees would have been left floating on the surface of the waters, as enormous ‘log mats’.These islands of vegetation, regularly watered by rainfall, could have easily supported plant and animal life over significant periods of time. Ocean currents would have moved these massive ‘rafts’ around the globe, sometimes washing them up beside land, where animals and insects might ‘embark’ or ‘disembark’, and then transporting them back out to sea. I’m not suggesting that land animals survived the Flood on rafts. Rather, these rafts would have facilitated their dispersal after the Flood, as they multiplied and migrated.The ability of ocean currents to distribute floating objects around the world was seen recently, when thousands of bathtub rubber ducks were lost off a container ship in the North Pacific in 1992. In less than three months, these had floated to Indonesia, Australia and South America, and subsequently into the Arctic and Atlantic oceans.10,11 Interestingly, the patterns of plant and animal distribution throughout the world are not random, as might be expected from evolutionary theory. Instead, we often find many different species clustered in what biogeographers describe as “areas of endemism”—where many different plants and animals are concentrated in the same distinct and often small regions.Moreover, and most significantly, the areas of high plant endemism generally correspond to areas of high animal endemism.12,13 This, together with the fact that there are often many floral and faunal similarities between areas of endemism14, provides strong support for the idea that the plants and animals were transported to these places—and by the same means.Further support for the rafting theory was provided by researchers at Bryan College, Tennessee, who showed that the intersections of ocean currents with land masses appear to correspond with the areas of endemism found throughout the world.15Explaining patterns of biogeography is difficult because the events in question all occurred many years outside of living memory. Plants and animals around the world Why are they found where they are? Figure 1. The movement of the continents according to old-earth geology by Dominic Statham In March 2010, internationally renowned atheist Richard Dawkins addressed the Global Atheist Convention in Melbourne, Australia. He said, “The pattern of geographical distribution [of plants and animals] is just what you would expect if evolution had happened.”1 However, a closer look at the science of biogeography (the study of the distributions of plants and animals) reveals a very different picture to the one Professor Dawkins painted.If plants and animals had evolved over millions of years then we would expect closely related species to be living close together geographically (figure 1). In some cases this is what we do find. On the Galápagos Islands, for example, there are similar species of finches, and, on the Hawaiian Islands, similar species of fruit flies and snails.However, this distribution of animals is also what we would expect following the Flood. Birds would have dispersed from the Middle East with some eventually settling on the Galápagos Islands. Subsequent variation and natural selection among the descendants of these finches would then have occurred because they had the inbuilt genetic capacity to change quickly, so as to adapt to different environments—something that seems to be a biological design feature. The same thing would have happened with the first fruit flies and snails to reach the Hawaiian Islands (perhaps on drifting log mats). These would also have diversified as they adapted to the different conditions. Disjunct distributions However, similar plants and animals are frequently found on different continents, separated by large stretches of land or ocean. This pattern is not what you would expect if they slowly evolved over millions of years, but is consistent with the young age account and the global Flood. For example, many similar plant and animal groups are found around the land bordering
oceans. This is such a consistent pattern that migration and transportation seems a much better explanation for biogeography than evolution.2 Wikipedia: KENPEI. Clethra These widely separated populations are so common that they have been given a name—disjunct distributions.Evolutionists sometimes try to explain disjunct distributions by continental drift. They say that the continents split apart millions of years ago, and when they did, similar species of plants and animals that once lived side by side were separated (figure 1). This is the explanation given, for example, as to why chironomid midges, which are like small flies, or gnats, are found in Antarctica, Southern Australia, South America, New Zealand and South Africa. 3One problem with this explanation is that, according to evolutionary theory, many species that are disjunct across previously-joined continents evolved after their separation.4,5 For example, South America and Africa allegedly separated around 100 million years ago, but species of cactus, which supposedly evolved in South America around 30 million years ago, are also found in Africa. In the same way, the evolutionary accounts of the emergence of rodents found in South America and Africa do not fit the generally accepted timing of continental drift.6 Many other puzzling disjunctions across these continents are known, such as those of cichlid fish, which are freshwater species.7Another problem is that disjunct species are frequently found on continents that were never joined together. For example, many plants and insects are known to be disjunct across the Pacific Ocean. 8,9 The distribution of the plant genus, Clethra, shown in figure 2, is a case in point. Interestingly, the opossum, Dromiciops, found in Chile, is much closer to Australian marsupials than to other South American marsupials. 10Other biogeographic anomalies abound that do not fit the expected evolutionary pattern. For example, the animal species of central and southern Africa are closer to those of southern Asia than those of northern Africa. 11 The plants found in Madagascar are remarkably similar to those of Indonesia.12 Crowberries (Empetrum) are found only in the more northern regions of the northern hemisphere and in the most southern regions of the southern hemisphere. Figure 2. Distribution of the plant genus Clethra across the Pacific Ocean Fossil surprises Significant disjunctions are also found in the fossil record. For example, many similar plant fossils are found in western North America and eastern Asia but, according to the ancient earth geologists’ account of slow continental drift, these rocks were laid down when Alaska and Russia were still thousands of kilometres apart. 13While living marsupials14 are largely restricted to Australia and South America (opossums), their fossils from rocks classified as Late Cretaceous (supposedly between 85 and 65 million years old) are found exclusively in Europe, Asia and North America. Richard Cifelli, an associate professor in the Department of Zoology at Oklahoma University said, “this geographical switch remains unexplained.”15 Interestingly, fossil marsupials have now been found on every continent.16,17According to evolutionary theory, placental animals (such as rabbits, elephants and cats 18) evolved in the northern hemisphere and did not appear in Australia until around 5 million years ago. However, a recent discovery of what appears to be a placental fossil in Australia, in rocks supposedly 120 million years old, has caused some evolutionists to suggest that placentals might have evolved first in the southern hemisphere, migrated north, and then become extinct in the southern continents! 19So, when we look at the biogeographical distribution of plants and animals in detail, we find it is not “just what you would expect if evolution had happened”. Rather, to explain the surprising distributions that are uncovered, evolutionary scientists are constantly inventing secondary ad hoc stories.On the other hand, the distribution of plants and animals is consistent with the young age account of Earth history. According to this, the entire land-based biosphere of the original world was uprooted and destroyed in the global Flood. After the waters receded, the surviving air-breathing, land-dwelling animals slowly dispersed to where they are found today. Some of these, and other animals such as insects and snails, together with the land plants, were likely dispersed on natural rafts—massive floating log mats left over from the destruction of the world’s original forests. Research reported in Journal of Creation is consistently confirming that this as a good explanation.20 Genetics and geographical distribution Published: 14 April 2011(GMT+10) The ability of ocean currents to distribute floating objects around the world is renowned. When thousands of bathtub rubber ducks were lost off a container ship in the North Pacific in 1992, they floated to Australia and South America, and subsequently into the Arctic and Atlantic oceans. See Biogeography. Not all the feedback we receive from atheists is necessarily hostile. Matthew B. writes in with a couple of scientific questions. His messages are printed in full, followed by responses from CMI-US’s Dr. Robert Carter.
Dear Creation.com, I am impressed and pleased for your level of devotion to this website, but unfortunately do not agree with it. I shall not attempt to waste your time by trying to answer questions which you have already tried to answer on this site, but restrict my email to just two questions which I feel have not been adequately explained/rebutted. 1) Do you dispute the evidence from genetic distribution of characteristics as evidence for evolution? It is scientifically proven that certain animals/plants share certain genetic characteristics, and it is accepted that they can be arranged into a hierarchy that fits independently with the hierarchy specified and predicted by evolution. Would you care to describe the creationist perspective? (NB/ Please do not use the traditional ‘God made that hierarchy’ answer; I would prefer to know why if that is the case, and have scientific reasons given). 2) Do you dispute the evidence for evolution from the geographical distribution of life? It is accepted that the distribution of plants and animals fits with the theories of evolution and plate tectonics. Having visited the (generally recognized) best examples of this theory’s consequences in person (Madagascar and the Galapagos), I am astounded that anyone can dispute the sound logic and hard proven science surrounding this issue. Please describe the creationist ‘rebuttal’ of this argument in a way that would satisfy a biologist/geographer (as myself). I hope to hear some good sound answers to increase my respect and understanding of the creationist worldview. Please bear in mind that I am an atheist, and as such do not see the Bible as evidence in any way for the view of creationism. Good luck! My kindest regards, Matthew B. Dear Matthew, I will do my best to answer your detailed challenge. 1) Evolution predicts similarity due to common ancestry. Creation predicts similarity due to common design. Finding hierarchical relationships, therefore, proves neither. True, creation makes no specific predictions about the nature of those similarities. We would happily incorporate many scenarios into our model. But the same is true of evolutionary theory (e.g., horses and bats sharing a close genetic relationship does not topple the theory in the minds of the holders of evolutionary theory). I would suggest you familiarize yourself with Walter ReMine’s The Biotic Message. He says the message is plain for all to see: near-hierarchical relationships that defy evolutionary explanation is what we would expect from a designer. One can most easily see this in the rise of horizontal gene transfer theory that has come out in light of the many surprises found at what was expected to be the base of the tree of life.1 There are other surprises, at all levels, in fact. 2) Biogeography is a fun topic, but it is not the death-knell of creation. I, too, have been to the Galápagos, and Madagascar is on top of my list of places I want to visit next. Unlike you, I have also been to the Wallace Line (I stood on the rim of the Gunung Agung volcano on Bali, looking out as the sun rose above the peaks of Lombok, and wondered why the plants and animals on the other side of the narrow strait were so different. The answer, of course, is that during the low water stand at the height of glaciation Bali and Lombok were the extreme ends of two separate landmasses.).We have several articles that discuss biogeography on creation.com, but the best summary of the creationist position appears in an article by Dominic Statham in the latest Journal of Creation.2 Are you sure biogeography is such a great case for evolution? While it is true that there are some cases that fit the model, there are many that do not. For example, up until recently, marsupial fossils had been found on all the continents except Australia (the Australian finds were recent and indicate that conclusions about fossil distributions should be held tentatively).3 Why? If one of the defences I have read in the evolutionary literature pops into your mind, I would be less than satisfied with your answer.The Galápagos is probably the best example of the creationist position. What mechanism brought the animals there in the evolutionary model? Rafting. In his report, Captain Fitzroy even commented about the piles of trees and shrubs washed up on the southern shores of the islands in the archipelago. 4 Huge rafts made of plant material, some over a mile in diameter, form even today off the mouth of the Guayas River (Guayaquil, Ecuador). I have seen some of the smaller ones from a plane. 5 It is possible for even large animals to survive for long periods of time on such rafts. What would one predict from the Global Flood? Huge vegetation rafts with plants and animals being distributed along oceanic currents—rapidly.Summary: Plant seeds, spores, and vegetative structures were dispersed across the globe by oceanic currents during the Flood. Post-Flood climate and environment dictated which plants could survive in a given locality. Transport by rafting, wind, animals, and people added to the distribution patterns. Air-breathing animals dispersed from the Ararat region by walking, flying, and rafting, arriving at the most distant locales in relatively short order. People dispersed in a single mass wave, with many localized permutations, from the Middle East. That is what we believe and we believe there is abundant evidence for this position. Sincerely, Dr. Robert Carter Matthew wrote back: Dear Dr Carter, Thank you very much for your reply! I am pleased that there is some good reasoning behind the creationist science of your response. However, I feel that there is one point you have not adequately justified. I am not sure that your theory actually requires that there be a flood in the history of Earth. You suggest that this flood requisitely dispersed seeds, animals and vegetative rafts (as in the example of Galapagos). Why is this? Surely over both the timeframes of evolutionary theory and creation theory rafts floating across the sea are possible, and do not necessitate the help of a cataclysmic ‘biblical flood’. Although I see it as very difficult to envision the mechanics of a flood on such a scale, I can see it being rather difficult for such rafts to remain hospitable and intact following the impact of a massive body of water with great velocity and potential. On a religious note, wasn’t the flood intended to purge the Earth? Wouldn’t a deity intending to wipe out life (save Noah and co.) consider the possibility of vegetation-rafts providing a safe haven for wildlife? Anyhow, I do not see any conflict of science or ‘belief’ between evolution and creation when it comes to the dispersal of seeds etc., as the mechanisms necessary would exist (as far as I am aware– please say if I am wrong) both in a godless world and a created one (i.e. wind, the sea, rivers, animals). Returning to the matter of the Galapagos, what is the creationist explanation for the adaptations of Galapagos Giant Tortoises and their different shell shapes relating to the niches on their respective islands? Hopefully we can agree that this is natural selection at work, as the species itself has not changed. Nevertheless, are these changes not homologous and translatable to the divergence of the ancestral iguana to become the different species of the marine and land iguanas? How is this explained differently to natural selection? Regarding marsupials, I shall not pretend to be an expert in the matter! Your point, however, sounds fascinating, and I would love to study it further to provide an evolutionary based theory for you to analyse, and refine your creation-based concepts accordingly.
My other issue is that of your answer to genetic hierarchies. Firstly, if it neither proves nor disproves evolution, it cannot be taken as evidence against it. Likewise, it cannot go in favour of creation theory. Secondly, the scientific method is the pursuit of truth based upon observation. If extensive observation points towards one hypothesis, then science will pursue the formation of a theory, which is then tested and peer reviewed (as I am sure you are aware). My problem therefore, is this. If we observe a distribution of characteristics both in the current pool of characteristics of living organisms and fossilized organisms, we can study it and form a theory. If the genetic distribution reflects this also, then the theory has more evidence. This is (from what I can glean) the case with evolution, where genetic hierarchies demonstrate the expected pattern and same pattern as with physical characteristics and properties. So, as you say, genetics is not conclusive ‘proof’ (if such a thing could exist for anything) of evolution, rather a ‘non-contradiction’ that give a bit more weight to the scientific model. I hope you appreciate my attitude to the ongoing ‘evolution vs creation’ debate. I accept that certain presuppositions between scientists and YECs prevent a universal agreement from being drawn up, but a lot of scientific inaccuracies exist between the theories which can be sorted by discussion and application of good science. My best wishes (and a merry Christmas!), Matthew B. Dr. Carter responded: Dear Matthew, The massive mats of vegetation would aid dispersion after the fact, not during. The Flood was amazingly destructive, as evidenced by many facts, including the massive deposits of coal (well-sorted plant material) on regional scales. I visited Mt. St. Helens a few months ago (See After devastation … the recovery). It was my first time there and I was struck by the fact that there is still a substantial log mat floating on Spirit Lake. This was thirty years after the eruption! It is residual material like this, floating on the oceans and drifting around the earth for decades that would aid dispersal of the air-breathing animals after the Flood.Galápagos tortoises, etc.: The creationist explanation for the species on the Galápagos is similar to our explanation of world-wide patterns: a few of these animals arrived on the Galápagos (via rafting), managed to survive, grew into a population, and spread to neighboring islands via small-scale dispersal events. Each of the islands is separated by enough water to provide limited isolation for each sub-population (on a short time scale) and founder effects, genetic drift, private mutation within each sub-population, and, perhaps, a dose of natural selection6 would drive each sub-population apart. Please note that many of the ‘species’ are freely interfertile, 7 but are prevented from interbreeding by geography alone. This is even true for species living together on a single island, as the females tend to stay at high elevation. Thus, the largest island has five main volcanic peaks and five ‘species’ of giant tortoise. I suppose, so far, that this is exactly the evolutionists’ position. We differ, however, in the time required for these changes to occur, the mechanisms behind it, and the extents of possible variation. Darwin said he could see no limit to the amount of variation that natural selection could produce. We believe quite strongly that life is not designed to be infinitely mutable, that a living organism is designed to change but that too much change will ruin the complex system keeping it alive, that Darwin failed to provide a mechanism that would allow for infinite mutability, and that modern genetics has not rescued him.Are you surprised that we believe in speciation, adaptation, genetic drift, etc.? If so, I suspect you have been taught that creationists believe in the fixity of species (search creation.com for "fixity of species" to see how we deal with this). Yes, most people in Darwin’s day believed it, but they were allowing the weight of one ancient authority to trump another.Scientific method: All science has to start with a set of presuppositions. Our methodology derives from this and I believe we have a solid and consistent line of reasoning. This approach, coming straight out of the Reformation, has borne tremendous fruit over the years as most branches of science were founded by a person with this view (See the many examples in Scientists of the past who believed in a Creator). Evolutionists start with the assumption of naturalism, that natural processes explain everything that ever was, is now, and ever will be. Thus, it is not the data we are quibbling over, but an overarching theory of how to collect, interpret, and act on the data.You said, "the scientific method is the pursuit of truth based upon observation," then showed how you see confirming trends from observation, correlation between living and fossil forms, genetic relationships of living species, and peer review. I would like to point out that this set of correspondences is all interpreted in the light of naturalism and that the peer reviewers are all naturalists. Throw a creationist on that review board and there is going to be very little agreement on your list of corresponding evidences! Why is this? It is because fundamental assumptions drive everything in science. We cannot escape them as people and our science is not free from the limits of humanity. Thank you for the refreshing discussion. It is not often that we get a level-headed exchange at this level and I hope you can see that I am trying to answer as forthrightly as possible. Robert Matthew responded one last time: Robert, Thank
you
again
for
some
logical
responses.
I think that the philosophy of your response has triumphed over the science, in that you have described how presuppositions (or as they are mathematically/epistemologically known, ‘axioms’) are fundamental to both science and creationism (if you will forgive me for separating them quite so unfairly). This, in my mind, justifies your position on a fundamental level; count it as a triumph for creationism, as you have persuaded an atheist that your points are justified! However, as you probably expected me to say, I am not a creationist (please do not take the sentence above without this). The argument from axiomatic construction of theory does not put either science or creation science higher than the other. Therefore, one could conclude that whilst creationists and scientists are ‘correct’ in their stances, neither is in a position to claim the ‘better’ theory. Therefore, I still disagree with attempts to dismantle, disprove or otherwise inhibit the theory of evolution from being taught to those whose scientific worldview pertains to evolution or related branches of science. Although I do think that it is worth creationism existing in the media for people of other persuasions to build on their worldviews. As should be clear from our correspondence, our shared intention is that of building upon and embellishing the intellectual adequacy of our worldviews. However, the reason that I choose to remain studying mainstream academia with evolution, cosmology etc. is that of nonaxiomatic (that is, derived) intellectual satisfaction. That is, if you like, very much a matter of opinion. Basically, I strongly feel that the axioms of science and mainstream mathematically derived academia build a stronger more justifiable theory than creationist axioms do. I feel that the fundamental truths taken to build our current model of science are of greater intellectual value*** than those taken by creationists, such as ‘God exists’, since this cannot be materially demonstrated (as far as I can see), as explained in the attachment below.
So in summary, creationism is valid (in my opinion), but equally valid as mainstream science on an epistemological level, as they are both relying on presuppositions/axioms. However, axioms needn’t be downright admissions to having no reason to assert them, as it may be that those particular axioms are more consistent with the way in which the world is observed to function than others, they do not contradict each other and have a certain intrinsic observability in the universe. Therefore, I feel that I have an intellectual reason to support evolution with mainstream academia over creationism. Since the two theories are derived from many of the same axioms (like a b=b a) there is much that they share in common, and as such I feel that it would be a good idea if both sides of the argument reduce their worldviews to the logical ‘bare roots’ I have been describing, to provide a better degree of communication and review between the camps and hopefully aid to wash over some of the militant hatred and anger that certain members of each persuasion demonstrate. Like a two party political system, science would potentially be a lot weaker without constructive criticism and persistent questioning that which creationist organizations supply, and equally creationism has many points to improve on or repair based on new scientific knowledge based on shared presuppositions. I agree with your last comment, that our discussion is very refreshing and unusual. I don’t suppose that such levelheadedness and logic is often supplied from either creationist or evolutionist when resent or unpleasantness is introduced into the argument. I have already specified that I would not mind any of this being published in any of your magazines etc., and would like to uphold that. I feel that should you wish to publish this then you should be encouraged to. Both sides have a lot to learn from this discussion. I may be in a position to hold discussion with Prof. Richard Dawkins in January next year. If I do, I shall certainly raise many of your points. I am a keen supporter of his worldview and have read many of his books, although certainly much of the resent and annoyance he displays is neither necessary, nor beneficial. Hopefully he is open-minded enough to take on some comments. A paradigm shift in the evolution vs creation community is needed, and these logical correspondences could be along the right lines of thinking required to achieve that. Thank you very much again for your replies; you are probably the best ambassador for creationism whom I have come across. Think of me as an atheist ally to creation science-I do not agree with it, but appreciate it, understand the reasoning and do not dislike it. Kind Matthew
regards, B.
***i.e. a b = b a, is an *axiom* for real-number algebra, but has a very real and evident place in our universe, as we can demonstrate that 4 sweets plus one sweet equals the same amount as if added the other way around. This axiom or presupposition builds a very satisfactory, intrinsic theory that supports evidence in the real world. In fact, Einstein’s model of General Relativity builds upon this very axiom and other real number axioms, with certain higher algebraic axioms to build a, in my opinion, equally satisfactory model of cosmology. This reasoning spreads outwards to encompass the entirety of modern science, save some of the more radical, abstract theory such as string theory which cannot really be considered to be ‘fact’ due to lack of conceptual and material evidence. Dr. Carter’s final response: Matthew, This has been a pleasure. If you see Dr. Dawkins, please tell him that you had a pleasant exchange with a man that shares an office with Dr. Jonathan Sarfati, author of Evolution: The Greatest Hoax on Earth? This has been a very popular book among the members of the creationist community and is a strong rebuttal to Dawkins’ Evolution: the Greatest Show on Earth. Greatest Hoax has material on pre-Darwinian creationist beliefs about the NON-fixity of species, Lyell’s ideas about fixity and his "centers of creation", biogeography, homology, and the christian roots of science, all of which are pertinent to our discussion. If you really wanted to learn what we believe and why, I could not recommend this book more highly. I understand that you hesitate to accord creationism the same scientific status as evolution. Thank you for at least admitting that we are on good philosophical grounds. As a former (briefly) evolutionist, I would encourage you to examine the philosophical underpinnings of ‘mainstream’ science. When I did this, the naturalistic construct collapsed like a house of cards. This is why I used that line of argumentation in my second message. Today, I feel that creation is a much better explanation for the world around us, and we are making great strides almost daily in multiple fields. Our case is getting stronger, not weaker, as we learn more about the complexity of the genome, catastrophic geology, cosmology, speciation, climate, radiometric dating, etc., etc. How did unique fish appear in particular areas? Stephanie from the United States wrote to ask about animal migration. Her question is highlighted in green. Wikimedia commons/Alexander Vasenin Hi, I was wondering how to answer this question. How did some fish only end up in certain lakes, ponds, etc. This one actually stumped me. Of course, I’m not about to deny the intelligent designer. This is actually one question I really can’t find an answer for. Thanks so much! Love the site by the way. CMI’s Jonathan O’Brien responds: Hi Stephanie, Your question is a good one. During the Flood the marine animals such as fish would have survived in the floodwaters, although many perished due to sedimentation and other factors. Immediately after the Flood the marine creatures that survived would have been distributed around the world in the oceans and other water bodies. These would have multiplied in the areas where they found themselves and migrated to other areas from
generation to generation. There are many ways that all sorts of organisms can get into particular locations where they are uniquely found. Once there, they find a ‘niche’ for themselves and are able to adapt to that location, if necessary. This of course is not Darwinian evolution in action, just biological adaptation in which pre-existing genetic information is sorted. No new or novel genetic information is created. Many unique organisms are now only found in very particular locations because this is where it so happens they managed to survive. They may indeed have made it to some other areas, but did not survive in that location. As to how organisms travel to where they are found, there are many possibilities. Fish eggs can stick to birds’ legs. When the bird lands for a drink or to look for food, the fish eggs detach and later hatch out. I think some eggs of certain organisms, such as insects and shrimps, can even be wind-blown, especially if stuck to leaves and things like that. Other organisms were introduced to new areas either deliberately or inadvertently by man, not long after the Babel dispersion. Explorers would have soon traveled to all of the farthest-flung places of the globe, soon after the Babel event, especially after sealevels fell and land bridges were temporarily created. Man also traveled far by boat and ship, taking all sorts of animals with him. The great Flood itself would have deposited many eggs of insects and marine animals, and transported juvenile marine creatures. The retreating waters left behind detritus such as tree limbs that had been floating in the waters. Land animals can travel enormous distances by clinging to driftwood—including reptiles, amphibians and mammals. It doesn’t take long for organisms to overtake new areas, such as is seen in the cane toad invasion of northern Australia.I highly recommend The Creation Answers Book for answers to many other questions regarding the Flood, and animal migration, including the question of how salt and fresh water fish survived the Flood. This is available from the store on Creation.com and as a free download from the books section. I hope this has helped you. Jonathan O’Brien W.F. from Australia writes in response to Mummified Trees. Carbon dating can only give dates of thousands of years, not millions. Dear Sir, In your Creation magazine, 2012, was an article by Jonathan O’Brien on Mummified trees. Was carbon-14 dating done on these wood samples? Surely if they appeared to be so young, then this dating method would have given the closest date than the 12 million years which were reasoned by Joel Barker. This should be a more positive evidence. Yours sincerely, W. F. CMI’s Jonathan O’Brien responds: Dear Mr F. Thank you for your question. I couldn’t find any reference to Carbon-14 dating having been done on these wood samples. This doesn’t surprise me as the researchers believe in long ages, and already believe that the wood is 2 to 12 million years old. Carbon dating can only give dates of thousands of years, not millions. They wouldn’t expect to find any Carbon-14 after about 50,000 years, and therefore wouldn’t bother to do such tests. Andreas Tille However, doing a Carbon-14 test on the wood would be an excellent project for creationists to undertake, and I expect that there would indeed be Carbon-14 found in the timber. Carbon-14 has been found over and over again in old wood samples, and also in coal samples. Carbon-14 has also been found at detectable levels in diamonds, indicating that the diamonds are far younger than commonly believed. Carbon-14 has even been found in dinosaur bones. If a sample has Carbon-14 in it, it is good evidence that it is not millions of years old. If Carbon-14 dating was undertaken on the wood, it is possible that the dating laboratory would come up with a date older than the true age. Carbon-14 dates of material older than about 3,500 years are inaccurate because such dates cannot be calibrated against historically-verified material of known age. Even younger, historically-calibrated Carbon14 dating is known to have anomalies and is not considered to be very accurate. Standard laboratories have developed a ‘calibration curve’ for carbon-14 dating to try to overcome the obvious discrepancies. In my opinion the wood found by Joel Barker is very likely post-Flood in origin, no more than about 4,500 years old, and possibly younger. If the wood was older, and was buried in the global Flood, it would give a Carbon-14 age of something like 30,000 years based on the carbon-14 ratio in today’s atmosphere, which is the basic way scientists who calculate such ages do their calculation. They do not take the global Flood into account. During the Flood, massive amounts of organic material
were buried, permanently altering the carbon balance.1 The Creation Answers Book, Chapter 4, has further helpful information on this.
Birds of a feather don’t breed together by Carl Wieland The fascinating phenomenon known as ‘ring species’ is sometimes quite incorrectly used to ‘prove’ evolution. The classic example is as follows.In Britain, the herring gull is clearly a different species from the lesser black-backed gull. Not only can they be easily told apart, but apparently they never interbreed, even though they may inhabit the same areas. By the usual biological definition, they are therefore technically different species.However, as you go westward around the top half of the globe to North America and study the herring gull population, an interesting fact emerges. The gulls become more like black-backed gulls, and less like herring gulls, even though they can still interbreed with herring gulls from Britain.Now go still further via Alaska and then into Siberia (see map). The further west you go, the more each successive population becomes less like a herring gull and more like the black-backed.At every step along the way, each population is able to interbreed with those you studied just before you moved further west. Therefore, you are never technically dealing with separate species. Until, that is, you continue your journey into Europe and back to Britain, where you find that the lesser black-backed gulls there ‘are actually the other end of a ring that started out as herring gulls. At every stage around the ring, the birds are sufficiently similar to their neighbours to interbreed with them.’ 1 Yet when the ends of the ring meet, the two do not interbreed and so are for all intents and purposes separate species. wikipedia.org As you travel west via the route shown by the yellow band, each successive population of herring gull seems more like the black-backed gull. Evolution? It is clear from such examples that species are not fixed and unchanging, and that two apparently different species may in fact be genetically related. New species (as man defines them) can form. The herring gull and the lesser blackbacked gull could not have been initially created as two separate groups reproducing only after their kind, or else they would not be joined by a chain of interbreeding intermediates.There are also observations of other wild populations from which a reasonable person must infer that certain very similar species did indeed share the same ancestor, even though there is no complete ‘ring’.Many have been misled into thinking this is evidence for evolution and against the young age model. However, some thought reveals otherwise. The key to understanding this is to consider the vast amounts of complex information in all living things, coding for functionally useful structures and processes.Virtually all the genetic information in today’s world was present in the beginning, contained in separate populations (the original created kinds). This information would not be expected to increase, but could decrease with time—in other words, any genetic changes would be expected to be informationally downhill. Evolution (in the normal meaning of the word) implies on the other hand that a single cell has become people, pelicans and palm trees. If true, then this is an uphill process—involving a massive increase of information.2 Change—but what sort?
The formation of new species actually fits the creation model very comfortably. The wolf, the dingo and the coyote are all regarded as separate species. However, they (perhaps along with several other species) almost certainly ‘split off’ from an original pair —a species representing the surviving information of one created kind. Is there evidence that this can happen, and that it can happen without adding new information, that is, within the limits of the information already present at creation? A ‘mongrel’ dog population can be ‘split’ into separate sub-groups, the varieties of domestic dog (breeders can isolate portions of the total information into populations which do not contain some other portions of that information). This sort of variation does not add any new information. On the contrary, it is genetically downhill. It involves a reduction of the information in each of the descendant populations compared to the ancestral one. Thus, a population of pampered lap-dogs has less genetic information/variability, from which nature or man can select further changes, than the more ‘wild’ population before evolution selection took place.But is it conceivable that such change (which is obviously limited by the amount of information already present in the original kind) can extend to full, complete formation of separate species without any new information arising, without any new genes? (In other words, since evolution means lots of new, useful genes arising with time, can you have new species without any real evolution?) Even leading evolutionist Richard Dawkins, who should know better, has erroneously cited ‘ring species’ as being evidence of the supposed inevitability of evolution. In his book The Ancestor’s Tale, Dawkins observed that ring species “are only showing us in the spatial dimension something that must always happen in the time dimension.”Richard Lewontin is Alexander Agassiz Professor of Zoology at Harvard. In his book The Genetic Basis of Evolutionary Change he says there are instances in which ‘speciation and divergence of new full species’ have obviously occurred using ‘the available repertoire of genetic variants’,3 without requiring any ‘novelties by new mutation’. In other words, an ancestral species can split into other species within the limits of the information already present in that kind—just as creationists maintain must have happened.4In the example we looked at, there is no reason to believe that the differences between the two gull species are the result of any new, more complex, functional genetic information not already present in an ancestral, interbreeding gull population. Because there is no evidence of any such information-adding change, it is misleading to say this gives evidence of evolution, of even a little bit of the sort of change required to eventually turn a fish into a philosopher.Ring species and similar examples actually highlight the great variety and rich information which must have been present in the original created kinds.5 They can be said to demonstrate evolution only to the gullible (pun intended). No evidence of evolution and ‘deep time’ by Dominic Statham There are many similar plants and animals found in eastern Asia and eastern North America, but not in the regions between them (fig. 1). These include arachnids, millipedes, wasps, freshwater fish, and over 150 different seed plants.1,2 Evolutionists try to explain this by saying that, many millions of years ago, the northern regions were warmer and eastern Asia and eastern North America were part of one continuous plant and animal distribution (fig. 2). Then, they say, around five million years ago, the climate cooled and the plant and animal life were separated (fig. 1).3 Figure 1. There are many similarities between the wildlife of eastern Asia and eastern North America. Figure 2. Similar and identical species found in eastern Asia and eastern North America suggest that these two regions were once part of one continuous plant and animal distribution. Figure 3. Pogonia ophioglossoides as found in North America (left) and Pogonia japonica as found in eastern Asia (right). ©Rogier van Vugt Figure 4. Pogonia ophioglossoides (left) andPogonia japonica (right) grown side by side. Some plants and fungi found in eastern Asia and eastern North America are so similar that they are classified as being the same species. 4,5 Others have been assigned different species names but probably should not have been. For example, the Snake Mouth Orchid is named Pogonia ophioglossoides when found in eastern North America, andPogonia japonica when found in eastern Asia (fig. 3). When grown under the same conditions, however, they appear indistinguishable (fig. 4).
The Sacred Lotus (eastern Asia) and Yellow Lotus (eastern North America) are classified as two different species, Nelumbo nucifera and Nelumbo lutea (fig. 5).6 However, their hybrid form is fertile, again indicating that they are really the same species.7 The remarkable similarities between the plants and fungi of these two regions present a serious problem for evolutionists and their belief in ‘deep time’. This is because, over millions of years, sister species, living on different continents and separated by huge distances over land/ocean, would be expected to evolve different characteristics. According to the theory of evolution, the ancestors of humans separated from other ape-like creatures around six million years ago. Between then and now, the evolutionary process allegedly gave rise to all the many changes that turned these creatures into the people we are today. It is difficult for evolutionists to explain why, over the same time period, the plants and fungi of eastern Asia and eastern North America did not evolve and change too! Figure 5. Nelumbo lutea as found in North America (left) and Nelumbo nucifera as found in eastern Asia (right). Their hybrid form is fertile, indicating that they are really the same species. The similarities between the wildlife of these two regions, however, present no problem for creationists. This is because, none of the habitats found on the earth today can be very old, the time of the global Flood. It is possible that a continuous plant and animal distribution grew up linking eastern Asia and eastern North America due to the warm climate that existed at high latitudes directly after the Flood (fig. 2). This region may then have been split into two by the ensuing Ice Age and also the rising sea levels following its waning, around 800 years after the Flood.8
Figure 6. The same species of mushroomTylopilus alboater grows wild in both China and North America east of the Rocky Mountains. Figure 7. The blue milk mushroom Lactarius indigo is found in Japan and eastern North America. Credit: Dan Molter
NATURAL SELECTION Refuting Evolution A handbook for students, parents, and teachers countering the latest arguments for evolution by Jonathan Sarfati, Ph.D., F.M. Variation and natural selection versus evolution First published in Refuting Evolution, Chapter 2 This chapter contrasts the evolution and creation models, and refutes faulty understandings of both. A major point is the common practice of Teaching about Evolution and the Nature of Science to call all change in organisms ‘evolution.’ This enables Teaching about Evolution to claim that evolution is happening today. However, creationists have never disputed that organisms change; the difference is the type of change. A key difference between the two models is whether observed changes are the type to turn particles into people. Evolution Evolution, of the fish-to-philosopher type, requires that non-living chemicals organize themselves into a self-reproducing organism. All types of life are alleged to have descended, by natural, ongoing processes, from this ‘simple’ life form. For this to have worked, there must be some process which can generate the genetic information in living things today. Chapter 9 on ‘Design’ shows how encyclopedic this information is.So how do evolutionists propose that this information arose? The first self-reproducing organism would have made copies of itself. Evolution also requires that the copying is not always completely accurate—errors (mutations) occur. Any mutations which enable an organism to leave more self-reproducing offspring will be passed on through the generations. This ‘differential reproduction’ is called natural selection. In summary, evolutionists believe that the source of new genetic information is mutations sorted by natural selection—the neo-Darwinian theory. Young age model The different kinds of organisms, which reproduced after their kinds. Each of these kinds was created with a vast amount of information. There was enough variety in the information in the original creatures so their descendants could adapt to a wide variety of environments.All (sexually reproducing) organisms contain their genetic information in paired form. Each offspring inherits half its genetic information from its mother, and half from its father. So there are two genes at a given position (locus, plural loci) coding for a particular characteristic. An organism can be heterozygous at a given locus, meaning it carries different forms (alleles) of this gene. For example, one allele can code for blue eyes, while the other one can code for brown eyes; or one can code for the A blood type and the other for the B type. Sometimes two alleles have a combined effect, while at other times only one allele (called dominant) has any effect on the organism, while the other does not (recessive). With humans, both the mother’s and father’s halves have 20,687 protein-coding genes, while 97% of the rest of the DNA has an important role in coding for RNA, for control of gene expression. Overall, the information equivalent to a thousand 500-page books (3 billion base pairs, asTeaching about Evolution correctly states on page 42). The ardent neoDarwinist Francisco Ayala points out that humans today have an ‘average heterozygosity of 6.7 percent.’1 This means that for every thousand gene pairs coding for any trait, 67 of the pairs have different alleles. If we consider only the proteincoding genes, this would mean 1,340 heterozygous loci overall. Thus, any single human could produce a vast number of different possible sperm or egg cells 21,340 or 2.4 × 10403. The number of atoms in the whole known universe is ‘only’ 1080, extremely tiny by comparison. So there is no problem for creationists explaining that the original created kinds could each give rise to many different varieties. In fact, the original created kinds would have had much more heterozygosity than their modern, more specialized descendants. No wonder Ayala pointed out that most of the variation in populations arises from reshuffling of previously existing genes, not from mutations. Many varieties can arise simply by two previously hidden recessive alleles coming together. However, Ayala believes the genetic information came ultimately from mutations, not creation. His belief is contrary to information theory, as shown in chapter 9 on ‘Design’. Adaptation and natural selection Also, the once-perfect environments have deteriorated into harsher ones. Creatures adapted to these new environments, and this adaptation took the form of weeding out some genetic information. This is certainly natural selection—evolutionists don’t have a monopoly on this. In fact, a creationist, Edward Blyth, thought of the concept 25 years before Darwin’s Origin of Species was published. But unlike evolutionists, Blyth regarded it as a conservative process that would remove defective organisms, thus conserving the health of the population as a whole. Only when coupled with hypothetical informationgaining mutations could natural selection be creative.For example, the original dog/wolf kind probably had the information for a wide variety of fur lengths. The first animals probably had medium-length fur. In the simplified example illustrated below,3 a single gene pair is shown under each dog as coming in two possible forms. One form of the gene (L) carries instructions for long fur, the other (S) for short fur.In row 1, we start with medium-furred animals (LS) interbreeding. Each of the offspring of these dogs can get one of either gene from each parent to make up their two genes.In row 2, we see that the resultant offspring can have either short (SS), medium (LS) or long (LL) fur. Now imagine the climate cooling drastically (as in the Ice Age). Only those with long fur survive to give rise to the next generation (line 3). So from then on, all the dogs will be a new, long-furred variety. Note that: They are now adapted to their environment. They are now more specialized than their ancestors on row 1. This has occurred through natural selection. There have been no new genes added. In fact, genes have been lost from the population—i.e., there has been a loss of genetic information, the opposite of what microbe-to-man evolution needs in order to be credible. Now the population is less able to adapt to future environmental changes—were the climate to become hot, there is no genetic information for short fur, so the dogs would probably overheat.Another information-losing process occurs in sexually reproducing organisms—remember, each organism inherits only half the information carried by each parent. For example, consider a human couple with only one child, where the mother had the AB blood group (meaning that she has both A and B alleles) and the father had the O blood group (both alleles are O and recessive). So the child would have either AO or BO alleles, so either the A or the B allele must be missing from the child’s genetic information. Thus, the child could not have the AB blood group, but would have either the A or the B blood group respectively. 4A large population as a whole is less likely to lose established genes because there are usually many copies of the genes of both parents (for example, in their siblings and cousins). But in a small, isolated population, there is a good chance that information can be lost by random sampling. This is called genetic drift. Since new mutant genes would start off in small numbers, they are quite likely to be eliminated by genetic drift, even if they were beneficial. 5In an extreme case, where a single pregnant animal or a single pair
is isolated, e.g., by being blown or washed onto a desert island, it may lack a number of genes of the original population. So when its descendants fill the island, this new population would be different from the old one, with less information. This is called the founder effect. Loss of information through mutations, natural selection, and genetic drift can sometimes result in different small populations losing such different information that they will no longer interbreed. For example, changes in song or color might result in birds no longer recognizing a mate, so they no longer interbreed. Thus a new ‘species’ is formed. The alleged evidence for evolution in action This section will deal with some of the examples used by Teaching about Evolution, and show that they fit the creationist model better. Antibiotic and pesticide resistance Teaching about Evolution claims on pages 16–17: The continual evolution of human pathogens has come to pose one of the most serious health problems facing human societies. Many strains of bacteria have become increasingly resistant to antibiotics as natural selection has amplified resistant strains that arose through naturally occurring genetic variation.Similar episodes of rapid evolution are occurring in many different organisms. Rats have developed resistance to the poison warfarin. Many hundreds of insect species and other agricultural pests have evolved resistance to the pesticides used to combat them—even to chemical defenses genetically engineered into plants.However, what has this to do with the evolution of new kinds with new genetic information? Precisely nothing. What has happened in many cases is that some bacteria already had the genes for resistance to the antibiotics. In fact, some bacteria obtained by thawing sources which had been frozen before man developed antibiotics have shown to be antibiotic-resistant. When antibiotics are applied to a population of bacteria, those lacking resistance are killed, and any genetic information they carry is eliminated. The survivors carry less information, but they are all resistant. The same principle applies to rats and insects ‘evolving’ resistance to pesticides. Again, the resistance was already there, and creatures without resistance are eliminated.In other cases, antibiotic resistance is the result of a mutation, but in all known cases, this mutation has destroyed information. It may seem surprising that destruction of information can sometimes help. But one example is resistance to the antibiotic penicillin. Bacteria normally produce an enzyme, penicillinase, which destroys penicillin. The amount of penicillinase is controlled by a gene. There is normally enough produced to handle any penicillin encountered in the wild, but the bacterium is overwhelmed by the amount given to patients. A mutation disabling this controlling gene results in much more penicillinase being produced. This enables the bacterium to resist the antibiotic. But normally, this mutant would be less fit, as it wastes resources by producing unnecessary penicillinase.Another example of acquired antibiotic resistance is the transfer of pieces of genetic material (called plasmids) between bacteria, even between those of different species. But this is still using pre-existing information, and doesn’t explain its origin. More information on antibiotic resistance can be found in the article Superbugs Not Super after All.6 Lacewing species Another example of ‘evolution’ is given on page 17, where Teaching about Evolution states: The North American lacewing species Chrysoperla carnea and Chrysoperla downesi separated from a common ancestor species recently in evolutionary time and are very similar. But they are different in color, reflecting their different habitats, and they breed at different times of year.This statement is basically correct, but an evolutionary interpretation of this statement is not the only one possible. A creationist interpretation is that an original Chrysoperla kind was created with genes for a wide variety of colors and mating behavior. This has given rise to more specialized descendants. The specialization means that each has lost the information for certain colors and behaviors. The formation of new species (speciation) without information gain is no problem for creationists.7 Adaptation/variation within Chrysoperla, which involves no addition of complex new genetic information, says nothing about the origin of lacewings themselves, which is what evolution is supposed to explain. Darwin’s finches On page 19, Teaching about Evolution claims: A particularly interesting example of contemporary evolution involves the 13 species of finches studied by Darwin on the Galápagos Islands, now known as Darwin’s finches … . Drought diminishes supplies of easily cracked nuts but permits the survival of plants that produce larger, tougher nuts. Drought thus favors birds with strong, wide beaks that can break these tougher seeds, producing populations of birds with these traits. [Peter and Rosemary Grant of Princeton University] have estimated that if droughts occur about every 10 years on the islands, then a new species of finch might arise in only about 200 years.However, again, an original population of finches had a wide variety of beak sizes. When a drought occurs, the birds with insufficiently strong and wide beaks can’t crack the nuts, so they are eliminated, along with their genetic information. Again, no new information has arisen, so this does not support molecules-to-man evolution. Also, the rapid speciation (200 years) is good evidence for the yong age model. Critics doubt that all of today’s species could have fitted on the ark. However, the ark would have needed only about 8,000 kinds of land vertebrate animals, which would be sufficient to produce the wide variety of species we have today.8 Darwin’s finches show that it need not take very long for new species to arise.9 Breeding versus evolution On pages 37–38, Teaching about Evolution compares the artificial breeding of pigeons and dogs with evolution. However, all the breeders do is select from the information already present. For example, Chihuahuas were bred by selecting the smallest dogs to breed from over many generations. But this process eliminates the genes for large size.The opposite process would have bred Great Danes from the same ancestral dog population, by eliminating the genes for small size. So the breeding has sorted out the information mixture into separate lines. All the breeds have less information than the original dog/wolf kind.Many breeds are also the victims of hereditary conditions due to mutations, for example the ‘squashed’ snout of the bulldog and pug. But their loss of genetic information and their inherited defects mean that purebred dogs are less ‘fit’ in the wild than mongrels, and veterinarians can confirm that purebreds suffer from more diseases.Actually, breeds of dogs are interfertile, even Great Danes and Chihuahuas, so they are still the same species. Not that speciation is a problem for creationists—see the section on lacewings above. But if Great Danes and Chihuahuas were only known from the fossil record, they would probably have been classified as different species or even different genera. Indeed, without human intervention, Great Danes and Chihuahuas could probably not breed together (hybridize), so they could be considered different species in the wild. Creationists regard the breeds of dogs as showing that much variability was programmed into the original dog/wolf kind. Darwin versus a faulty creation model On pages 35–36, Teaching about Evolution discusses some of Darwin’s observations. For example, living and fossil armadillos are found only in South America. Also, animals on the Galápagos Islands are similar to those in Ecuador, while creatures on islands off Africa’s coast are related to those in Africa. The book then states:Darwin could not see how these
observations could be explained by the prevailing view of his time: that each species had been independently created, with the species that were best suited to each location being created at each particular site. Actually, this is setting up a straw man, as this is not what creationists believe, because it completely ignores the global flood. The flood wiped out all land vertebrates and would have totally re-arranged the earth’s surface. So, there’s no way that anything was created in its present location.Also, all modern land vertebrates would be descended from those which disembarked from the ark in the mountains of Ararat—over generations, they migrated to their present locations. It should therefore be no surprise to the creationists that animals on islands off Africa’s coast should be similar to those in Africa— they migrated to the islands via Africa.Darwin’s observations were thus easily explainable by the young age model. However, by Darwin’s time, most of his opponents did not believe the model, but had ‘re-interpreted’ it to fit into the old-earth beliefs of the day.A prevalent belief was a series of global floods followed by re-creations, rather than a single flood followed by migration. Darwin found observations which didn’t fit this non-creationists model. An interesting experiment by Darwin, cited by Teaching about Evolution on page 38, also supports the creation-flood model.By floating snails on salt water for prolonged periods, Darwin convinced himself that, on rare occasions, snails might have ‘floated in chunks of drifted timber across moderately wide arms of the sea.’ … Prior to Darwin, the existence of land snails and bats, but not typical terrestrial mammals, on the oceanic islands was simply noted and catalogued as a fact. It is unlikely that anyone would have thought to test the snails for their ability to survive for prolonged periods in salt water. Even if they had, such an experiment would have had little impact.Thus, Darwin helped answer a problem raised by skeptics of the young age model and its account of the flood. This also showed that some invertebrates could have survived the flood,10 possibly on rafts of pumice or tangled vegetation, or on driftwood as Darwin suggested. Other experiments by Darwin showed that garden seeds could still sprout after 42 days’ immersion in salt water, so they could have traveled 1,400 miles (2,240 km) on a typical ocean current. 11 This shows how plants could have survived—again by floating on driftwood, pumice, or vegetation rafts even if they were often soaked.Therefore, the flood-dispersion model could also have led to such experiments, despite what Teaching about Evolution implies.12 Refuting Evolution 2 A sequel to Refuting Evolution that refutes the latest arguments to support evolution (as presented by PBS and Scientific American). by Jonathan Sarfati, Ph.D. with Michael Matthews Argument: Natural selection leads to speciation Evolutionists say, ‘Natural selection has been observed to cause profound changes in populations—providing abundant evidence for speciation.’ First published in Refuting Evolution 2, Chapter 4 Galápagos finches—evolution in action? The opening episode of the PBS Evolution series makes much of the Galápagos finches—considered one of the classic evidences of ‘evolution in action.’ But PBS admits that Darwin didn’t even realize that the birds were finches and he failed to label which island they came from. All the same, he managed to acquire this information, and he eventually concluded that they had descended from mainland finches with modification just as the model would predict! He correctly realized that finch beak size was the result of adaptation to different food sources. The problem is that Darwin and the PBS series taught that this adaptation could explain the general theory of evolution (GTE). But the finch beak variation is merely the result of selection of existing genetic information, while the GTE requires new information. Also, an 18-year study by zoologist Peter Grant showed that a new species could arise in only 200 years,1which is inadvertent support for the young age model of rapid speciation.2However, another problem with using these finches is that the variation seems to be cyclic—while a drought resulted in a slight increase in beak size, the change was reversed when the rains returned. So it looks more likebuilt-in adaptability to various climatic conditions than anything to do with the GTE.PBS also discusses the change in beak length of hummingbirds, to adapt to changes in the lengths of flowers where they obtain nectar. But the same points apply—no evidence was produced that any new information is required for these changes, as opposed to selection of already-existing information. What is the creationist model? Perhaps the most frequently repeated mistake that evolutionists make in their attacks on creation is to assert that ‘natural selection’ and ‘speciation’ prove evolution and disprove the account of origins. Their bait-and-switch arguments imply that creationists believe in ‘fixity of species.’ The glossary for the PBS Evolution series Online Course for Teachers: Teaching Evolution explicitly makes this empty allegation:In creationism, species are described as ‘fixed’ in the sense that they are believed not to change their form, or appearance, through time.But no reputable creationist denies speciation—in fact, it is an important part of creationist biology. In the previous chapter, I showed that the real issue is whether evolution can explain the increase of genetic information content—enough changes to turn microbes into men, not simple change through time. Before laying to rest the evolutionists’ pointless arguments on this issue, it might be helpful to review the creationist model in detail. The ‘kinds’ are not modern species The kinds would have originallybeen distinct biological species, i.e., a population of organisms that can interbreed to produce fertile offspring but that cannot so breed with a different biological species.But creationists point out that the ‘kind’ is larger than one of today’s ‘species.’ Each of the original kinds was created with a vast amount of information. The original creatures had enough variety in their genetic information so that their descendants could adapt to a wide variety of environments.Creationists have made several deductions about the modern descendants of the original creations. They deduce, for example, that as long as two modern creatures can hybridize with true fertilization, the two creatures are descended from the same kind.3Also, if two creatures can hybridize with the same third creature, they are all members of the same kind.4 The hybridization criterion is a valid operational definition, which could in principle enable researchers to list all the kinds. The implication is one-way—hybridization is evidence that two creatures are the same kind, but it does not necessarily follow that if hybridization cannot occur then they are not members of the same kind (failure to hybridize could be due to degenerative mutations). After all, there are couples who can’t have children, and we don’t classify them as a different species, let alone a different kind.The boundaries of the ‘kind’ do not always correspond to any given man-made classification such as ‘species,’ genus, family, etc. But this is not the fault of the term ‘kind’; it is actually due to inconsistencies in the man-made classification system. That is, several organisms classified as different ‘species,’ and even different genera or higher groupings, can produce fertile offspring. This means that they are really the same species that has several varieties, hence a polytypic (many type) species. A good example is Kekaimalu the wholphin, a fertile hybrid between a male false killer whale (Pseudorca crassidens) and a female bottlenose dolphin (Tursiops truncatus), i.e., between two different so-called genera.5 There are more examples in reference 3.Biologists have identified several ways that a loss of genetic information through mutations (copying mistakes) can lead to new species—e.g., the loss of a protein’s
ability to recognize ‘imprinting’ marks, ‘jumping genes,’ natural selection, and genetic drift. When these mutations take place in small populations, they can sometimes result in sterile or nonviable offspring. Or changes in song or color might result in birds that no longer recognize a mate, so they no longer interbreed. Either way, a new ‘species’ is formed. Thus, each created kind may have been the ancestor of several present-day species.But again, it’s important to stress that speciation has nothing to do with real evolution (GTE), because it involves sorting and loss of genetic information, rather than new information. The young age model predicts rapid speciation The model would also predict rapid formation of new varieties and even species. This is because all the modern varieties of land vertebrates must have descended from comparatively few animals .In contrast, Darwin thought that this process would normally take eons. It turns out that the very evidence claimed by evolutionists to support their theory supports the young age model.Biologists have identified several instances of rapid adaptation, including guppies on Trinidad, lizards in the Bahamas, daisies on the islands of British Columbia, and house mice on Madeira. 6 Another good example is a new ‘species’ of mosquito that can’t interbreed with the parent population, arising in the London Underground train system (the ‘Tube’) in only 100 years. The rapid change has ‘astonished’ evolutionists, but should delight creationists.7 Scientific American admits as much.These days even most creationists acknowledge that microevolution has been upheld by tests in the laboratory (as in studies of cells, plants and fruit flies) and in the field (as in Grant’s studies of evolving beak shapes among Galápagos finches). [SA 80]And why should creationists deny such things? All of this so-called microevolution is part of a created and fallen world, but has never been observed to add new genetic information. In fact, the sorts of changes which are observed are the wrong type to drive the evolutionary story.8 Scientific American is forced to make a pointless claim about evidence of ‘profound’ changes:Natural selection and other mechanisms—such as chromosomal changes, symbiosis, and hybridization —can drive profound changes in populations over time. [SA 80]Again, do these profound changes increase information? No populations are seen losing information, and adapting within the constraints of the information they already have. In contrast, goo-to-you evolution requires something quite different—the progressive addition of massive amounts of genetic information that is novel not only to that population, but to the entire biosphere. Straw man 1: Natural selection can’t explain new species Scientific American falls for the same straw-man argument as PBS, failing to recognize that creationists accept new species arising within the kind. Creationists recognize how reproductive isolation can result from information loss. (See discussion above.) 11. Natural selection might explain micro-evolution, but it cannot explain the origin of new species and higher orders of life. Evolutionary biologists have written extensively about how natural selection could produce new species. For instance, in the model called allopatry, developed by Ernst Mayr of Harvard University, if a population of organisms were isolated from the rest of its species by geographical boundaries, it might be subjected to different selective pressures. Changes would accumulate in the isolated population. If those changes became so significant that the splinter group could not or routinely would not breed with the original stock, then the splinter group would be reproductively isolated and on its way toward becoming a new species. [SA 82]Indeed, creationists point out that Mayr’s allopatric model would explain the origin of the different people groups (‘races’) after the confusion of languages at Babel induced small population groups to spread out all over the earth.9 Of course, the modern people groups are notreproductively isolated and are still a single biological species. Note that the reproductive isolation is an informationally negative change, even if beneficial, because it blocks the interchange of genetic information between populations.Evolutionists brag that natural selection is the best studied of the evolutionary mechanisms, but these studies show that it has nothing to do with evolution of more complex life forms! All we observe it doing is removing information, not adding it. Scientific American suggests that there are other feasible mechanisms to explain evolution, but they do not hold up, either.Natural selection is the best studied of the evolutionary mechanisms, but biologists are open to other possibilities as well. Biologists are constantly assessing the potential of unusual genetic mechanisms for causing speciation or for producing complex features in organisms. Lynn Margulis of the University of Massachusetts at Amherst and others have persuasively argued that some cellular organelles, such as the energy-generating mitochondria, evolved through the symbiotic merger of ancient organisms. [SA 82]The endosymbiosis theory has many problems, such as the lack of evidence that prokaryotes are capable of ingesting another cell and keeping it alive, and the large differences in genes between mitochondria and prokaryotes.10 Scientific American admits that it’s open to any other mechanism to explain nature—as long as it excludes God!Thus, science welcomes the possibility of evolution resulting from forces beyond natural selection. Yet those forces must be natural; they cannot be attributed to the actions of mysterious creative intelligences whose existence, in scientific terms, is unproved. [SA 82]We have already cited more honest admissions by evolutionists Lewontin and Todd about their a priori rejection of a Designer before even examining the evidence. But evolutionary propaganda for public consumption persists in claiming that evolution is accepted purely on scientific grounds. Straw man 2: Evolutionists have seen species evolve Scientific American tries to make hay with this straw man, devoting two points to ‘proving’ natural selection and speciation. Informed creationists don’t teach against these biological processes—even though some ‘day-age’ advocates, like Hugh Ross, do.11 12. Nobody has ever seen a new species evolve. Speciation is probably fairly rare and in many cases might take centuries. [SA 82] It might take centuries, but it need not. In fact, speciation can happen much faster than most evolutionists (and ‘day-age’ advocates) realize. Creationists following the young age model expect such rapid non-evolutive speciation, as we pointed out earlier.Furthermore, recognizing a new species during a formative stage can be difficult, because biologists sometimes disagree about how best to define a species. The most widely used definition, Mayr’s Biological Species Concept, recognizes a species as a distinct community of reproductively isolated populations—sets of organisms that normally do not or cannot breed outside their community. In practice, this standard can be difficult to apply to organisms isolated by distance or terrain or to plants (and, of course, fossils do not breed). Biologists therefore usually use organisms’ physical and behavioral traits as clues to their species membership. [SA 82]We agree. It’s important to note this difficulty in defining ‘species’ whenever evolutionists claim that creationists don’t have a consistent definition of ‘kinds’ (which we do, as discussed before). We also agree with Scientific American’s recognition of recent experiments that have caused artificial speciation.Nevertheless, the scientific literature does contain reports of apparent speciation events in plants, insects, and worms. In most of these experiments, researchers subjected organisms to various types of selection for anatomical differences, mating behaviors, habitat preferences, and other traits and found that they had created populations of organisms that did not breed with outsiders. For example, William R. Rice of the University of New Mexico and George W. Salt of the University of California at Davis demonstrated that if they sorted a group of fruit flies by their preference for certain environments and bred those flies separately over 35 generations, the resulting flies would refuse to breed with
those from a very different environment. [SA 82–83]None of this is news to informed creationists. Once again, there is no new information, but sorting and loss of already existing information. Ecology proves evolution? While evolutionists claim that natural selection is the best-studied mechanism for evolution, they also must explain the reallife processes behind natural selection. Their discussion of ecology is very interesting (and factual), but it tells us nothing about GTE. Changing populations within healthy forest ecosystems For example, PBS 3 devotes a whole segment to show how a healthy forest ecosystem has a large carnivore at the top of the food chain, which can cause drastic changes in the population of the forest. It takes 100 pounds of plant to feed 10 pounds of herbivore, which in turn feed 1 pound of carnivore. So the existence of carnivores indicates the health of the supporting animals and plants. Later on in the program, Wildlife Conservation Society biologist Alan Rabinowitz claims that this healthy forest exhibits ‘evolution going on around us,’ but all he means is the replacement of one species with another. Of course, already-existing species replacing other already-existing species has nothing to do with the origin of new species with new genetic information. Once again, ‘evolution’ is a vacuous catch-all term, with any change in population numbers tossed out to the unwary listener as evidence of the goo-to-you theory. Founder effect Then the PBS program moves on to isolated habitats and the ‘founder effect.’ This is where a single breeding pair or pregnant female colonizes a new niche, and carries only a fraction of the gene pool. Therefore its descendants also contain a small fraction of the original gene pool, so the new population can be very different from the old. This also offers no comfort or support to the notion of evolution because the new population has less information than the old. Invasion—the leafy spurge Another ecological topic is biological invaders, the bane of all countries that depend on agriculture and livestock to feed their people and earn export dollars. The invaders are often more mobile and adaptive, so they out-compete native species. Modern technology has vastly increased the rate of hostile invasions, as animals stow away on ships and in the undercarriage of airplanes, although some species have been introduced deliberately. Fordham University paleoecologist David Burney investigated what happened in Hawaii when Polynesians and then Europeans introduced new species. He claimed:Evolution has now entered a new mode. Something altogether new is happening, and it has to do with what humans do to the evolutionary process. [PBS 3]Ho hum, this is just another example of replacement of one species with another, which again has nothing to do with showing how particles could have turned into people.Pioneers introduced a weed called leafy spurge into North Dakota from Russia, and it ‘threatens to kill off all native grasses.’ A cattle rancher claimed on PBS that ‘it is a cancer to the land … it makes the land just totally useless.’ Actually, the first claim is an exaggeration, and the second is a matter of perspective—sheep and goat farmers would have no problems.But the rancher said that herbicides were very expensive, so the narrator asks:… what’s left? … The solution may be another invader— discovered when scientists learned what kept leafy spurge in check in its native Russia. It’s the flea beetle—a case of fighting evolutionary fire with fire. [PBS 3]Canisters of flea beetles are dropped from airplanes, then the narrator says: So now we’re in a race most of us don’t even know we’re running—to learn as much as possible about evolution before it’s too late. [PBS 3]Huh? Using already-existing enemies of the leafy spurge requires ‘evolution’? This must be the nadir of the contentless nature of this word, even by the pathetic standards of the PBS series. Farmers have used such common-sense biological controls for centuries, well before Darwin. Interestingly, one of the classic cases of successful biological control was the defeat of Australia’s cactus invader, the prickly pear, through the introduction of the Cactoblastis organism. John Mann, the scientist responsible for saving Australia from ecological and economic ruin in this way, was heaped with accolades and honors for his feat. Mann was a convinced creationist, who was interviewed byCreation before his death.12 Symbiosis PBS 3 also describes the leaf-cutting ants of Brazil. They form colonies containing eight million insects, and they cut leaves into pieces and bring them to the nest, but they don’t eat them. Rather, other leafcutter ants mulch them and use the mulch to grow a fungus ‘garden.’ This fungus is used as food for the young leafcutters, which thus depend on the fungus for survival, but the fungus depends on the ants to provide the mulch.But this fungus garden has a ‘weed,’ a virulent mold that badly hinders the fungal growth. To combat this, some ants have a white waxy coating that is now known to be tangled mats of bacteria that produce antibiotics that kill the mold.Presumably, by this stage in the series, the producers hope that viewers are so indoctrinated in evolution that they don’t even need to try to produce evidence. To the diehard evolutionist, any phenomenon at all can be adduced as ‘evidence’ for evolution. In this case, they don’t bother to explain how such a complex symbiosis could have evolved, but merely assert that the bacteria and mold are products of an arms race lasting 50 million years. Predator–prey, driving force of evolution? While evolutionists discuss natural selection and speciation, they like to emphasize the bloodshed and violence that drives these biological changes. They see ‘Nature, red in tooth and claw,’ in the memorable phrase from the very long 1850 poem In Memoriam, A.H.H. by Alfred Lord Tennyson (1809–1892). In debates they love to pull out this as ‘knock-down’ evidence against creationists, believing it disproves the possibility of a benevolent, wise designer —following Darwin. The fact that Tennyson’s poem predated Darwin’s Origin indicates that Darwin was greatly influenced by philosophical ideas of his day.Episode 4 of the PBS Evolution series aims to show that these violent biological forces, rather than the environmental ones, drive evolution most strongly, based largely on extensive interviews with the atheistic sociobiologist Edward O. Wilson. The title of PBS 4, ‘The Evolutionary Arms Race!’ reflects the struggle between predator and prey: as a prey evolves stronger defense mechanisms, an attacker must evolve stronger mechanisms to survive, and vice versa. Of course, evolutionary biologists think there is no design behind this: the only prey that survive have chance copying mistakes in their genes that confer a strong defense, and they pass on these genes to their offspring. Faced with these stronger defense mechanisms, only those predators that happen to have mutations conferring better attacking power will be able to eat the prey, while the others starve and fail to pass on their genes.But as explained earlier, real evolution requires changes that increase genetic information, while non-information-increasing changes are part of the creation model. None of the examples presented in episode 4 prove that information has increased, so they provide no support for evolution or against creation. Poison newt PBS takes viewers to Oregon, where there were mysterious deaths of campers, but it turned out that newts were found boiled in the coffee pot. These rough-skinned newts (Taricha granulosa) secrete a deadly toxin from their skin glands so powerful that even a pinhead-sized amount can kill an adult human. They are the deadliest salamanders on earth. So scientists investigated why this newt should have such a deadly toxin.They theorized that a predator was driving this ‘evolution,’ and they found that the common garter snake (Thamnophis sirtalis) was the newt’s only predator. Most snakes will be killed by the newt’s toxin, but the common garter snake just loses muscle control for a few hours, which could of
course have serious consequences. But the newts were also driving the ‘evolution’ of the snakes—they also had various degrees of resistance to the newt toxin. Are these conclusions correct? Yes, it is probably correct that the predators and prey are driving each other’s changes, and that they are the result of mutations and natural selection. Although it might surprise the ill-informed anti-creationist that creationists accept mutations and selection, it shouldn’t be so surprising to anyone who understands the young age model .So is this proof of particles-to-people evolution? Not at all. There is no proof that the changes increase genetic information. In fact, the reverse seems to be true.The snakes with greater resistance have a cost—they move more slowly. Since PBS provided no explanation of the poison’s activity, it’s fair to propose possible scenarios to explain the phenomenon under a creation framework (it would be hypocritical for evolutionists to object, since they often produce hypothetical ‘just-so’ stories to explain what they cannot see).Suppose the newt’s poison normally reacts with a particular neurotransmitter in its victims to produce something that halts all nerve impulses, resulting in death. But if the snake had a mutation which reduced the production of this neurotransmitter, then the newt’s poison would have fewer targets to act upon. Another possibility is a mutation in the snake altering the neurotransmitter’s precise structure so that its shape no longer matches the protein. Either way, the poison would be less effective. But at the same time, either mutation would slow nerve impulses, making the snake’s muscle movement slower.So either of these would be an information loss in the snake that happens to confer an advantage. This is far from the only example. The best known is sickle-cell anemia, a common blood disorder in which a mutation causes the sufferer’s hemoglobin to form the wrong shape and fail to carry oxygen. People who carry two copies of the sickle-cell gene (homozygous) often develop fatal anemia. But this misshapen hemoglobin also resists the malaria parasite (Plasmodium). So humans who are heterozygous (have both a normal and abnormal gene) have some advantage in areas where malaria is prevalent, even though half their hemoglobin is less effective at its job of carrying oxygen. Another example is wingless beetles, which survive on windy islands because they won’t fly and be blown into the sea. 14As for the newt, likewise, increased secretion of poison can result without any new information. One possibility is an information-losingmutation that disables a gene controlling the production of the poison. Then it would be over-produced, which would be an advantage in defending against the snake, but a wasteful use of resources otherwise.There are other related examples, e.g., one way that the Staphylococcus bacteria becomes resistant to penicillin is via a mutation that disables a control gene for production of penicillinase, an enzyme that destroys penicillin. When it has this mutation, the bacterium over-produces this enzyme, which means it is resistant to huge amounts of penicillin. But in the wild, this mutant bacterium is less fit, because it squanders resources by producing unnecessary penicillinase.Another example is a cattle breed called the Belgian Blue. This is very valuable to beef farmers because it has 20–30% more muscle than average cattle, and its meat is lower in fat and very tender. Normally, muscle growth is regulated by a number of proteins, such as myostatin.However, Belgian Blues have a mutation that deactivates the myostatin gene, so the muscles grow uncontrolled and become very large. This mutation has a cost, in reduced fertility.15 A different mutation of the same gene is also responsible for the very muscular Piedmontese cattle. Genetic engineers have bred muscular mice by the same principle.In all these cases, a mutation causes information loss, even though it might be considered ‘beneficial.’ Therefore it is in the opposite direction required for particles-to-people evolution, which requires the generation of new information. Evolution of pathogens If evolutionists hope to find evidence of modern-day evolution, they have a perfect opportunity with pathogens. In just a few months, bacteria can go through hundreds of thousands of generations, equivalent to ‘millions of years’ in vertebrates. Yet in spite of this rapid change, the bacteria that we see today are essentially the same as the bacteria retrieved from the tombs of the pharaohs, and even with those discovered in salt crystals ‘dated’ millions of years old.21 HIV resistance to drugs PBS 1 claims that Darwin didn’t really see evolution in action, but now we do. Supposedly HIV, the cause of AIDS, evolves resistance to drugs faster than we can make them. Because the virus can produce billions of copies per day, it can ‘evolve’ in minutes to hours. One researcher said that this rapid change would be a ‘surprise’ if we didn’t have the concept of evolution. PBS also attempted to tug heartstrings, by portraying AIDS patients as ‘victims of evolution.’First, we see the equivocation—HIV producing HIV is supposed to show that particles could turn into people; but they’re still HIV—they haven’t changed into something else.Second, in PBS 4, it’s made clear that the related phenomenon of antibiotic resistance in bacteria took the medical community by surprise—this means that it wasn’t a prediction of evolution, except after the fact. Third, they fail to demonstrate that new information is involved, and in fact the next segment of the program showed that the opposite is true. Veronica Miller of Goethe University in Germany experimented by ceasing all antiviral drug treatments to a patient. Without the drugs, the few surviving original (‘wild’) types that had infected the patient could grow more easily. It turned out that they easily out-competed the vast numbers of resistant forms that had developed in the hospital. She said this was a risk because the wild types were also more dangerous—more efficient than the new strains that had survived the earlier drug treatments. The superior efficiency and reproductive success of the wild type implies that the other ‘evolved’ strains acquired resistance due to a loss of information somewhere.This should not be surprising, because the same is true of many examples of antibiotic resistance in bacteria. For example, some bacteria (seePoison newt, above) have an enzyme that usually has a useful purpose, but it also turns an antibiotic into a poison. That is, it’s not the antibiotic per se that’s damaging, but its chemical byproduct from the bacterium’s metabolism. So a mutation disabling this enzyme would render the antibiotic harmless. But this bacterium is still disabled, because the enzyme is now hindered, so the bacterium would be unable to compete in the wild with non-resistant ones. The information loss in both HIV and the bacterium is the opposite of what evolution requires.22 Tuberculosis and antibiotic resistance PBS describes the microbe as a ‘predator’ of humans, although ‘parasite’ would be more accurate. Mummies show that the tuberculosis bacillus (TB) affected Egyptians 4,000 years ago. The Black Death wiped out one-third of Europe’s population in 1347–1351, and the influenza pandemic of 1918–1919 killed 20 million people—more than World War 1 that had just ended.After the world wars, antibiotics were considered the ‘magic bullet,’ and there were optimistic claims even as late as 1969 that ‘infectious diseases were a thing of the past.’ But they failed to anticipate the development of resistance. This shows that bacterial resistance was hardly a ‘prediction’ of evolution, but is really a phenomenon they try to explain ‘after the fact’ as due to evolution. As will be shown, there is nothing to support molecules-to-man evolution; rather, a properly understood creation model makes good sense of the evidence.PBS 4 discussed a new strain of TB that had arisen in the overcrowded Russian prison system, containing malnourished prisoners with weakened immune systems. One inmate, ‘Sasha’ (Alexandr), had failed to complete his course of antibiotics. This meant that a few bacteria survived because they had some resistance to the antibiotic, and then proliferated once the treatment stopped. But the program itself makes it clear that the resistance was already present, so this is not evolution, although it is natural selection.These resistant bacteria are not confined to the prison, but have spread because of travel. One 19-year-old Russian student, ‘Anna,’ has a strain resistant to five antibiotics. Immunologists predict that TB could soon claim 2–3 million lives per year.But as shown, there is no proof that any antibiotic resistance is due to increased genetic information. The above example shows that the
information was already present, and I previously explained how a loss of information could confer resistance. Sometimes bacteria can pass genes to each other by exchanging plasmids, and sometimes these genes confer resistance. But of course, these examples involve no new information produced in the biosphere. Evolution of less harmful bacteria? Paul Ewald of Amherst College claimed on PBS 4 that ‘evolution’ may not only be a problem, but could also be harnessed to ‘evolve’ less harmful bacteria. If a pathogen spreads by close contact between people, then it’s in its best interest not to make people so sick that they can’t move around. But those pathogens spread by water and insects tend to be deadly.In the 1991 cholera epidemic in South America, a million people were infected, and 10,000 died. The bacterium (Vibrio cholerae) was spread by contaminated water, so ‘evolved’ high levels of toxicity. The solution was to clean the water supply, so that only healthier people could spread the germ. So the germ ‘evolved’ mildness, and many infected people didn’t even develop symptoms.But here again, there is indeed natural selection, but the result is that Vibrio cholerae turn into Vibrio cholerae! There is no proof that any new information was produced, but rather, selection of existing genetic variation.PBS 4 compared this phenomenon to breeding domestic dogs from wolves, but again this involved loss of information. Pathogens and creation Some people wonder where disease germs fit into the young age framework, if everything was created very good. The phenomenon described in the previous section can provide some insights. It clearly shows that even something usually known as a deadly germ can have a mild variant that causes no illness. Even today, Vibrio cholerae has a role in the ecosystems of brackish waters and estuaries, and the original may have had a role living symbiotically with some people. Even its toxin probably has a beneficial function in small amounts, like most poisons. The virulence arose after the Fall, by natural selection of varieties producing more and more toxin as contaminated water became more plentiful. No new information would be needed for this process. Recent evidence shows that the loss of chemotaxis—the ability to move in response to changes in chemical concentrations—will markedly increase infectivity in an infant mouse model of cholera.23Another likely example of virulence arising by information loss is the mycoplasmas, the smallest known selfreproducing organisms (parasitic bacteria with no cell walls and fewer than 1,000 genes, found in the respiratory system and urogenital tracts of humans). Loss of genetic information, e.g., for amino acid synthesis, could have resulted in the mycoplasmas becoming increasingly dependent on their hosts for survival.24 Some clues to possible benign pre-Fall roles for viruses can be gleaned from functions they have even today. Viruses are non-living entities, which function like seeds and spores, transporting genes among plants and animals. They also help keep soil fertile, keep water clean, and regulate gases in the atmosphere.25 So once again, some alleged evidence for evolution actually provides support for the creation/Fall model. Has immunity evolved? In PBS 4, Stephen O’Brien of the National Cancer Institute wondered why the big cats have ‘evolved’ resistance to a disease deadly to humans. There is a Feline Immunodeficiency Virus (FIV) that should cause AIDS-like symptoms. Supposedly the cats’ ancestors were almost wiped out by the virus, but some had resistant genes. Supposedly, the FIV evolved to mildness.More interesting was the claim that about 10 percent of humans have a ‘whopping mutation’ that confers resistance to HIV. This turns out to be the loss of certain receptors on the immune cells preventing the HIV from docking on them. Again, this change is in the opposite directionrequired to change particles into people.From mycoplasmas to big cats, from TB to poison newts, there’s not a shred of evidence that might explain the evolution of new genetic information, but the loss that we see fits nicely with young age model. Muddy Waters Clarifying the confusion about natural selection by Carl Wieland ‘Natural selection’ is often referred to as ‘survival of the fittest’ or, more recently, ‘reproduction of the fittest’. Many people are confused about it, thinking that evidence for natural selection is automatically evidence for the idea that molecules turned into microbes, which became millipedes, magnolias and managing directors. Most presentations of evolution add to the confusion by conveniently failing to point out that even according to evolutionary theory, this cannot be true; natural selection by itself makes no new things. Darwin the plagiarist? Natural selection is really a very straight-forward, commonsense insight. A creationist, the chemist/zoologist Edward Blyth (1810–1873), wrote about it in 1835–7, before Darwin, who very likely borrowed the idea from Blyth. 1 An organism may possess some inheritable trait or character which, in a given environment, gives that organism a greater chance of passing on all of its genes to the next generation (compared with those of its fellows which don’t have it). Over succeeding generations that trait or character has a good chance of becoming more widespread in that population. Such an improved chance of reproductive success (i.e. having offspring) might be obtained in several ways: A greater chance of survival. I.e. the organism is ‘more fit to survive’. This is what ‘survival of the fittest’ means, by the way; it does not necessarily refer to physical fitness as commonly understood. If you are more (or less) likely to survive, you are correspondingly more (or less) likely to have offspring, and thus to pass your genes on. For instance, genes for longer hair will improve an animal’s chances of surviving in a cold climate. Genes for white colouring will improve the camouflage of a bear in a snowy wilderness (camouflage does not just help an animal avoid being caught and eaten; it can also help a predator to sneak up on prey). By thus being more likely to avoid starvation, a lighter-coloured bear is more likely to be around to pass its lighter colouring on to the next generation. A greater chance of finding a mate. If the females of a fish species habitually prefer mates with longer tails, then male fish with genes for longer tails will have more chance of reproducing, on average, so that their genes (which include those for long tails) have more chance of getting copied. The long-tail genes (and thus the long-tail variety) will therefore become more common in that population. Any other way of enhancing reproductive success. Consider a plant species, the seeds of which are dispersed by wind. If it has genes which give its seeds a shape that confers on them slightly better aerodynamic ‘lift’ than the seeds of its fellows, then the genes for that particular trait (and thus the trait itself) will be favoured, i.e. ‘selected’ in this ‘natural’ way, hence the term. Conversely, if that plant species happens to be on a small island, seeds which travel far are going to be more likely to be ‘lost at sea’. Hence genes which give less ‘lift’ will be favoured. Presuming that genes for both shortdistance and long-distance seed air travel were available, this simple effect would ensure that all the members of an island population of such plants would eventually produce only ‘short-flight’ seeds; genes for ‘long-flight’ seeds would have been eliminated.
Adaptation In such a way, creatures can become more adapted (better suited) to the environment in which they find themselves. Say a population of plants has a mix of genes for the length of its roots. Expose that population over generations to repeated spells of very dry weather, and the plants most likely to survive are the ones which have longer roots to get down to deeper water tables. Thus, the genes for shorter roots are less likely to get passed on (see diagram above). In time, none of these plants will any longer have genes for short roots, so they will be of the ‘long root’ type. They are now better adapted to dry conditions than their forebears were. Darwin’s belief This adaptation, really a ‘fine-tuning to the environment’, was seen by Darwin to be a process which was essentially creative, and virtually without limits. If ‘new’ varieties could arise in a short time to suit their environment, then given enough time, any number of new characteristics, to the extent of totally new creatures, could appear. This was how, he believed, lungs originally arose in a lungless world, and feathers in a featherless one. Darwin did not know how heredity really works, but people today should know better. He did not know, for instance, that what is passed on in reproduction is essentially a whole lot of parcels of information (genes), or coded instructions.It cannot be stressed enough that what natural selection actually does is get rid of information. It is not capable of creating anything new, by definition. In the above example, the plants became better able to survive dry weather because of the elimination of certain genes; i.e. they lost a portion of the information which their ancestors had. The information for the longer roots was already in the parent population; natural selection caused nothing new to arise in, or be added to, the population.The price paid for adaptation, or specialization, is always the permanent loss of some of the information in that group of organisms. If the environment were changed back so that shorter roots were the only way for plants to survive, the information for these would not magically ‘reappear’; the population would no longer be able to adapt in this direction. The only way for a short-rooted variety to arise as an adaptation to the environment would be if things began once more with the ‘mixed’ or ‘mongrel’ parent population, in which both types of genes were present. Built-in limits to variation In such an information-losing process, there is automatically a limit to variation, as gene pools cannot keep on losing their information indefinitely.This can be seen in breeding, which is just another version of (in this case, artificial) selection—the principle is exactly the same as natural selection. Take horses. People have been able to breed all sorts of varieties from wild horses—big working horses, miniature toy ponies, and so on. But limits are soon reached, because selection can only work on what is already there. You can breed for horse varieties with white coats, brown coats and so forth, but no amount of breeding selection will ever generate a green-haired horse variety—the information for green hair does not exist in the horse population.Limits to variation also come about because each of the varieties of horse carries less information than the ‘wild’ type from which it descended. Common sense confirms that you cannot start with little Shetland ponies and try to select for Clydesdale draft horses—the information just isn’t there anymore! The greater the specialization (or ‘adaptation’, in this case to the demands of the human breeder, who represents the ‘environment’), the more one can be sure that the gene pool has been extensively ‘thinned out’ or depleted, and the less future variation is possible starting from such stock.These obvious, logical facts make it clear that natural selection is a far cry from the creative, ‘uphill’, limitless process imagined by Darwin (and many of today’s lay-folk, beguiled by sloppy public education).Evolutionist theoreticians know this, of course. They know that they must rely on some other process to create the required new information, because the evolution story demands it. Once upon a time, it says, there was a world of living creatures with no lungs. Then the information for lungs somehow arose, but feathers were nowhere in the world—later these arose too. But the bottom line is that natural selection, by itself, is powerless to create. It is a process of ‘culling’, of choosing between several things which must first be in existence. Natural election Charles Darwin, TFE Grafik In 1872, an attempt was made to elect Charles Darwin (left) to the prestigious Zoological Section of the French Institute, but this failed because he received only 15 out of 48 votes. A prominent member of the Academy gave the reason as follows:‘What has closed the doors of the Academy to Mr. Darwin is that the science of those of his books which have made his chief title to fame—the "Origin of Species," and still more the "Descent of Man," is not science, but a mass of assertions and absolutely gratuitous hypotheses, often evidently fallacious. This kind of publication and these theories are a bad example, which a body that respects itself cannot encourage.’ 1However, later on 5 August 1878, Darwin was elected a Corresponding Member in the Botanical Section of the same French Institute. Darwin wrote to Asa Gray as follows:‘It is rather a good joke that I should be elected in the Botanical Section, as the extent of my knowledge is little more than that a daisy is a Compositous plant and a pea is a Leguminous one.’2 How do evolutionists explain new information? Since natural selection can only cull, today’s evolutionary theorists rely on mutations (random copying mistakes in the reproductive process) to create the raw material on which natural selection can then operate. But that is a separate issue. It
has been shown convincingly that observed mutations do not add information, and that mutation is seriously hampered on theoretical grounds in this area.2 One of the world’s leading information scientists, Dr Werner Gitt from Germany’s Federal Institute of Physics and Technology in Braunschweig, says, ‘There is no known natural law through which matter can give rise to information, neither is any physical process or material phenomenon known that can do this.’ 3 His challenge to scientifically falsify this statement has remained unanswered since first published. Even those mutations which give a survival benefit are seen to be losses of information, not creating the sorely needed new material upon which natural selection can then go to work.4 (See ‘Blindingly obvious?’.) In summary: Natural selection adds no information, in fact it reduces it. Evolution requires a way to add new information. Mutations (genetic copying mistakes) must be invoked to explain how new information arose in order for natural selection to ‘guide’ the assumed evolutionary process. Mutations studied to date all appear to be losses of information—not surprising for a random process.5 It is thus quite illegitimate to use instances in which natural selection is happening (reducing the information in populations) as examples of ‘evolution happening’. Natural selection, operating on the created information in the original gene pools, makes good sense in a fallen world. It can fine-tune the way in which organisms ‘fit’ their environment, and help stave off extinction in a cursed, dying world. By ‘splitting’ a large gene pool into smaller ones, it can add to the amount of observed variety within the descendants of an original kind, just as with the many varieties of horse from one type. Even new ‘species’ can come about like that, but no new information. This helps to explain greater diversity today.Perhaps if evolution’s ‘true believers’ really had convincing evidence of a creative process, they would not feel obliged to muddy the waters so often by presenting this ‘downhill’ process (natural selection) as if it demonstrated their belief in the ultimate ‘uphill’ climb—molecules-to-man evolution. We need to tell this increasingly educated world how the facts about biological change connect to the real history of the world. Blindingly obvious? A CMI speaker visiting a cave in Australia was told by the guide about a blind shrimp which, in that lightless environment, had ‘evolved the ability not to see’. (!)Obviously, a mutation (genetic copying mistake) causing blindness in a shrimp living in the light would normally hinder its ability to survive. However, it would not be a handicap where there was no light, and as a side benefit, the shrimp would not be susceptible to eye infections like its still-seeing relatives.This slight advantage is enough to ensure that, after a few dozens of generations, all the shrimps will carry the defective gene, and thus will all be blind. They have not in fact evolved any abilities, they have lost one.A loss can be a survival advantage, but it is still a loss. The evolutionary belief demands that massive amounts of new information have arisen over time; showing how information is lost or corrupted can scarcely be said to support this belief.
Refutation of New Scientist’s Evolution: 24 myths and misconceptions Evolution v natural selection by Jonathan Sarfati Published: 5 December 2008(GMT+10) Ed. Note: this is the third instalment of a detailed critique of a major New Scientist anti-creationist diatribe (seeintroduction and index page). This one deals the widespread confusion between evolution and natural selection, actually a process discovered by creationists and an important part of the creation model. Evolution: 24 myths and misconceptions It will soon be 200 years since the birth of Charles Darwin and 150 years since the publication of On the Origin of Species , arguably the most important book ever written. In it, Darwin outlined an idea that many still find shocking – that all life on Earth, including human life, evolved through natural selection. Yet even many evolutionists admit that his book actually didn’t demonstratewhat the title indicated: the origin of species. One of Darwin’s highly qualified contemporaries, Professor Johann H. Blasius, director of the Duke’s Natural History Museum of Braunschweig (Brunswick), Germany, was highly critical: ‘I have also seldom read a scientific book which makes such wide-ranging conclusions with so few facts supporting them. … Darwin wants to show that Arten [types, kinds, species] come from other Arten. I regard this as somewhat of a highhanded hypothesis, because he argues using unproven possibilities, without even naming a single example of the origin of a particular species.’ 1 If truth be told, evolution hasn’t yielded many practical or commercial benefits. … Evolution cannot help us predict what new vaccines to manufacture because microbes evolve unpredictably. But hasn’t evolution helped guide animal and plant breeding? Not very much. Most improvement in crop plants and animals occurred long before we knew anything about evolution, and came about by people following the genetic principle of ‘like begets like’. Even now, as its practitioners admit, the field of quantitative genetics has been of little value in helping improve varieties.—Antitheistic evolutionist Jerry Coyne And despite its hyped up ‘importance’, evolution provides no practical benefit to biology—see the detailed discussion in Does science need evolution? A modern evolutionist—and ardent misotheist—Jerry Coyne, argues that evolution is important as his (atheistic) theory of ‘How did we get here?’, but had to admit:[I]f truth be told, evolution hasn’t yielded many practical or commercial benefits. Yes, bacteria evolve drug resistance, and yes, we must take countermeasures, but beyond that there is not much to say. Evolution cannot help us predict what new vaccines to manufacture because microbes evolve unpredictably. But hasn’t evolution helped guide animal and plant breeding? Not very much. Most improvement in crop plants and animals occurred long before we knew anything about evolution, and came about by people following the genetic principle of ‘like begets like’. Even now, as its practitioners admit, the field of quantitative genetics has been of little value in helping improve varieties. Future advances will almost certainly come from transgenics, which is not based on evolution at all.2And even the claim about bacteria ‘evolving’ drug resistance is overstated, because this took evolutionists by surprise when it first occurred, and the changes involved are not those that would evolve bacteria into biologists. See the discussion in Anthrax and antibiotics: Is evolution relevant?
Darwin presented compelling evidence for evolution in On the Origin and, since his time, the case has become overwhelming. Often those who declare the evidence to be ‘overwhelming’ or that ‘the debate is over’ say this to avoid debate. That’s why opposition is censored by ‘peer review‘ and opponents often demonized ordiscriminated against, as documented in the new film Expelled. As Thomas Sowell (1930– ) pointed out in another context (in his book Race and Culture about politically correct theories on race): ‘No belief can be refuted if it cannot be discussed.’ Countless fossil discoveries allow us to trace the evolution of today’s organisms from earlier forms. Yet experts point out that it’s impossible to tell from fossils whether one creature was an ancestor of another, such as the late Colin Patterson. Furthermore, the fossil record should show gradual change from one kind of creature to another, millions of times over and it does not. Evolutionist Stephen Jay Gould called the scarcity of transitional fossils the ‘ trade secret of paleontology’ (see this analysis as well asThe Links Are Missing). For example, one evolutionist admitted: ‘The oldest bat fossils, belonging to an extinct lineage, were unearthed from rocks about 54 million years old, but the creatures that they represent aren’t dramatically different from living bats, says Mark S. Springer, an evolutionary biologist at the University of California, Riverside. Hallmark features of these creatures [the ‘earliest’ fossil bats] include the elongated fingers that support the wing membranes and the extensive coiling of bony structures in the inner ears, a sign that they were capable of detecting the high-frequency chirps used in echolocation ‘Hallmark features of these creatures include the elongated fingers that support the wing membranes and the extensive coiling of bony structures in the inner ears, a sign that they were capable of detecting the high-frequency chirps used in echolocation.’3 DNA sequencing has confirmed beyond any doubt that all living creatures share a common origin. Ipse dixit (a dogmatic assertion without supporting evidence). All it can show are similarities; common origin as opposed to common design is an interpretation, and one fraught with problems. Rather, they support the biotic message theory, as proposed by Walter ReMine in The Biotic Message. That is, the evidence from nature points to a single designer, but with a pattern which thwarts evolutionary explanations because of the many similarities that cannot be explained by any theory of common ancestry—such as the incredible similarities between many marsupials and their placental counterparts (e.g. flying squirrels and flying phalangers—see Are look-alikes related?). Also, in most cultures that have ever existed, a consistent unifying pattern ‘brought honour to a designer and would also indicate his authority over and mastery of His creation.’4 Innumerable examples of evolution in action can be seen all around us, from the pollution-matching pepper moth to fastchanging viruses such as HIV and H5N1 bird flu. Is this the best they can offer? These are examples of a theory invented by the creationist, Edward Blyth, wrongly claimed as Darwin’s invention, and today is an important part of the creation model: natural selection (see also Darwin and the search for an evolutionary mechanism, which shows the historical and philosophical influences on Darwin’s ostensibly scientific theory). They have nothing to do with turning moths into motorists or viruses into vets, because the changes are in the wrong direction, i.e. removing information instead of addingit as goo-to-you evolution requires. Conflating natural selection and evolution is a staple of evolutionary propaganda. Recognizing this alone would almost be enough to see through the dogma. I’ll address these specific examples in later instalments when Le Page, the New Scientist author, cites them in more detail. Evolution is as firmly established a scientific fact as the roundness of the Earth. ‘Evolution has been observed. It’s just that it hasn’t been observed while it’s happening.’—leading misotheist Richard Dawkins The roundness of the earth can be observed (see also these articles refuting the flat earth myth); but evolution can’t be. Or in the words of Dawkins: ‘Evolution has been observed. It’s just that it hasn’t been observed while it’s happening.’5 And yet despite an ever-growing mountain of evidence, most people around the world are not taught the truth about evolution, if they are taught about it at all. That’s true: the government schools and MMM (Mendacious Mainstream Media) teach evolution as fact, which is not the truth about it! Even in the UK , the birthplace of Darwin with an educated and increasingly secular population, one recent poll suggests less than half the population accepts evolution. So, despite the huge amount of evolutionary indoctrination, the indoctrinators are unhappy that it’s not working on everyone. And this includes even deliberately misleading students as long as it convinces them that evolution is true, since they believe, ‘Education is a subversive activity that is implicitly in place in order to counter the prevailing … deeply conservative religious culture.’ For those who have never had the opportunity to find out about biology or science, claims made by those who believe in supernatural alternatives to evolutionary theory can appear convincing. Meanwhile, even among those who accept evolution, misconceptions abound. Yes, we have already encountered some propounded by Le Page, arguing that examples of an observable process (natural selection) is equivalent to proving the historical goo-to-you claim. Most of us are happy to admit that we do not understand, say, string theory in physics, True enough. Indeed, New Scientist itself has documented that even experts are confused by it,6,7 and reported the joke about why our universe is unique: it’s the only one string theory can’t explain. See also String theory unstrung. yet we are all convinced we understand evolution. In fact, as biologists are discovering, its consequences can be stranger than we ever imagined. Evolution must be the best-known yet worst-understood of all scientific theories. Then blame the propaganda pieces — like this one — that are more interested in point-scoring and word games than educating. So here is New Scientist’s guide to some of the most common myths and misconceptions about evolution. So here is New Scientist’s admission of ownership of this shoddy drivel, so they deserve all they get as a result. The gossip on the skeptics’ own websites suggested that Scientific American (SciAm) had suffered a financial downturn as a result of their ‘mistake’ in producing their anti-creationist article. A rebuttal on this site to a National Geographic anti-creationist tirade also resulted in people switching subscriptionsto what is now our Journal of Creation. There are already several good and comprehensive guides out there. But there can’t be too many. However, one of the allegedly good guides was the SciAm article that we demolished! Others were on skeptics websites, which so often prove not be at all objective and reliable. Shared misconceptions: Everything is an adaptation produced by natural selection
We tend to assume that all characteristics of plants and animals are adaptations that have arisen through natural selection. Many are neither adaptations nor the result of selection at all. The 20-nanometer motor (height), ATP synthase (one nanometer is one thousand-millionth of a metre). These rotary motors in the membranes of mitochondria (the cell’s power houses) turn in response to proton flow (a positive electric current). Rotation of the motor converts ADP molecules plus phosphate into the cell’s fuel, ATP.This is all true. But when it comes to the complex machinery of life, such asATP synthase and the DNA winding motors, natural selection is the only game in town to try to avoid the overwhelming improbability of these machines arriving by chance (that is avoiding the abundantly clear implication that a super-intelligent designer created them). Why do so many of us plonk ourselves down in front of the telly with a microwave meal after a tiring day? Because it’s convenient? Or because TV meals are ‘the natural consequence of hundreds of thousands of years of human evolution‘? Stop laughing. You’ve probably made similar assumptions. Hence our article Evolution made me do it! For just about every aspect of our bodies and behaviour, it’s easy to invent evolutionary Just So stories to explain how they came to be that way. Don’t blame the public; blame the evolutionary establishment that tolerates such Just So stories and then feed them to the public. And why the tolerance of the scientific community for Just So stories? An a prioricommitment to materialism, according to atheist genetics professor Richard Lewontin. We tend to assume that everything has a purpose, but often we are wrong. This is a criticism of prominent evolutionary ‘adaptationism’. Gould and Lewontin invented the term ‘spandrel’ for features that supposedly arose not because of any direct adaptation, but as a by-product. This comes from cathedral architecture, a spandrel being the space between a rectangular corner and an inside curve such as an arch. It is also used of the space under a staircase. In cathedrals, this arch could be filled with a richly decorated panel or stained glass, and space under stairs is often used for a cabinet. But although the spaces could be put to use, the spaces were not intended per se, but were merely a consequence of something designed for another purpose (structural strength). Since artists use spandrels as a ‘canvas’ on which to paint their decorations, Gould argued that organisms could likewise use ‘functionless’ artefacts of anatomy for some new purpose.8 Take male nipples. Male mammals clearly don’t need them: they have them because females do and because it doesn’t cost much to grow a nipple. So there has been no pressure for the sexes to evolve separate developmental pathways and ‘switch off’ nipple growth in males. We agree, except that it has nothing to do with ‘evolution’ switching or not switching as shown in Male nipples prove evolution? … Then there’s our sense of smell. Do you find the scent of roses overwhelming or do you struggle to detect it? Can you detect the distinctive odour that most people’s urine acquires after eating asparagus? People vary greatly when it comes to smell,largely due to chance mutations in the genes that code for the smell receptors rather than for adaptive reasons. Certainly. So this has nothing to do with evolution, and it could be a built-in high-mutation system that can scan a wide range of chemicals. The elaborate design of the olfactory system, likely based on the principles of vibrational spectroscopy, would make this very easy, because the mutations could cause small changes in the quantum energy levels of the receptors. The elaborate olfactory system speaks of incredible design, not evolution. Yet other features are the result of selection, but not for the trait in question. For instance, the short stature of pygmies could be a side effect of selection for early childbearing in populations where mortality is high, rather than an adaptation in itself. That’s reasonable. But once again, nothing here is incompatible with the young age model, of which variation, natural selection and speciation are important parts. Multiskilled genes Another reason why apparent adaptations can be side effects of selection for other traits is that genes can have different roles at different times of development or in different parts of the body. So selection for one variant can have all sorts of seemingly unrelated effects. This is called pleiotropy, and is a huge problem for evolution directed by natural selection. I.e. natural selection may not be able to improve one characteristic so straightforwardly without deleterious effects on other characteristics. The fact that on average each human gene codes for 4 or 5 proteins underlines the problem. One well known example of pleiotropy is one form of blindness in cave fish—see Christopher Hitchens blind to salamander reality: A well-known atheist’s eureka moment shows the desperation of evolutionists. Male homosexuality might be linked to gene variants that increase fertility in females, for instance. This presupposes a genetic basis for homosexual behaviour in the first place (see for example Homosexual animals). This will be discussed in later instalments, but meanwhile see the articles under Homosexuality: What are the biblical and scientific issues? A non-adaptive or detrimental gene variant can also spread rapidly through a population if it is on the same DNA strand as a highly beneficial variant. This is one reason why sex matters: when bits of DNA are swapped between chromosomes during sexual reproduction, good and bad variants can be split up. Indeed, there is no dispute that sexual reproduction has its advantages. But explaining how this arose in the first place is a problem for evolutionists—see Evolution of sex? Other features of plants and animals, such as the wings of ostriches, may once have been adaptations but are no longer needed for their original purpose. As we have argued in Vestigial Organs: What do they prove?: There are at least three possibilities as to why ostriches, emus, etc have wings: a) They derived from smaller birds that once could fly. This is possible in the creationist model. Loss of features is relatively easy by natural processes; acquisition of new characters, requiring new DNA information, is impossible. b) The wings have a function. Some possible functions, depending on the species of flightless bird, are: balance while running, cooling in hot weather, warmth in cold weather, protection of the rib-cage in falls, mating rituals, scaring predators (I’ve seen emus run at perceived enemies of their chicks, mouth open and wings flapping), sheltering of chicks, etc. If the wings are useless, why are the muscles functional that allow these birds to move their wings? c) It is a result of ‘design economy’. Humans use this with automobiles, for example. All models might have mounting points for air conditioning, power steering, etc. although not all have them. Likewise, all models tend to use the same wiring harness, although not all features are necessarily implemented in any one model. In using the same embryological blueprint for all birds, all birds will have wings. Such ‘vestigial traits’ can persist because they are neutral, because they have taken on another function or because there hasn’t been enough evolution to eliminate them even though they have become disadvantageous.
If they have another function, then it is compatible with being created that way. Often the ‘vestigial organ’ argument is an appeal to ignorance: we don’t know a function, therefore it has none. There are so many times when organs thought to be useless turn out to have important functions, e.g. short muscle fibres in horse legs that turn out to have a vital role in dampening vibrations, as well as the important thyroid and thymus glands. Take the appendix. There are plenty of claims that it has this or that function but the evidence is clear: you are more likely to survive without an appendix than with one. This is outdated. The appendix has long been known to be rich in lymphatic tissue, and is now thought to be a ‘safe-house’ for bacteria, to ‘reboot’ the colon flora in case of an infection that clears them out. 9 See Appendix: a bacterial safe house : New research suggests function for appendix in maintaining good digestive bacteria populations. The problem of appendicitis seems to result from a fibre-poor Western diet and perhaps even ‘another case of an overly hygienic society triggering an overreaction by the body’s immune system. Also, if this vestigial idea were true, then we would expect that more ‘primitive’ primates would have a more developed appendix, but this is not so. Rather, the appendix is more prominent in humans and gorillas. So one evolutionist researcher claimed that it gradually progressed to the current ‘fully developed organ’, so it ‘should not be regarded, in the anthropoid apes and man, as a purely degenerative structure’.10 See also More musings on our useless appendix: A not-so-recent study on the pattern of the appendix among our alleged primate cousins showed that, even using evolutionary assumptions, it cannot be a degenerate evolutionary structure. So why hasn’t it disappeared? Because evolution is a numbers game. The worldwide human population was tiny until a few thousand years ago, and people have few children with long periods between each generation. That means fewer chances for evolution to throw up mutations that would reduce the size of the appendix or eliminate it altogether — and fewer chances for those mutations to spread through populations by natural selection. Another possibility is that we are stuck in an evolutionary Catch-22 where, as the appendix shrinks, appendicitis becomes more likely, favouring its retention. Yet in this supposed numbers game, there were enough mutations to cause bipedalism and development of a large brain enabling languagedevelopment. Wisdom teeth are another vestigial remnant. A smaller, weaker jaw allowed our ancestors to grow larger brains, but left less room for molars. Yet many of us still grow teeth for which there is no room, with potentially fatal consequences. One possible reason why wisdom teeth persist is that they usually appear after people reach reproductive age, meaning selection against them is weak. This is also outdated. Wisdom teeth are rarely a problem for people, except those enjoying a modern western diet with soft, processed foods. This means less hard chewing during childhood jaw development, which causes a reduction in jaw size, and less stimulation of natural forward tooth movement in the jaw that would normally leave room for the third molar. Also, many dental surgeons caution against removal of these teeth unless they cause actual problems, not just as a preventive measure. See also Are wisdom teeth (third molars) vestiges of human evolution? For all these reasons and more, we need to be sceptical of headline-grabbing claims about evolutionary explanations for different behaviours. Evolutionary psychology in particular is notorious for attempting to explain every aspect of behaviour, from gardening to rape, as an adaptation that arose when our ancestors lived on the African savannah. Yes, see for example Rape and evolution: Evolution shows its true colours and Evolution of mankind. This cites Jerry Coyne, a strong opponent of evolutionary psychology, as saying that memes are ‘but a flashy new wrapping around a parcel of old and conventional ideas.’ … Natural selection is the only means of evolution Much change is due to random genetic drift rather than positive selection. It could be called the survival of the luckiest. Take a look in the mirror. The face you see is rather different to that of a Neanderthal. Why? The unflattering answer could be for no other reason than random genetic drift. With features that can vary somewhat in form without greatly affecting function, such as the shape of the skull, chance might play a bigger role in their evolution than natural selection. Random genetic drift happens, but it has nothing to do with explaining how some reptiles changed into birds, for example. Such random changes do not explain the origin of the complex, integrated DNA coding necessary to specify how to make new features such as feathers.Neandertals were likely post-Babel humans adapted for the post-Flood Ice Age. The DNA in all organisms is under constant attack from highly reactive chemicals and radiation , and errors are often made when it is copied. As a result, there are at least 100 new mutations in each human embryo, possibly far more. Some are harmful and are likely to be eliminated by natural selection — by death of the embryo, for instance. Most make no difference to our bodies, because most of our DNA is useless junk anyway. More outdated nonsense, and largely derived from the evolutionary assumption that we have been around for millions of years. I.e. if much of our genome were functional, such a high rate of mutation would lead to error catastrophe unless most were non-functional. However, at least 97% of our DNA is now known to be transcribed, but much of it into regulatory RNA molecules rather than proteins. See Astonishing DNA complexity uncovered and update. This is further evidence that the evolutionary timescale is false because if we had been here for millions of years we would be extinct from the damage that mutations cause. Dr John Sanford inventor of the gene gun, explains this in his new book Genetic Entropy and the mystery of the genome (see also Plant geneticist: Darwinian evolution is impossible , and his research papers published in secular journals. A future instalment will discuss ‘junk DNA’ further, but meanwhile see the articles under What about Vestigial ( junk ) DNA that evolutionists claim is a useless leftover of evolution? A few cause minor changes that are neither particularly harmful nor beneficial. You might think that largely neutral mutations would remain restricted to a few individuals. In fact, while the vast majority of neutral mutations die out, a few spread throughout a population and thus become ‘fixed’. It is pure chance — some just happen to be passed on to more and more individuals in each generation. Although the likelihood of any neutral mutation spreading by chance is tiny, the enormous number of mutations in each generation makes genetic drift a significant force. It’s a little like a lottery: the chance of winning is minuscule but because millions buy a ticket every week there is usually a winner. And this drift has a good chance of eliminating even the rare beneficial mutations. This is a big problem for the gradualistic theories of evolution: the smaller the effect of a mutation, the more likely that drift will swamp its selective advantage. See this discussion in a review of Dawkins Climbing Mount Improbable. As a result, most changes in the DNA of complex organisms over time are due to drift rather than selection, which is why biologists focus on sequences that are similar, or conserved, when they compare genomes. Natural selection will preserve sequences with vital functions, but the rest of the genome will change because of drift.
The actual evidence says the opposite. Most mutations have a small effect, so are immune from selection pressure. And genetic drift can often eliminate beneficial mutations. See diagram (right) from Dr Sanford’s book (below) Far more mutations are deleterious than advantageous. Individually, most have too small an effect to be acted upon by natural selection. Drifting through bottlenecks Genetic drift can even counteract natural selection. Many slightly beneficial mutations can be lost by chance, while mildly deleterious ones can spread and become fixed in a population. The smaller a population, the greater the role of genetic drift. This is true. But then there is a lower supply of mutations, so it will take much longer for mutations to throw up anything useful. Population bottlenecks can have the same effect. Imagine an island where most mice are plain but a few have stripes. If a volcanic eruption wipes out all of the plain mice, the island will be repopulated by striped mice. It’s a case of survival not of the fittest, but of the luckiest. And nothing to do with evolution, because the disaster merely removed some information from the gene pool by chance. Random genetic drift has certainly played a big role in human evolution. Human populations were tiny until around 10,000 years ago, and went through a major bottleneck around 2 million years ago. Other bottlenecks occurred when a few individuals migrated out of Africa around 60,000 years ago and colonised other regions. The evidence for bottlenecks is consistent with the young age model of creation (e.g. mitochondrial Eve) and the Flood. See also Out of Africa theory going out of style? There is no doubt that most of the genetic differences between humans and other apes — and between different human populations — are due to genetic drift. However, most of these mutations are in the nine-tenths of our genome that is junk, so they make no difference. The interesting question is which mutations affecting our bodies or behaviour have spread because ofdrift rather than selection, but this is far from clear. Since at least nine-tenths of our genome is known to be functional, this argument collapses. But see also Decoding the dogma of DNA similarity and Greater than 98% Chimp/human DNA similarity? Not any more: A common evolutionary argument gets reevaluated by evolutionists themselves. Natural selection leads to ever-greater complexity In fact, natural selection often leads to ever greater simplicity. And, in many cases, complexity may initially arise when selection is weak or absent. If you don’t use it, you tend to lose it. Evolution often takes away rather than adding. For instance, cave fish lose their eyes, while parasites like tapeworms lose their guts. Sure, there are many natural ways to destroy information, but evolution needs a viable, believable way to generate it. See Let the blind see Breeding blind fish with blind fish restores sight. Such simplification might be much more widespread than realised. Some apparently primitive creatures are turning out to be the descendants of more complex creatures rather than their ancestors. For instance, it appears the ancestor of brainless starfish and sea urchins had a brain. Which is compatible with the Fall which was cosmic in scope. Nevertheless, there is no doubt that evolution has produced more complex life-forms over the past four billion years. The tough question is: why? It is usually simply assumed to be the result of natural selection, but recently a few biologists studying our own bizarre and bloated genomes have challenged this idea. No doubt? Well of course there is no doubt if you are a true believer and have decided that you don’t want to believe in a universal designer; then evolution is the only game in town, by definition. See A tale of two fleas. And once again New Scientist promotes the outmoded idea that our genomes are full of junk (‘bloated’). Rather than being driven by selection, they propose that complexity initially arises when selection is weak or absent. How could this be? Suppose an animal has a gene that carries out two different functions. If mutation results in some offspring getting two copies of this gene, these offspring won’t be any fitter as a result. In fact, they might be slightly less fit due to a double dose of the gene. In a large population where the selective pressure is strong, such mutations are likely to be eliminated. In smaller populations, where selective pressure is much weaker, these mutations could spread as a result of random genetic drift (seeNatural selection is the only means of evolution) despite being slightly disadvantageous. Gene or chromosome duplication is hardly the answer. In plants, but not in animals (possibly with rare exceptions), the doubling of all the chromosomes may result in an individual which can no longer interbreed with the parent type—this is called polyploidy. Although this may technically be called a new species, because of the reproductive isolation, no new information has been produced, just repetitious doubling ofexisting information. If a malfunction in a printing press caused a book to be printed with every page doubled, it would not be more informative than the proper book. (Brave students of evolutionary professors might like to ask whether they would get extra marks for handing in two copies of the same assignment.)Duplication of a single chromosome (which contains many genes) is normally harmful, as in Down’s syndrome. Insertions are a very efficient way of completely destroying the functionality of existing genes, so if a duplicated gene is inserted randomly, it would likely cause damage to other functioning genes.The evolutionist’s ‘gene duplication idea’ is that an existing gene may be doubled, and one copy does its normal work while the other copy is non-expressed. Therefore, it is free to mutate free of selection pressure (to get rid of it). However, such ‘neutral’ mutations are powerless to produce new genuine information. Dawkins and others point out that natural selection is the only possible naturalistic explanation for the immense design in nature (not a good one, as Spetner and others have shown). Dawkins and others propose that random changes produce a new function, then this redundant gene becomes expressed somehow and is fine-tuned under the natural selective process.This ‘idea’ is just a lot of hand-waving. It relies on a chance copying event, genes somehow being switched off, randomly mutating to something approximating a new function, then being switched on again (how?) so natural selection can tune it.Furthermore, mutations do not occur in just the duplicated gene; they occur throughout the genome. Consequently, all the deleterious mutations in the rest of the genome have to be eliminated by the death of the unfit. Selective mutations in the target duplicate gene are extremely rare—it might represent only 1 part in 30,000 of the genome of an animal. The larger the genome, the bigger the problem, because the larger the genome, the lower the mutation rate that the creature can sustain without error catastrophe; as a result, it takes even longer for any mutation to occur, let alone a desirable one, in the duplicated gene. There just has not been enough time, even with mythical evolutionary time, for such a naturalistic process to account for the amount of genetic information that we see in living things. Two geneticists argue: gene duplications are aberrations of cell division processes and are more likely to cause malformation or diseases rather than selective advantage duplicated genes are usually silenced (no longer produce proteins) and subjected to degenerative mutations
regulation of supposedly duplicated gene clusters and gene families is irreducibly complex, and demands simultaneous development of fully functional multiple genes and switching networks, contrary to Darwinian gradualism.11 The more widely the duplicated genes spread in a population, the faster they will acquire mutations. A mutation in one copy might destroy its ability to carry out the first of the original gene’s two functions. Then the other copy might lose the ability to perform the second of the two functions. As before, these mutations won’t make the animals any fitter – such animals would still look and behave exactly the same – so they will not be selected for, but they could nevertheless spread by genetic drift. This is another problem for the gene duplication idea. Use your mutations In this way, a species can go from having one gene with two functions to two genes that each carry out one function. This increase in complexity occurs not because of selection but despite it. Once the genome is more complex, however, further mutations can make a creature’s body or behaviour more complex. For instance, having two separate genes means each can be switched on or off at different time or in different tissues. As soon as any beneficial mutations arise, natural selection will favour its spread. If this picture is correct, it means that there are opposing forces at the heart of evolution. Complex structures and behaviour such as eyes and language are undoubtedly the product of natural selection. Undoubtedly? Once again the philosophy of materialism reigns over rational thought and proper scepticism. Also, evolution does not explain the origin of eyes or language. But when selection is strong—as in large populations—it blocks the random genomic changes that throw up this greater complexity in the first place. Yet natural selection is the only real materialistic solution to the origin of complexity. That’s why atheists such as Dawkins defend(ed) it so strongly (see A Who’s Who of evolutionists). This idea might even explain why evolution appears to speed up after environmental catastrophes such as asteroid impacts. Such events would slash the population size of species that survive, weakening selection and increasing the chances of greater genomic complexity arising through non-adaptive processes, paving the way for greater physical or behavioural complexity to arise through adaptive processes. Sure, so lets improve the human race by exposing it to nuclear radiation, or chemical carcinogens that will speed up the mutation rate. This is the sort of fact-free story telling that the author has supposedly eschewed. Evolution produces creatures perfectly adapted to their environment You don’t have to be perfectly adapted to survive, you just have to be as well adapted as your competitors. The apparent perfection of plants and animals may be more a reflection of our poor imaginations than of reality. It’s a theme repeated endlessly in wildlife documentaries. Again and again we are told how perfectly animals are adapted to their environment. It is, however, seldom true. Take the UK ‘s red squirrel. It appeared perfectly well adapted to its environment. Until the grey squirrel arrived, that is, and proved itself rather better adapted to broadleaf forests thanks, in part, to its ability to digest acorns. Certainly there is a gradation in complexity and a variety of features that enable plants and animals to adapt to different environments. But one would not claim that the Wright brother’s first man made (but not first overall) heavier-than-air flying machine was not designed, simply because there are far more complex planes now. A future instalment will discuss alleged design flaws further. But remember that we live in a fallen world where things are no longer perfect. There are many reasons why evolution does not produce ‘designs’ that are as good as they could be. Natural selection’s only criterion is that something works, not that it works as well as it might. Botched jobs are common, in fact. The classic example is the panda’s thumb, which it uses to grasp bamboo. ‘The panda’s true thumb is committed to another role. So the panda must… settle for an enlarged wrist bone and a somewhat clumsy, but quite workable, solution,’ wrote Stephen Jay Gould in 1978. On closer inspection, however, there is nothing clumsy at all about the panda’s design. 12 Instead, the ‘thumb’ is part of an elaborate and efficient grasping structure that enables the panda to quickly strip leaves from bamboo shoots.13 Claims that the panda’s thumb is some kind of non-designed ‘contraption’ is a smokescreen to distract from the real question—that evolution simply does not explain how life could start in a pond and finish with a panda.14 As this example shows, evolution is far more likely to reshape existing structures than to throw up novel ones. The lobed fins of early fish have turned into structures as diverse as wings, fins, hoofs and hands. See illustration and discussion in The horse shows that similarities are due to creation! We have five fingers because our amphibian ancestors had five digits, not because five is necessarily the optimal number of fingers for the human hand. Yet the creatures they claim to be possible common tetrapod ancestors did not have five digits! Acanthostega had eight, while Ichthyostegahad seven. Credit Vij Sodera: One Small Step to Man (see below) Difference between reptile’s bellows lung and bird’s one-way lung. Click here to view larger image. Many groups simply never evolve features that might have made them even more successful. Sharks lack the gas bladder that allows bony fish to control their buoyancy precisely, for example, and instead have to rely on swimming, buoyant fatty livers and, occasionally, a gulp of air. Similarly, mammals’ two-way lungs are far less efficient than birds’ one-way lungs. But still good enough. On evolutionists’ dating, sharks have thrived for 300 million years without the gas bladder. One could ask why fish evolved such a thing that was clearly not necessary! And the transition from a bellows lung (as reptiles also possess) to an avian flow-through lung (see Blown away by design) has not been explained by evolutionists. One evolutionary expert in lungs explains the problem: ‘The earliest stages in the derivation of the avian abdominal airsac system from a diaphragmatic-ventilating ancestor would have necessitated selection for a diaphragmatic hernia [i.e. hole] in taxa transitional between theropods and birds. ‘Such a debilitating condition would have immediately compromised the entire pulmonary ventilatory apparatus and seems unlikely to have been of any selective advantage.’ 15 And sometimes creatures evolve features that actually reduce their overall fitness rather than increase it, such as the peacock’s tail. Vij Sodera: One Small Step to Man (see below) Hypothetical stage of evolution of bird’s lung. The complex design of the peacock tail is indeed a problem for evolutionists, especially as the sexual selection theory, which did not explain its intricate design anyway, has been disproven for this case—the very thing that Darwin invoked sexual selection to explain! See Peacock tail tale failure. Use it or lose it Continual mutation also means that if you don’t use it, you lose it. For instance, many primates cannot make vitamin C, because of a gene mutation. This mutation makes no difference to animals that get plenty of vitamin C in their diet.
However, when the environment changes, such loss of function can make a big difference, as one primate discovered on long sea voyages. This may well be true. The Creation/Fall model predicts some deterioration in design. But this doesn’t help evolution, because guinea pigs likewise are unable to produce vitamin C, but share some of the apparent degrading errors seen in the human DNA. Here is a case where theshared mistakes are not due to common ancestry. For a detailed treatment that shows that this evolutionary story fails the test see: Why the shared mutations in the Hominidae exon X GULO pseudogene are not evidence for common descent Evolution’s lack of foresight can produce inherently flawed designs. The vertebrate eye – with its back-to-front wiring and blind spot where the wiring goes through the retina – is one example. Not this boring old canard again! It would be nice if the propagandists for evolution actually researched the reason for the backwardly wired retina : the need for a blood supply behind the photoreceptors. They should also learn how the Müller glial cells act as a fibre optic plate to guide the light through the nerve network without distortion . So the vertebrate eye is superbly designed, as the eyesight of eagles testifies! … Evolution’s peak? Humans are not running fast enough. Evolving through natural selection is about time and numbers. The number of new mutations that appear, and the number of chances that natural selection has to eliminate the harmful and favour the beneficial ones, depends on the size of a population, the number of offspring each individual has and on the number of generations, among other things. We might like to think of ourselves as the most ‘highly evolved‘ species but, in terms of how many rounds of mutation and selection we’ve undergone, we are one of the least evolved species. Around 10 billion new viral particles can be produced every day in the body of a person infected with HIV. By contrast, the total human population on Earth was no more than a few million until a few thousand years ago. Indeed, Dr John Sanford (see above), shows that the known rate of harmful mutations accumulation really would have resulted in error catastrophe (i.e., extinction!) if we had really been around for millions of years 16 (see his research papers published in secular journals17,18). Furthermore, in a decade bacteria can produce 200,000 generations — about the number of generations of humans there have been since our lineage split from that of chimpanzees. So it’s hardly surprising that in less than a human lifespan we’ve seen the evolution of new diseases such as HIV and numerous antibiotic-resistant bacteria. Behe’s second book, The Edge of Evolution,19 covers the issue of beneficial mutations and the limits of Darwinian processes. As his Ph.D. research involved malaria, he applies his expertise to the malarial parasite (Plasmodium falciparum) and the mutations humans have to deal with it, and the parasite’s counter-measures to human-made drugs.One of the most effective anti-malarial drugs is chloroquine, because the parasite took longer to develop resistance to this. Behe shows that chloroquine resistance likely involves two specific mutations occurring together in the one gene. This explains why resistance to chloroquine took a long time to develop, whereas resistance to other anti-malarial drugs, which only needs one mutation, occurs within weeks. Behe works out the probability of this double mutation occurring in the same gene, using other scientists’ figures for the parasite’s population, etc.If it took so much time for a double mutation to occur in an organism that has a huge population and short life cycle (and therefore huge opportunity for all manner of mutations to occur), then how long would it take for a double mutation to occur in an organism like a human, with a long generation time and small population? Behe showed that it would never occur even with evolutionary time assumed. And this is just one double mutation in a gene. So, any adaptation that requires two specific mutations in one gene to work, will never evolve in a human, and yet such must have happened numerous times if humans arose through evolutionary processes.Behe also points out that the chloroquine-resistant parasites do worse than the non-resistant ones where there is no chloroquine. This suggests that the double mutation is informationally downhill, as usual. It seems that the reason that the parasite is resistant to chloroquine is that concentration in the parasite’s vacuole is reduced, and one mechanism is impaired uptake. According to one paper:‘Chloroquine-resistant parasite isolates consistently have an import mechanism with a lower transport activity and a reduced affinity for chloroquine.’This is the same principle that explains some antibiotic-resistant bacteria, where a mutation confers resistance by impairing a cell pump so the germ pumps in less of its would-be executioner.20 [Antibiotic resistance] is not so much an arms race as trench warfare or a scorched earth policy. Many of the changes are destroying machinery that the enemy could otherwise use. This leads to another of Behe’s major points: there is not so much an arms race as trench warfare or ascorched earth policy. Many of the changes are destroying machinery that the enemy could otherwise use. E.g. defenders will destroy their own bridges to prevent an enemy crossing, sabotage their own factories if the enemy is using them to churn out armaments, burn their own crops so the enemy will run out of food … This is why the world-class expert on sickle cell anemia, Dr Felix Konotey-Ahulu, rejects this icon of evolution .Behe further reinforced the point by citing microbiologist Barry Hall on carbapenemeantibiotics: ‘Instead of assuming that [the chief kind of enzyme that might destroy these antibiotics] will evolve rapidly, it would be highly desirable to accurately predict their evolution in response to carbapeneme selection.’21 Hall showed that most antibiotics failed, but one (‘iminepen’) did not, simply because neither single nor double point mutations would suffice, but it would require more than two simultaneous mutations. Hall wrote that this was beyond the reach of mutation + selection: ‘The results predict, with >99.9% confidence, that even under intense selection the [enzyme] will not evolve to confer resistance to imipenem.’ See also the explanations of nylon-eating bacteria, Lenski’s citrate-eating bacteria, and B-cell hypermutation, showing why these cases are irrelevant to goo-to-you evolution. Biophysicist Dr Lee Spetner in his book Not By Chance analyzes examples of mutational changes that evolutionists have claimed to have been increases in information, and shows that they are actually examples of loss of specificity, which means they involved loss of information (which is to be expected from information theory). See also this discussion, Is antibiotic resistance really due to increase in information?
DOES NATURAL SELECTION SUPPORT EVOLUTION Too dry for a fly by David Catchpoole
The rainforest fly Drosophila birchii likes living in, not surprisingly, rainforests, where the air is humid and everything is nice and moist.But Australia ’s pockets of tropical rainforest are becoming more fragmented by land clearing for roads, agriculture and urban development. Increasing penetration of drier air from outside alters the ‘microclimate’ inside the rainforest— particularly humidity. So scientists decided to test Drosophila birchii in the laboratory to see how quickly this rainforest fly would be able to adapt to a drier environment.1They exposed flies to a dessication (drying) stress until 80 to 90% had died, and then bred from the survivors. But the offspring were no better than their parents at surviving drier-than-normal conditions. With mounting surprise, the researchers repeated the process—for 30 cycles over 50 fly generations—but still no increase in dessication resistance.The astonished researchers thought something must have gone wrong with that particular batch of D. birchii flies. After all, when the lab tested other species of Drosophila from less humid environments—D. melanogaster, D. simulans and D. serrata— they saw a two- to five-fold increase in dessication resistance.Even after dry-stressing fresh batches of the flies from four separate rainforest populations, the researchers noted that ‘the most resistant population lacks the ability to evolve further resistance even after intense selection for over 30 generations’. As other evolutionists have commented, this was ‘a complete surprise’. 2 For creationists, this is a classic example of the built-in limits to genetic variation! How so? Evolutionary theory claims that life arose by a process which is ultimately creative, and virtually without limits.But the yong age account implies that virtually no new genetic information3 has arisen since the beginning . So we would expect today’s various Drosophila species to each carry less genetic variety than the original created kind from which allDrosophila flies are descended.4 Why? Because natural selection eliminates genes. It cannot create new ones.This is most noticeable in extreme environments—e.g. in dry conditions, flies that lose body moisture too quickly will die out and, without offspring, their genes will be lost from that population. But in a wet rainforest environment, there’s no advantage in conserving body moisture; what’s needed is just the opposite—the ability to withstand high humidity and the rampant diseases which thrive in such conditions. Hence Drosophila birchii populations have become highly adapted to life in the rainforest, but it has come at a cost. The price paid for such specialization is the permanent loss of genetic information useful for survival in a drier environment.In contrast, the Drosophila flies from intermediate (less humid) environments, D. melanogaster, D. simulans, and D. serrata, still contain sufficient genetic variation to enable the population to adapt to drier conditions.1,5 So, what we have here is not evolution, just natural selection. 6,7 Not a creative, limitless process, but one of culling genes already in existence. Bighorn horns not so big by David Catchpoole Trophy hunters making the pilgrimage to Canada’s Ram Mountain, Alberta, home to the world’s biggest bighorn sheep, are being increasingly disappointed. Ram Mountain has long been a magnet for sport shooters of North America’s mountain sheep,1 but rams with the large horns so highly prized by hunters are now hard to find.A world-class trophy ram is regarded as an extremely valuable commodity, with hunting permits being auctioned for very large sums. How large? One sport shooter paid over a million Canadian dollars in 1998 and 1999 for permits to hunt trophy rams in Alberta.But such is the decline in horn size of Ram Mountain’s rams, that in recent years hunters have gone home empty-handed, not having found any sheep with horns larger than the minimum regulation size.Researchers who documented the decline in horn size over the past three decades say it is “an evolutionary response to sport hunting of bighorn trophy rams” (emphasis added).2,3 They noted that ram body weight has also declined, essentially confirming earlier suspicions that selective removal of large-horned rams was reducing the overall genetic fitness of the bighorn sheep population. 4,5By killing the largest rams “of high genetic quality” before they reach their breeding peak, the hunters have depleted the genes for big horns and fast growth. These “undesirable evolutionary consequences” of trophy hunting “will be extremely difficult to reverse”, say the researchers (emphasis added).2 It’s not evolution! To the extent that the researchers have observed that selective culling of large-horned rams at Ram Mountain has diminished the size of rams and their horns, with concomitant reduction in variety in the gene pool and a deterioration in the population’s “genetic fitness”, the researchers are correct. But these changes are not an “evolutionary response” or “evolutionary consequence” as they have nothing to do with evolution. Evolution—the supposedly information-gaining process by which, over millions of years, some primeval soupy ‘seep’ became sheep—is nowhere in evidence here.Instead, Ram Mountain’s bighorn sheep population has lost genetic information, not gained it. Note the researchers’ own admission that “such changes will be extremely difficult to reverse”. Indeed, despite the recent dropoff in hunting (because hunters could not find rams with horns larger than the minimum legal size), “horn size has not recovered”. 3 This strongly parallels the “crash” of the cod fishery off the Canadian coast, where cod have failed to return to their former size despite the Canadian government’s closure of the fishery in 1992 in order to let it recover. 6 It seems that once the genes for large size are lost, they’re gone forever.7Hunting seems to have had similar impacts upon moose, too, which now have smaller antlers than was the case just a few decades ago. And selective ivory poaching is thought to be the cause of a dramatically increased frequency of tuskless elephants in many African populations.Note that in all these instances the selection pressure is essentially an artificially-imposed version of ‘natural selection’. Neither such ‘artificial’ nor ‘natural’ selection is in any way ‘evolution’ as it can only favour certain genes over others, it cannot generate any new genetic information. Rather, selection (whether artificial or natural) can only operate on (i.e. cull out) genetic information that already exists.8 And that’s exactly what’s been happening on Ram Mountain.
Defining terms Evolutionist Dr John Endler’s refreshing clarity about ‘natural selection’ has been largely ignored by David Catchpoole Illustrated by Caleb Salisbury Dr John Endler, an evolutionist, is certainly no slouch in the academic stakes. Born in Canada, Endler has a PhD from Scotland’s Edinburgh University and subsequent research and professorial experience at the University of California, USA, as well as Australia’s James Cook University and Deakin University, and England’s University of Exeter. In 2007 he was elected as a Fellow of the American Academy of Arts and Sciences. In 2008 the European Research Council announced that he was among the first cohort of Life Scientists to receive an award under its Advanced Grants scheme. His fellow evolutionists are happy to cite Endler’s research work on natural selection and adaptation in guppies but have all but ignored key observations in his definitive 1986 book, Natural Selection in the Wild. Many times we have pointed out,1 in relation to natural selection and evolution, that: Natural selection is a fact—it was recognized by creationists before Darwin, as it is by informed creationists today.2 Natural selection favours certain already-existing genetic traits in populations by culling genes out of the gene pool;3,4,5 thus it helpsadaptation of a population to its environment.6,7 (Sometimes the new population is given a new species name— adaptation and speciation are accepted by informed creationists.)8,9 Natural selection by itself generates no new genetic information. So any adaptations that are purely the result of natural selection acting on pre-existing genetic information are not changes in the right direction to drive particles-to-people evolution.10 So, natural selection is not the same thing as evolution!11,12,13However, proponents of evolution repeatedly cite examples of natural selection—examples in which populations lose genetic information—as evidence of microbes-toman evolution (which would require an increase in genetic information). This is clearly unjustified.The evolutionists’ vague and ambiguous definition of terms facilitates thatbait-and-switch tactic, so often employed by Richard Dawkins.14In theory, evolutionists look to mutations as being the process responsible for generating the new genetic information evolution requires, which is then sorted by natural selection. But in practice, does that really happen? 15When pressed to give specific evidence of mutations that increase the information in the genome, Dawkins and his cohorts cannot give coherent answers.16 They ought to be able to point to hundreds of examples of such mutations by now. But they can’t. There is at best a tiny handful—one or two to our current knowledge—which could represent a modicum of information increase, and the lead candidate, the ability of a bacterium to digest the man-made substance nylon, involves considerable doubt.17 ‘The term “natural selection” means different things to different people, and this often leads to confusion’—John Endler,Natural Selection in the Wild, 1986 Only a very few evolutionists have been upfront about this. However, they have been largely ignored. Our attention was recently drawn (see Box) to one such evolutionist, Dr John Endler, whose 1986 book Natural Selection in the Wild18spelt out the problem clearly.Endler’s book may have been ignored, but Endler and his research papers have not. E.g., Richard Dawkins happily cites Endler’s famous research on natural selection and adaptation in guppies—but this is a classic example of the bait-and-switch ruse we have so often warned about. 19,20In Natural Selection in the Wild, Endler beautifully identifies the inherent confusion about the key terms which we would say enables Dawkins and other outspoken evolutionists to so often go publicly unchallenged (page xii):“A major problem in this subject is that there is a multiplicity of meanings for the same terms, and the same terms mean different things to different people.”And Endler makes it clear (p. 8) that the confusion is not just at a public layman level, but also in the scientific community and their technical publications: “The term ‘natural selection’ means different things to different people, and this often leads to confusion in the literature.” ‘Natural selection does not explain the origin of new variants, only the process of changes in their frequency’—John Endler,Natural Selection in the Wild, 1986 The gist of the problem (just as we point out repeatedly) is that people wrongly use ‘natural selection’ and ‘evolution’ interchangeably, and Endler specifically (p. 8) warns against this:“Natural selection must not be equated with evolution, though the two are intimately related.”Note that Endler is no creationist, as is clear from his pro-evolution commentary throughout. But on p. 245, where he toes the evolutionary line that natural selection is a key component of the microbes-toman process, he also candidly admits that natural selection is insufficient by itself to explain how pond scum became people:“Natural selection is common enough in natural populations to have been detected in a wide variety of organisms, and strong selection is not as rare as has been previously assumed; natural selection is therefore likely to be important in evolution. However, natural selection does not explain the origin of new variants, only the process of changes in their frequency.” (Emphasis added.)Many times Endler is upfront about this difficulty, i.e. that those who use the term “evolution” cannot sidestep the problem of the origin of the genetic variation; how the variants came into existence in the first place. On page 5, he thus defines evolution:“Evolution may be defined as any net directional change or any cumulative change in the characteristics of organisms or populations over many generations … It explicitly includes the origin as well as the spread of alleles, variants, trait values or character states.”The ambiguity of the terms, however, means that many do indeed sidestep the issue (p. 14):“To put this usage into a broader perspective, those who restrict ‘natural selection’ to phenotypic selection also call natural selection, as defined in this book, ‘evolution’; those who are more careful call it ‘evolution by natural selection.’ But evolution is more than merely a change in trait distributions or allele frequencies; it also includes the origin of the variation. ” (Emphasis added—note that ‘alleles’ are alternative forms of the same gene, e.g. a gene for hair may have versions that code for long or short hair respectively.)And some not only blithely avoid the challenge, but deliberately seek to redefine the terms in order to define the origins problem out of their sphere of operation (p. 7):“Population geneticists use a different definition of evolution: a change in allele frequencies among generations. This meaning is quite different from the original; it now includes random as well as directional changes, but it does not require the origin of new forms.”In other words, whether the change goes uphill, or downhill, or just back-and-forth aimlessly, it is all still called ‘evolution’ by population geneticists. Endler goes on:“Unfortunately, the use of the population genetics definition often results in an overemphasis on changes in allele frequencies and an underemphasis on (or no consideration of) the origin of the different alleles and their properties. Both are important in evolution.”Note his insightful analysis that defining the terms in that manner results in “ … an underemphasis on (or no consideration of) the origin of the different alleles … ”. Just how little consideration has been given to this issue by evolutionists is evident in this highly significant observation by Endler (p. 246): John Endler is credited with having rediscovered in 1975 the colourful fish now named Endler’s guppy, or Endler’s livebearer, in his honour. (Although first recorded in 1937, in Venezuela, Endler was the first
to properly study and document it.) The live specimens ofPoecilia wingei that Endler collected himself were the first examples of this fish to make it to the aquarium trade.“Thus natural selection may affect the patterns of the origins of combinations of traits, even though it will not explain the mechanisms of their origins. This was tangentially discussed by Fisher (1930),21 Simpson (1944),22 and Rensch (1959),23 but has received virtually no attention since then. It would repay further study.” (Emphasis added.)So, “tangentially” discussed by notable evolutionists in 1930, 1944 and 1959, and here by Endler in 1986. And since Endler? His words in 1986 still ring true today: “virtually no attention since then.” And the issue sorely is in need of the “further study” by evolutionists that Endler identifies (p. 241):“… a fundamental understanding of the origin of new variants would allow us to address how morphological and genetic changes actually take place, as well as how they affect the rate and direction of evolution. Natural selection only affects changes in the frequency of the variants once they appear; it cannot directly address the reasons for the existence of the variants.” Whoever defines the terms, wins the debate. But is this key problem for evolutionists ever likely to get the consideration Endler says it warrants? Not if the dearth of attention since Endler’s book in 1986 is any guide. And Endler probably had fair warning that his attempt to clarify ‘natural selection’ was unlikely to be enthusiastically heralded by his own evolutionist colleagues. In the preface, he conceded about his book that “I expect that nobody will find it wholly satisfactory”, going on to explain (pp. xi–xii, emphases added):“Among the many people who have read it in manuscript, some find parts exceedingly helpful, while others find the very same parts boring or superfluous. To many the most irritating parts will probably be found in Chapters 1, 2 and 8 because they attempt to put the various points-of-view, definitions, and meanings of natural selection in perspective, and everyone thinks that his own emphasis is most important. A typical reaction is: ‘I find it fascinating that more than 100 years after the Origin and Mendel there can be two major positions on this everyday phrase’; … .” So, in context of the creation/evolution controversy, the battleground is still very much raging around the “terms” of the debate, i.e. thedefinition of the terms themselves. As astute observers have noted, “Whoever defines the terms, wins the debate.”From the evolutionists, then, we can no doubt expect ‘muddy waters’ for some time yet. Proving Endler’s point A 2010 New Scientist article by Professor Keith Bennett (Queen’s University, Belfast) alerted us to evolutionary biologist John Endler’s 1986 book Natural Selection in the Wild, saying that it chronicled how Endler had “scrutinised claimed examples of natural selection but found a surprising lack of hard evidence.”1 To our surprise, however, the opposite was true; Endler provided much evidence of real natural selection taking place—but he did highlight a “surprising lack of hard evidence” that this resulted in any evolution. So, it is almost certain that Bennett was using “natural selection” as if it meant the same as “evolution”. Ironically, then, in the very act of favourably citing Endler’s book, Bennett seems to have done the very thing that Endler’s book warns against—something that was probably lost on the majority of New Scientist readers. No wonder confusion reigns. Bennett, K., The Chaos Theory of Evolution, New Scientist 208(2782):28–31, 16 October 2010.
The evolution train’s a-comin’ (Sorry, a-goin’—in the wrong direction) by Carl Wieland The atmosphere in the crowded lecture theatre foyer was alive with curious anticipation. It was the late 1970s, the heady early days of the creation movement in South Australia. The creation/evolution debate I was about to take part in, before some 40 science teachers and involving a prominent academic evolutionist, was a first for the region.As the words of an animated conversation drifted across to me, I realized that my opponent-to-be was only a few metres to my left. A senior lecturer (associate professor in US terms) in population biology, he was holding forth to a small group of supporters, clearly unaware that his creationist protagonist was within earshot.‘This is really frustrating’, I heard him say. ‘I feel like an astronaut who’s come back from the moon, seen the spherical Earth, and now he’s supposed to debate with someone who tries to tell people it’s flat. In my job we seeevolution happening in front of our eyes.’Back then, before creationist arguments had had a good airing, it was understandable for him to think like that. Biology teachers could perhaps be excused for perpetuating such a naïve belief. They simply assumed that the easily observable genetic changes in many types of living populations were an obvious demonstration that evolution from microbes to man was fact. Just give it enough time, and voilá , such ‘micro’ changes would accumulate, continually filtered and guided by natural selection. It seemed obvious and logical to expect these ‘little steps’ to keep adding up so as to lead to the ‘macro’ changes—the really big jumps, frog-to-prince, fish-to-philosopher, that type of thing. (As we will show later in this article, though, the very opposite is true.)In that light, this biology lecturer’s perplexed frustration can be readily understood, because he thought that he was often seeing a small bit of what would in time become a large chunk of change. We need to understand that most evolutionists, even today, still think this way. Which is, frankly, why the usual answers given by most young age believers, when challenged on the subject of biological change, are inadequate.For instance, a challenger might say, ‘Mosquitoes have evolved resistance to DDT in just 40 years. If that’s not evolution happening before our eyes, what is?’ Most people responses focus on the amount of change. For instance, they will say, ‘Well, that’s just variation within a kind.’ Or they reply, ‘But the mosquito’s still a mosquito, isn’t it? It hasn’t turned into anything else.’Both of these replies are true. But they are inadequate and seldom impress the challenger, who thinks, ‘Well, that’s just a copout for the creationists. Evolution takes millions of years, and here we have all this change in only 40 years. So, give it a million years and imagine what sort of change we’ll have then!’The analogy I have for many years used in explaining this in public lectures is that of a railway train. Imagine you see a train pulling out of a station in, say, Miami, Florida, headed north to Chicago.1 The distance you see it travel is only a few hundred metres. But you can reasonably presume that, given enough time, it will end up in Chicago. You have seen sound evidence to indicate that it is in principle capable of making the whole journey, you don’t need to see it make the whole trip. This is just how evolutionists see the little changes (often called
‘microevolution’, but seeaside below) happening all around us. If a mosquito has changed a little in 40 years, you don’t need to see it turning into an elephant—it has shown that it is in principle capable of making a similarly radical journey.What we need to be aware of, and focus on in our answers, I tell audiences, is not the amount of change, but the type or direction of change. It is not just that the train has not gone far enough, but that it is headed in the wrong direction . The types of changes observed today, though they can be accommodated within an evolutionary framework, are, we will see, precisely and demonstrably the opposite of the ones which evolutionists really need in order to give some semblance of credibility to their belief system.So while you may be seeing the train pulling out of the station at Miami, if the reality is that it is not heading north, up to Chicago, but is headed in the opposite direction, downwards to where the line (if there was one) would end in the deep blue ocean, then it will never get to Chicago. Time will not solve the problem, since it is in principle an impossibility to reach Chicago by train in that downward direction. Just so, once we can point out to people that the ‘evolution train’ (really the train of biological change) is headed downwards, not upwards, then the more time there is, the less likely the whole evolution scenario becomes.Before explaining what I mean by biological changes having a ‘direction’, I will share what triggered this article. It was a book review 2 by well-known evolutionary biologist Dr Jerry Coyne, of the University of Chicago, who could not resist an opportunity to lash out at the creationists. 3Amazingly, Coyne uses the train journey analogy himself, reinforcing my point of how evolutionists see the issue. Though his intention is to mock creationists, he unwittingly provides a great opportunity to show how misplaced this common reasoning is.The book he was reviewing4 uses familiar examples of rapid human-induced biological changes (antibiotic resistance in bacteria, pesticide resistance in insects, changes in growth rate of fish from overfishing) to get people to ‘consent’ to the bigger idea of microbes-to-man evolution.Coyne deplores the fact that the book’s examples will probably not change the minds of creationist advocates, who have already accepted such changes as ‘adaptation within a species’ (‘variation within a kind’ would have been more precise). He says that creationists argue that ‘such small changes cannot explain the evolution of new groups of plants and animals’, and goes on to say: ‘This argument defies common sense. When, after a Christmas visit, we [presumably his family in Chicago—CW] watch grandma leave on the train to Miami, we assume that the rest of her journey will be an extrapolation of that quarter-mile.’ Thus, says Coyne, a ‘creationist unwilling to extrapolate from micro- to macroevolution’ is being ‘irrational’. Reason vs rhetoric Why can one say with confidence, concerning the biological changes observable today (man-induced or otherwise) that the train is headed in the wrong direction? Why is it that when evolutionists use this ‘grandma’s train’ extrapolation argument, it can be turned around to make the opposite point? Because the real issue in biological change is all about what happens at the DNA level, which concerns information.5 The information carried on the DNA, the molecule of heredity, is like a recipe, a set of instructions for the manufacture of certain items.Evolutionists teach that one-celled organisms 6 (e.g. protozoa) have given rise to pelicans, pomegranates, people and ponies. In each case, the DNA ‘recipe’ has had to undergo a massive net increase of information during the alleged millions of years. A one-celled organism does not have the instructions for how to manufacture eyes, ears, blood, skin, hooves, brains, etc. which ponies need. So for protozoa to have given rise to ponies, there would have to be some mechanism that gives rise to new information.Evolutionists hail natural selection as if it were a creative goddess, but the reality (which they invariably concede when pressed) is that selection on its own always gets rid of information, never the opposite.7 To have a way to add information, the ‘only game in town’ for evolution’s true believers is genetic copying mistakes or accidents, i.e. random mutations (which can then be ‘filtered’ by selection). 8However, the problem is that if mutations were capable of adding the information required, we should see hundreds of examples all around us, considering that there are many thousands of mutations happening continually. But whenever we study mutations, they invariably turn out to have lost or degraded the information. This is so even in those rare instances when the mutational defect gives a survival advantage—e.g. the loss of wings on beetles on windy islands.9 What’s in a word? Micro vs macro Many creationists will say, ‘We accept microevolution, but not macroevolution.’ As our main article points out, the ‘micro’ changes (i.e. observed genetic variation) are not capable of accumulating into macro ones, anyway.We suggest, however, that it would be wiser to avoid the use of the term ‘microevolution’. To most people, it sounds as if you are conceding that there is a ‘little bit of evolution’ going on. I.e. a little bit of the same process that, given enough time, will turn microbes into millipedes, magnolias and microbiologists. Thus, you will be seen as churlish or, as in Dr Coyne’s inverted ‘train’ example, as irrational for putting what they see as an arbitrarydistinction between the ‘micro’ and ‘macro’.If the use of such potentially misleading terminology is unavoidable, always take the opportunity to point out that the changes often labelled ‘microevolution’ cannot be the same process as the hypothetical ‘goo-to-you’ belief. They are all information-losing processes, which thus depend on there being a store of information to begin with.As creatures diversify, gene pools become increasingly thinned out. The more organisms adapt to their surroundings by selection, i.e. the more specialized they become, the smaller the fraction they carry of the original storehouse of created information for their kind. Thus, there is less information available on which natural selection can act in the future to ‘readapt’ the population should circumstances change. Less flexible, less adaptable populations are obviously heading closer to extinction, not evolving.We see that, just like with the train pulling out from Miami and headed south, if the sorts of changes we see today are extrapolated over time, they lead to extinction, not onwards evolution.Remember, evolutionary belief teaches that once upon a time, there were living things, but no lungs—lungs had not evolved yet, so there was no DNA information coding for lung manufacture. Somehow this program had to be written. New information had to arise that did not previously exist, anywhere.Later, there were lungs, but no feathers anywhere in the world, thus no genetic information for feathers. Real-world observation has overwhelmingly shown mutation to be totally unable to feed the required new information into the system. 10 In fact, mutations overall hasten the downward trend by adding genetic load in the form of harmful mutations, of which we have all accumulated hundreds over the generations of our ancestry.11In other words, populations can change and adapt because they have a lot of information (variety) in their DNA ‘recipe’. But unless mutations can feed in new information, each time there is variation/adaptation, the total information decreases (as selection gets rid of the unadapted portions of the population, some information is lost in that population). Thus, given a fixed amount of information, the more adaptation we see, the less the potential for future adaptation. The train is definitely headed downhill, destined to fall off the jetty of extinction.The supreme irony is that, of all the examples lauded by Dr Coyne as ‘evolution’, whether antibiotic resistance 12 or changes in fish growth rates, not one single one supports his ‘train’ analogy, but rather the reverse. Not one involves a gain of information; all show the opposite, a net loss. Pondering all this, I feel a sense of the same sort of frustration (only in reverse) that my evolutionist opponent was airing all those years ago, which he could have paraphrased as: ‘Why can’t they see it? It’s obvious, isn’t it?’Who knows, perhaps somehow this article will get into Dr Coyne’s hands. Maybe it will give him, and some other evolutionist apologists, food for thought the next time they put one of their grandmothers on a train. From ape to man via genetic meltdown: a theory in crisis
A review of Genetic Entropy & The Mystery of the Genome by John C. Sanford, Ivan Press, Lima, New York, 2005 by Royal Truman I write this review with very mixed feelings. On the one hand, for the first time some key data are being divulged which we need to include in our models, and which honest thinkers who question evolutionist theory need to digest. But I have a problem. In the Prologue professor Sanford wrote, ‘I knew I would be at odds with the most “sacred cow” of modern academia. Among other things, it might even result in my expulsion from the academic world.’ I know John personally and treasure his intelligence and integrity. In further drawing attention to his book, I may be contributing to having his ties to academia severed, a world to which he has such strong emotional ties and to which he has made so many contributions. I know academics and journalists who have already lost their jobs for questioning Darwinian theory.He is not exaggerating. I myself have also had my experiences in this matter.‘I started to realize (again with trepidation), that I might be offending a lot of people’s religion,’ he confides early on. How correct he is. I recently discussed the issue of life’s origins with a dear friend I’ve worked together with for years. He brought up three arguments contra creation which I easily answered on strictly scientific terms. Suddenly he leaped to his feet. Trembling with rage he pointed a finger at me, and yelled that what I was doing was dangerous! The fundamentalists in America are dangerous! They are fighting against tolerance! They refuse to accept science! They are irrational and have no facts!Dr Sanford is an applied geneticist semi-retired from Cornell University and now with the Institute of Creation Research. He is also the inventor of the ‘gene gun’, widely used in the genetic modification of crops. In this book the reader is confronted with compelling reasons to reject the claim that mutations plus natural selection have led to the marvels found in nature.Many scientists do not believe man is merely the product of random mutations plus natural selection, what Sanford calls the Primary Axiom. One line of reasoning, that of irreducible complexity, has been very capably championed by professor Behe:1 molecular machines require many complex components, the absence of only one rendering that entity non-functional. Evolutionary processes cannot be expected to provide the necessary building blocks.Others have argued that the high fidelity of DNA replication leads to very low rates of mutation. Developing humans from an ape-like forefather would just take too long. In a much cited paper, Drake has estimated2 that the rate of spontaneous mutations for humans is about 5 x10–11 nucleotides per generation. In some 6 million years from a claimed split from the chimpanzee lineage, no humans could be generated if this is true.Sanford forces us to recognize clearly that the relentless net effect of random mutations is degradation or complete destruction of function.Sanford was a practising evolutionist and at heart a eugenicist (p. 116), who ‘gradually realized that the seemingly “great and unassailable fortress” which has been built up around the Primary Axiom is really a house of cards. … Its apparent invincibility derives largely from bluster, smoke, and mirrors’ (Prologue). But we will learn that evolutionary theory fails on grounds most people did not suspect. Mutations are bad Sanford forces us to recognize clearly that the relentless net effect of random mutations is degradation or complete destruction of function. After decades of research, if even one mutation out of a million really unambiguously created new information (apart from fine-tuning), we would all have heard about it by now (p. 17). This is to be distinguished from certain changes in for example bacteria (p. 19), which merely fine-tune a component of a system already in place. The changes typically involve modification of one or two nucleotides, and in huge bacterial populations these are usually already present, a solution waiting for the precise niche. In other words, ‘When we use a rheostat to dim a light, we are not creating a new circuit, nor are we in any way creating new information’ (p. 19).Mutagens have been used for years in plant breeding, creating billions of mutation events: mostly small, sterile, sick, deformed and aberrant plants (p. 25). One improvement, low phytate corn, was caused by mutations which damaged the metabolism of phytic acid, making hungry cows happy, but hardly explaining the origin of this biochemical process (p. 25). ‘However, from all this effort, almost no meaningful crop improvement resulted. The effort was for the most part an enormous failure, and was almost entirely abandoned’ (p. 25). Indeed, no one is suggesting replacing incubators with X-ray machines to help evolution along. On the contrary, health policies are in place aimed at reducing or minimizing mutations (p. 15). Disastrously high mutational rates Now Sanford provides a key fact, inimical to evolutionary theory, but fully consistent with the Second Law of Thermodynamics. The genetics community now accepts that point mutations in human reproductive cells are in the range of at least 100–300 per individual each generation (p. 34). In fact, additional kinds of mutations, such as deletions, insertions, duplications, translocations, inversions, micro-satellite mutations and all mitochondrial mutations exacerbate the situation. Mitochondrial mutations alone would add about another mutation per individual each generation within the reproductive cell line, and macro-mutations can generate more sequence divergence than all point mutations combined. The overall contributions imply more than 1,000 nucleotide changes in every person, every generation (p. 37).Using the unrealistic lower bound of 100 mutations, and assuming 97% of the genome has no function, implies three new relevant mutations per individual each generation are generated (p. 34). Before someone attempts to shrug off these new findings, let us evaluate whether it is true that only 3% of the human genome is relevant. If the percent is twice as high, then we would double the proportion at risk through mutations. Junk DNA or masterpiece? The genome is full of countless loops and branches—like a computer program using analogue and Boolean logic.Driven by an incorrect model, genomes are generally characterized as chaotic and full of meaningless evolutionary relics. The irony is that the more advanced the organism, the more so-called ‘junk DNA’ is claimed to be present (p. 37). Perhaps we should be exposing our babies to radioactivity after all?! Biochemists discover ever more complex metabolic networks, with elaborate regulatory schemes to provide feedback inhibition or acceleration. The genome is full of countless loops and branches—like a computer program using analogue and Boolean logic. It has genes that regulate genes that regulate genes, able to set in motion complex cascades of events (p. 3).But the fact that research is steadily decreasing the proportion of supposed nonfunctional DNA has not been properly integrated into evolutionist thinking. ‘In just a few years, many geneticists have shifted from believing that less than 3% of the total genome is functional, to believing that more than 30% is functional—and that fraction is still growing’ (p. 21). Seriously now, when we examine organisms, such as dolphins, swallows or humans, do we get the impression of final products driven by a chaotic information processing system? In any event, in our thinking we need to start getting used to the fact that over 30 new genetically relevant, function-altering mutations occur per individual each generation. Unity of complexity
Reductionist, materialistic thinking prevents more effective reasoning constructs from being developed. If we could understand to the finest detail the properties of all atoms in a computer we’d still fail to grasp the logic of algorithms programmed to solve a mathematical problem. We would not even suspect its existence. None of the individual components of an airplane can fly, but the integrated unity can. The purpose of a back-up in-flight computer may appear to be ‘parasitic junk’, especially if we limit our analysis to the material properties of the atoms it is constructed with. When it is to be brought into action, why and in response to what circumstances, would not be discerned by researching individual characteristics such as atomic vibrations and molecular rotations and bond strengths.Before we assume that the information in the genome used to generate mature organisms is mostly junk, we would be wise to examine the final morphological product with more humility. Good and bad mutations inseparable Are mutations really causing all that much damage? Many Hollywood stars (and my wife!) sure seem awfully attractive. Since interchange of the genes provided from the father and the mother occurs, might this not provide a means of avoiding passing on defective genes? Might not ‘bad’ sperms and eggs lead to defective offspring which simply don’t survive, leaving many ‘good’ versions in the population? Well, unfortunately not. A huge number of mutations are added to the germline of every baby born, and these are spread throughout the various chromosomes. Human nucleotides exist in large linked clusters or blocks, ranging in size from 10,000 to a million, inherited in toto, and never break apart (p. 55, 81). A desirable trait will be accompanied by an undesirable trait, within the same individual (p. 79).Therefore, within any physical linkage unit, on average, thousands of deleterious mutations would accumulate before a beneficial mutation would arise (p. 82). All of the individual 100,000–200,000 linkage blocks in genomes are deteriorating.Furthermore, recombination appears to be primarily between genes rather than randomly between nucleotides. This means that an inferior gene is doomed to remain in that lineage, unless a back-mutation occurs, which is vanishingly unlikely. This means that the good mutations and the bad mutations cannot be separated, another example of the one-way direction of degradation known as ‘Müller’s ratchet’.Being now clearly persuaded that the net effect of mutations will be loss of information-guided functionality, we are ready to digest another insight. Tragic as a devastating mutation may be to the affected and family, the effects of this ‘curse’ would be limited to the victim if no offspring survive. But for the population as a whole, the major damage turns out not to be the severe mutations. Near neutrals Figure 1. Far more mutations are deleterious than advantageous. Individually, most have too small an effect to be acted upon by natural selection (p. 32). The majority of deleterious mutations have individually a negligible effect on viability of the organism. This is especially true if the ‘competitors’ are also accumulating non-deadly but nevertheless undesirable mutations. This is like the rusting of a car, one iron atom at a time (p. 72). Even one extra unnecessary nucleotide is slightly deleterious—as it slows cell replication and wastes energy (p. 21).This issue has been mostly ignored in the literature. Mutations in the ‘near-neutral box’ (figure 1) are redefined as being completely neutral, and so dismissed. It is then claimed that more severe mutations to the left of the near-neutral box can be entirely eliminated by natural selection (p. 23). I supposed that if we are talking about a very small number of mutations this would be to a first approximation reasonable. But the accumulation of dozens or hundreds of such mutations every generation presents a totally different picture.Incidentally, we must remember that essentially all hypothetical beneficial mutations also fall within Kimura’s ‘effectively neutral’ zone (p. 24). Therefore, positive selection would also be too weak to have an effect!It would be desirable if natural selection could remove at least some damaging mutations. In fact, this remains our last hope to avoid a fitness meltdown. Before abandoning hope, we need to consider natural selection carefully. Natural selection is ineffective The same environmental factor is unable to severely penalize different deleterious mutations. It is not realistic to invoke strongly negative selection to quickly eliminate a large number of unrelated mutations. As the number of minor mutations increases, each mutation becomes noise for the others (pp. 77, 78).Now, in a laboratory one can intelligently favour natural variability to accentuate some chosen trait (p. 98). This requires carefully crafting the external environment (nutrition, temperature, natural enemies, etc.) to minimize mutational noise. Nevertheless, no one has ever claimed to have created brand new functions not already coded for on the genome in this manner. And inevitably the organisms fine-tuned in the laboratory for a single trait are less viable long-term, living freely in nature where all natural ranges of environmental challenges occur. It is possible to optimize things such as the amount of sugar a beet produces, as long as this plant is later protected from full competition with the original stock. The changes may be in man’s interest, but at the price of the organism’s natural fitness (e.g. the large sugar production might result from a mutation damaging its control mechanism so it over-produces; in the wild, this could not compete because it is wasting valuable resources).Outside of the laboratory the matter is much worse. There is no intelligent guidance. The judge is also nearly blind (p. 7). There is a very long chain of events separating the direct effects of a genetic change and the consequences for the whole organism level. There is a logarithmic dilution at each step, a huge loss of cause-effect resolution and correspondence. ‘It is like measuring the impact of a butterfly’s stroke—on a hurricane system which is a thousand miles away’ (p. 49). ‘It is a little like trying to select for a specific soldier, based upon the performance of his army’ (p. 49).The literature is full of statements and abstruse computer programs claiming natural selection can perform near miracles.3–5 But after 25 years of searching, I have yet to find an analogy or computer model backing up this claim which has any biological relevance. Generally it is enough to simply ask what kind of organism would be suitable to check and perhaps calibrate the claims against, to reveal the irrelevance. Sanford offers an illustration of how natural selection really works, which reflects formally the issues involved very realistically, which I will modify to maximize correspondence to how selection really works in nature (p. 50).Let’s imagine a new method for improving biochemistry textbooks. A few students are randomly selected who will get a biochemistry textbook each semester during the next four years, whether or not they take a biochemistry course. Each new book will have 100 random changes in the letters. Those receiving the textbook are forced to read it (whether they take the biochemistry course or not). Different teachers assign grades to all courses taken by all students across the country each
semester (whether they received the biochemistry textbook or not). The correlation between true ability and each grade (math, history, Latin … ) is weak and often wrong. At the end of the semester we compare the average grades of all students nationwide and identify from among the best students those in possession of a mutated biochemistry textbook. Each of these latter textbooks are borrowed, 100 new random changes are made, and then returned to the owner. The whole cycle of reading and grading is repeated, multiple times. Will a better textbook result in this manner? No, since there is no meaningful correlation between the small differences in textbooks and the grades. Too many other factors (‘noise’), such as home life, lack of sleep, classroom setting etc. override the effect of a few misspellings.Any trait such as intelligence, speed or strength depends on gene characteristics and environmental factors (nutrition, training, etc.) (p. 90). For example, height is about 30% (h2 = 0.3) heritable. For complex traits such as ‘fitness’ heritability values are low (i.e. 0.004). ‘This is because total fitness combines all the different types of noise from all the different aspects of the individual’ (p. 91). Low heritability means bad genotypes are very difficult to eliminate. Survival becomes primarily a matter of luck, and not better genes:‘If Kimura’s estimate is correct, then 99.6% of phenotypic selection for fitness will be entirely wasted. This explains why simple selection for total phenotypic fitness can result in almost no genetic gain.’ (p. 93)Natural selection is a probabilistic matter. ‘Mother Nature’ does not compute for each member of a population a ‘total fitness value’ based upon all phenotypic traits (p. 94).Furthermore, almost all mutations are recessive, camouflaging their presence and hindering selection against them (pp. 56, 76). Another consideration, not explicitly brought out in this book, is that key environmental factors (disease, temperature, mutation, predators, etc.) affecting survival vary over time. Strong selection must be present for a huge number of generations if fixation of a (temporarily) favourable trait throughout a population is to occur. Relaxation for just a few generations could undo this process, since selection for a different trait would then be at the expense of the preceding one.We must recognize clearly this lack of strong correlation between a mutation (whether having a positive or negative effect) and reproductive success. It is a fact of nature, yet most people attribute incorrectly near miraculous creative powers to natural selection.But then how could natural selection supposedly develop optimized proteins, such as enzymes, one nucleotide mutation after the other, leading to almost identical versions throughout nature?6–8 Each improved nucleotide would have to be selectable in the presence of all the other noise-causing mutations within the same linkage blocks. This cannot occur by somehow selecting for superior individuals on average—which inherently involves thousands of different genes and millions of different nucleotides (p. 117).We conclude that evolutionary theory has a major problem. If mutation/selection cannot preserve the information already within the genome, it is even more difficult to argue that billions of slight improvements were selected gradually over time (p. 106). The matter is not merely an issue of low probabilities. Theoretically a huge number of offspring could be generated, each differing by many random mutations. Might not a lot of luck bordering on the miraculous cherry-pick out the best? Not really. Sanford explains why there are physical constraints as to what natural selection could do in the real world. The cost of selection The number of offspring which humans can produce is rather small. For a human population to maintain its size, about three individuals per couple would be needed. This is because not all who live go on to have children, due to personal choice, accidental death, etc. Eliminating individuals carrying bad mutations would require that additional children be born, to be sacrificed to natural selection (p. 57). ‘All selection has a biological cost—meaning that we must remove (or ‘spend’) part of the breeding population’ (p. 56). In other words, deleterious mutations in man must be kept below one mutation for every three children for flawless, 100% effective selection to be able to eliminate all the mutations and still allow the population to reproduce (p. 32).There are several kinds of costs, all additive, which must be paid for before ‘real’ selection can be covered (p. 59).9 As mentioned above, fitness has low heritability, meaning environmental factors are much more important than genetic factors in determining who survives. This means that a very large number of additional offspring is needed, which must die due to natural selection independent of genetic causes, simply to remove non-heritable variations (p. 59). In these circumstances, having to additionally select the worse culprits which carry 100 or more mutations, every generation, is not physically possible (p. 62). Haldane’s Dilemma
A process which steadily degrades a genome cannot produce a better organism. Having demonstrated conclusively that the degradation of the human genome (in the presence of such high mutations rates, preponderance of deleterious mutations and lack of huge expendable proportions of offspring) cannot be avoided, we return to what evolutionary theory claims happened. Ever more complex and sophisticated genomes are supposed to have arisen, step by step, over eons.In the 1950s, one of the most famous population geneticists, John Burdon Sanderson Haldane, presented an observation known as ‘Haldane’s dilemma’ (p. 128): it would take (on average) 300 generations to select a single new mutation to fixation. However, his calculations were only for independent, unlinked mutations. He assumed constant and very strong selection for a single trait, which is not realistic. The interference by hundreds of random mutations was not taken into account. Even so, selection for only 1,000 specific and adjacent mutations could not happen in all putative evolutionary time. There is no way an ape-like creature could have been transformed into a human (p. 129). Man and chimp differ at roughly 150 million nucleotide positions (p. 130) and humans show remarkably little variation worldwide. Think for yourself Advanced education is dominated by evolutionary theory taught as established fact. But ‘are you really just a meaningless bag of molecules—the product of nothing more than random molecular mutations and reproductive filtering?’ (Prologue). This doctrine is presented as unquestioned truth, an axiom accepted by faith because many scientists present it as obviously true (p. 5). But if you come to the point where you feel that the Primary Axiom is no longer obviously true to all reasonable parties, then you must not accept it on blind faith (p. 10). At best the materialist model could be basically right, but it is absurd to continue believing that it is self-evident. At the very least, critical thought and fair discussion is required, something scorned and denigrated by the current high priests of biology.Historically, the entire field of population genetics was developed by a small, tightly knit group of people radically committed to the Primary Axiom. They were free to explore many scenarios and adjust multiple parameters unconstrained by objective calibrations, and to optimize frameworks to appear internally consistent. Their mathematical approach was to define the unit of selection as discrete genetic units, such
a gene or nucleotide, instead of whole organisms with all the contradictory influencing factors (p. 52).‘For the most part, other biologists do not even understand their work—but accept their conclusions “by faith”’ (p. 46). The theorists’ models can be shown to never have matched biological reality to the minimal degree expected of useful models, but these men were undeniably intelligent and had an incredible aura of intellectual authority (p. 53). In many ways they deserve our admiration, since transforming any scenario, correct or not, into an appropriate mathematical formulation requires a great deal of skill. One can also admire honestly the brilliant lawyer who argues ever so cleverly against the truth in his client’s interest. How we wish they would contribute their gifts within a correct paradigm! There is hope Finally, professor Sanford makes it clear that no amount of human intervention can salvage the relentless degradation of our genomes. We will experience much and increasing suffering on the part of our children and grandchildren. ‘Read this book twice. Then read it again with a highlighter. Technical aspects are easy to follow, and the specialist will benefit very much for the highly relevant references offered. Islands’ weeds don’t support evolution Any claim that evolutionary biologists have witnessed evolution in action is of interest to creationists. We recently talked about a claim by Dr Jared Diamond (Creation 16(3):41) that evolution has been observed. He cited the changes in peppered moths and insecticide resistance in mosquitos. We showed (from the work of other evolutionists around 20 years before) that these were definitely not cases in which evolution was happening.Evolutionists of course claim large-scale evolution has occurred (non-life turned into life, then the first ‘simple’ life evolved all the way up to people). Yet all they point to as proof of this are minor changes — such as varying beaks in finches, or different colours in moths. Also, evolution is supposed to be a process generating lots of new genetic information. Yet the examples they cite invariably turn out to show no such thing. So we were interested to read in the scientific journal Nature, 14 March 1996, page 103, in another item by Dr Diamond, that a case of rapid evolution had allegedly been observed off Canada’s Pacific coast.Researchers Martin Cody and Jacob Overton had reported ‘direct detection of both rapid evolutionary change and the "founder effect" in populations of wild plants. (The founder effect is the phenomenon whereby new colonies of a species may become instantly distinct from the parent population, as a result of their few founding individuals being an atypical sample.)’But is this a genuine case of evolution? Was new information added to the plants’ DNA, so that something truly new could be said to have arisen? The answer again is a resounding ‘no’. In essence, what happened was this: The researchers studied the ‘loss of dispersal ability’ of plants confined to islands. Many species that are found only on remote islands seem to lack any way of reaching those islands in the first place. So why are they different from similar plants on the mainland?Cody and Overton did a detailed study over 10 years of some weeds whose seeds were dispersed by the wind (in the way we see dandelion fluff distributed by the wind). The design features in these airborne seeds show some natural variation; some of the plants produce airborne seeds which are able to travel further than others.They found that in only a few generations, these plants on the island produced seeds less able to travel far and wide (on average) than those plants on the mainland from which they had descended. This was said to be ‘an especially clear and simple example of evolution through natural selection, witnessed historically’.While this may be a clear example of natural selection, it must be realized that natural selection is not evolution (in the sense in which evolution is normally understood) since by itself it cannot generate anything new.Natural selection does not produce any truly novel characteristics, such as feathers on reptiles to turn them into birds. It simply operates on characteristics that are already present in the genetic code, like varying shapes, colours, or sizes.This is what happened with the weedy plants on Canada’s islands. On a small island, highly mobile seeds would be likely to travel beyond the boundaries of the land. Or to put it another way, plants with genes for less mobile seeds are more likely to establish their offspring on that island.The diagram makes it clear how this effect can happen. It is an expression of the variation which was there all along, and has nothing to do with the imagined process of how a one-celled creature could turn into peacocks, pears, and people.In fact, rather than proving evolution in the way Charles Darwin thought it did, natural selection is really a wonderful example of the creationists’ principle of conservation in operation. The genetic system maintains its identity as a specific kind, while the distribution of characteristics within that kind is rearranged to allow the plant or animal population to survive changes more readily in the environment.Despite the fact that Dr Jared Diamond opens his article with a sideswipe at creationists, the clear evidence is that the weed research on Canada’s islands points not to evolution, but to creation. How selection might operate on weed species ‘x’ (‘x-weeds’) with airborne seeds x-weeds with genes coding for mostly far-ranging seeds = = =
x-weeds with genes coding for mostly short-range seeds x-weeds with genes coding for both, producing mostly medium-range seeds but also occasional seeds of both short- and long-range.
STEP 1 — before the x-weeds colonize the island
A mixtureEmpty of gene typesweeds in the x-weed population STEP
of
x-
STEP
4
The longer-range a plant’s seeds are, the more likely it is that it will NOT contribute its genes to the next generation of plants on the island. Plants with genes producing short-range seeds will be more likely to transmit their genes to the next generation, and so with each generation, these become more common on the island, even though they began in the minority. 2STEP 5
Some of the wider-ranging seeds colonize the island Most of the seeds on the island are now of the short-range type, (short-ranging seeds can’t easily reach it) creating the apparent (but easily resolved) conundrum of how their seeds could have arrived here in the first place. STEP 3
The offspring of the original seeds to reach the island have a preponderance of ‘long-range’ type genes. This makes the population appear a little different from that on the mainland — an example of the so-called ‘founder effect’. Well-armed water fleas and radishes Startling new findings show acquired changes ‘arming’ the next generation. But it’s no help to evolution. by Carl Wieland When August Weisman cut off the tails of mice last century, he was trying to disprove a belief held by evolutionists like Lamarck (and Darwin, whom he otherwise admired). That is, that changes acquired during a creature’s lifetime, such as the stretching of the neck from efforts to reach for food in higher trees, could be inherited.None of the offspring of Weisman’s mice had any tail shortening. Thus arose one of the ‘central dogmas’ of modern biology, that changes caused by the environment cannot be inherited.1 However, recent findings have seemed to suggest otherwise.Wild radishes normally respond to caterpillar attack by greatly increasing both the number of protective spikes in their leaves, and the production of natural toxins which make the plant less palatable. 2,3 A careful, controlled study has shown that at least some of this resistance to attack is passed on to the next generation.Similarly, water fleas (Daphnia) respond to certain chemicals called kairomones, released by their natural predators when these are around, by growing ‘protective helmet-like structures’. A surprising finding was that the offspring of mothers exposed to kairomones always had larger helmets than ones ‘whose mothers had never been exposed to the danger signal’. And so did their offspring!2,3Since inheritance takes place through coded instructions, using the DNA language convention, it makes sense that the environment should not affect inheritance. It seems far-fetched to contemplate any way in which the cutting off of a tail, or the stretching of a neck, could specifically ‘re-write’ genetic instructions. So in general, this ‘dogma’, of information flowing only one way (from the DNA to the rest of the organism), holds true.Do these new findings support ‘Lamarckian inheritance’, and do they suggest a new mechanism for evolution? No, and no.The water fleas have a built-in mechanism to respond via larger helmets within their lifetime. Evolutionists would say it somehow evolved through chance mutations and natural selection. Creationists would say it was designed. Both agree that it aids the survival of the water flea.This may be via the ‘switching on’ of genes which would otherwise be dormant. (Other recent discoveries show that genes can be switched on or off depending on which parent they are inherited from).4,5 If so, the findings discussed earlier may merely show a simple extension to this mechanism—the switched-on genes stay switched on in the offspring. Or else there is a secondary mechanism which switches on genes that are passed on to the offspring. In either case, it is clearly not a random response, but a programmed mechanism—one which helps the offspring to survive and propagate the line.A key point of this new discovery is that even in the parent generation, the environment did not cause the response—e.g. the larger helmets—so much as induce it. In other words, it is not a change caused by the environment, but a pre-programmed response induced by it. So there is no evidence that any new information is generated—it is all there already.The central problem for all evolutionary theories is explaining how all the new information arose to progressively transform microbes, over billions of years, into magpies, molecular biologists and magnolia trees.6 Thus this finding, as such, gives no support to either Lamarckian or neo-Darwinian evolutionary belief.What it does suggest is that there is another level of complexity in living things, which are even more ingeniously designed than previously realized. This makes it even more difficult for those who insist that living things were not designed but arose by natural processes. What! … no potatoes? by Don Batten Governments are waking up to the need to preserve the ‘wild’ varieties of our food plants, with their rich stores of information. A highly qualified plant scientist tells us how this highlights the fallacy of evolution.
Why are there so many people of Irish descent in North America and Australia? It harks back to the Irish Potato Famine of the 1840s. Over 1.5 million people died in Ireland when the potato crops failed due to a disease known as potato blight. Many people emigrated.Why did the potatoes succumb to the disease? Potatoes came from the Andes mountains of South America, where many different varieties were
grown, including some which could resist potato blight disease. When potatoes were introduced to Europe in the 1500s, this did not include varieties with resistance to this disease.Therefore the crops in Europe were all susceptible to the disease when it arrived. (Ireland suffered the most because of its very high dependence on potatoes for the complex carbohydrate portion of their diet, whereas others had more grain crops). They succumbed because of the lack of genetic variety, which included the genes for resistance to blight.The pattern has been repeated many times since. In 1970 in the U.S., genetic uniformity resulted in loss of almost a billion dollars worth of maize because 80% of the varieties being grown were susceptible to a virulent disease known as ‘southern leaf blight.’1 Too successful? Plant breeders have been very successful in increasing the yields of all sorts of crop plants—so successful that farmers have been replacing the local, traditional varieties with the new varieties. For example, in China, at least 9,000 varieties of wheat have been lost since 1949.The ‘Green Revolution’ saw the development of high-yielding rice and wheat varieties and their rapid replacement of traditional, community-bred varieties (‘landraces’). For example, by 1984 in Bangladesh, 96% of the wheat grown consisted of Green Revolution varieties.A Losing information on the farm single variety of the Some of our best cultivated plants have obviously lost genetic information—for example, ‘miracle wheat’ navel oranges do not produce seeds. However, genetic uniformity also causes loss of accounted for 67% of information. Many crops are made genetically uniform by inbreeding 4 so that the farmer all the wheat will get consistent performance from each plant—for example, all the sunflower plants 2 planted. This has will ripen their grain at the same time. Wild sunflower plants have a range of ripening contributed to the times, seed size, etc.This means that the varieties bred for agriculture are lacking feeding of many millions of people. genetic information present in the wild strains—and they have to be this way to be most However, the loss of the traditional suitable for agriculture.The problem also applies to farm animals. Breeds of cattle, for varieties, and the reliance on relatively example, breed true-to-type. Friesian milking cows, mated with Friesian bulls, will few new varieties, poses problems. produce further Friesian milking cows, not a Beef Shorthorn (which does not produce as Problems much milk, but produces more meat). To get a strain of animal to breed true-to-type, Large areas of a uniform variety are they are inbred until variant individuals or ‘off-types’ are no longer produced. This results susceptible to new strains of pests and in the two copies (one from each parent) of many genes being the same, whereas in disease for which the variety lacks wild animals, the two copies can be different, resulting in variation in the offspring. So resistance. These new pest or disease domestic breeds of animals are missing a lot of the genetic information in wild animals. strains can be introduced from overseas, or new varieties can occur through normal reproduction which results in new combinations of existing genes. Just as with antibiotic resistance, these new disease strains do not arise through the development of new, functional genes,3 so this has nothing to do with particles-to-people evolution.To try to keep ahead of new strains of pests and diseases, plant breeders introduce new genes from wild plants of the crop species, or from ‘landraces,’ into new varieties. New varieties generally last only five to seven years before they are replaced.However, with loss of the wild types and landraces, plant breeders could lack the sources of genes for the further breeding needed to increase yields, decrease dependence on fertilizers and pesticides, improve quality, breed for drought resistance, cold/heat tolerance, salt tolerance, and many other things. So the loss of the genetic information needed to achieve these objectives is a serious problem. The U.N.’s Food and Agriculture Organisation (FAO) estimates that about 75% of genetic diversity in agricultural crops has been lost this century—largely by the replacement of landraces with the new varieties. Authorities are beginning to respond to this problem—see banking on genes. Denying evolution Many scientists believe the dogma that the blind, purposeless forces of evolution (random mutations and natural selection) created all the genetic information in plants.Yet the (belated) push to preserve the wild varieties of our food plants highlights the fact that no amount of selection (artificial, by breeders, or natural) can generate information which is not there! If random copying mistakes (mutations) originally generated all the information, surely it should not be too hard for highly intelligent scientists to create the required genes for breeding new improved varieties? However, with all that we now know about genes, no one can yet create a gene—for example, for rust resistance—from scratch.7 Plant breeders recognize that the information in the genes of plants is irreplaceable.The evolutionist E.O. Wilson wrote: Why don’t strawberries taste like Dad’s used ‘Each species is the repository of an immense to? amount of genetic information. The number of Many people remember the deliciously sweet, genes range from about 1,000 in bacteria and fragrant strawberries picked from their home 10,000 in some fungi to 700,000 or more in many garden. They were smaller than the ones flowering plants and a few animals … . If stretched available today, but they tasted and smelled out fully, the DNA [in one cell] would be roughly a better. What has happened?People buy with meter long. But this molecule is invisible to the their eyes, so nice big, red strawberries sell well. naked eye. … The full information contained Plant breeders therefore concentrated on therein, if translated into ordinary-size letter of breeding big, red strawberries with high yield printed text, would just about fill all 15 editions of and good shelf life. In concentrating on these the Encyclopædia Britannica published since characteristics, flavour has been neglected. 1768.’8Biologist David Janzen, University of Indeed it is possible that selecting for high yield may (inadvertently) Pennsylvania, said that destroying tropical forests have selected for low flavour!The point is that selecting for one for paper manufacture would be ‘like pulping the characteristic can be at the expense of something else. One Library of Congress to get newsprint.’ 8Just as the character can be accentuated while another is diminished. There are information in books comes from an intelligent biological limits to what can be achieved. Breeding cannot ‘create’ source, so the information in the genes of living new features for which there are no genes, or which exceed the things also comes from an intelligent source.This biological capabilities of the organism. source is clearly far more knowledgeable and intelligent than we who cannot yet create the genetic information ourselves and so we have to be concerned about the loss of genetic diversity.In their concern for the loss of this diversity, plant breeders agree that the genetic information is irreplaceable, and tacitly admit that it did not arise through random, non-intelligent processes, and that selection cannot re-create it, once lost.Faith that the blind forces of ‘evolution’ created all the genetic information is indeed a blind faith.
Banking on genes In recognition of the problem with crop plants, ‘gene banks’ for various crops have been set up around the world. For example, more than 80,000 rice varieties are maintained at the International Rice Research Institute (IRRI) in the Philippines. The gene bank provides rice seed samples on request. When Cambodia got through the notorious evolution-inspired Pol Pot upheavals, the rice farmers could resume growing their lost varieties from seed supplied from the rice seed collection.However, seeds held in gene banks are vulnerable because of the need to grow the seed periodically to produce fresh seed. Gene banks are labour intensive, costly to maintain, and not easy to raise funds for. Storage at –20°C enables some seed to remain viable for up to 100 years, but this depends on continuous maintenance of refrigeration facilities. From a survey, FAO estimated that almost half of all stored seeds need to be regenerated—that is, these strains are liable to be lost. 5Also, only major crop plants are covered by such gene banks. Non-cereal plants which are an important source of food in subsistence agriculture in the tropics tend to be neglected in gene banks. For example, wheat accounts for 14% of all gene banks, whereas cassava, a major poor people’s crop, accounts for only 0.5%.6In addition to the large gene banks, there are ‘Seed Saver’ groups who voluntarily collect and grow traditional varieties no longer grown commercially by farmers. Folk involved in such seed saving actions network with one another to share rare varieties.Organizations concerned with conserving genetic resources, such as The International Plant Genetic Resources Institute (IPGRI) in Rome, Italy, now recognize the importance of getting farmers themselves to maintain their traditional varieties. Non-government organizations (NGOs) have been leading the way with this approach.
Dawkins playing bait and switch with guppy selection by Jonathan Sarfati In September 2009, Richard Dawkins released his book The Greatest Show on Earth: The Evidence for Evolution. In it, he disparagingly referred to creationists as “history-deniers”. But it’s Dawkins who is denying true history, and his interpretation of the evidence is (sadly) faulty. Published: 18 February 2010(GMT+10)In Dawkins’ new book The Greatest Show on Earth, he supposedly presents proof of evolution, as he admits that “the evidence for evolution is nowhere explicitly set out” in his previous books. But much of his book is guilty of the logical fallacy ofequivocation or “bait-and-switch”, that is, switching the meaning of a single word (evolution) part-way through an argument. For example, the real point of debate is whether all living things come from pond scum, but Dawkins says:“ … when there is a systematic increase or decrease in the frequency with which we see a particular gene in a gene pool, that is precisely what we mean by evolution.” (p. 33)Yet throughout his book, Dawkins rails against “history deniers” or “40 percenters” who deny “evolution”. But if this is what he means by evolution, then I can’t think of anyone who denies it, including the staff at CMI!Dawkins uses many of the pages in his book to prove that natural selection is a fact. Once again, creationists taught this before Darwin, and it’s an important part of the modern young age model, explaining how creatures adapt to the environment.However, Dawkins himself compares most examples of natural selection to a human sculptor removing clay, i.e. “chiselling” genes from the gene pool (p. 34). Such changes are in the opposite direction required to turn bacteria into biologists. [Sexual selection theory]fails to account for the peacock tail, the very thing Darwin invented the theory to explain! It also hindered discovery of animportant function for the huge toucan beak: temperature regulation. Also, creationists have little problem with sexual selection, i.e. the selection of characteristics preferred by the opposite sex in mate choice. This is potentially a strong effect, since only those creatures that find mates can pass on their genes to the next generation. However, it fails to account for the peacock tail, the very thing Darwin invented the theory to explain ! It also hindered discovery of an important function for the huge toucan beak: temperature regulation.Dawkins does set out some good evidence that both natural selection and sexual selection happen, but knocks down a straw man in thinking that this somehow proves particles-to-people evolution or disproves the young age model. The following is a draft extract from our forthcoming book, The Greatest Hoax on Earth? Refuting Dawkins on Evolution. Guppies Dawkins’ colleague Dr John Endler studied many populations of guppies in mountain streams in Trinidad, Tobago and Venezuela. (pp. 133–9).1 Brightly coloured males seem to impress the females, who “sexually selected” such colours. But they stand out to predators, who would “naturally select” against this. As strong support for this, streams with strong predators contain drabber males, while streams with weak predators have more brightly coloured males with larger, gaudier spots.Endler noticed that the “drab” ones are camouflaged by spots as well, which blend in with the pebbles at the bottoms of their native streams. So he set up experiments in a number of ponds, half with fine gravel and half with coarse. He allowed guppies to breed freely. The number of spots shot up, presumably since only sexual selection was at work. Then after six months, he left some ponds predator-free; in others, a fairly weak predator (given that no natural stream is really totally predator-free); and in the remaining, he introduced a strong predator, a pike cichlid. In the ponds with weak or no predation, the number of spots continued to rise, as sexual selection was still operating. But in the ponds with the strong predator, the number of spots dropped sharply. Evidently males with lots of spots were easily spotted and devoured, so despite the females’ preferences, they had to be content with the survivors.Also, Endler found that gravel size made a difference. Both strong and weak predators promoted larger spots in pools with coarse gravel, and smaller spots with finer gravel. This makes sense—the closer spot size matches gravel, the more camouflaged the fish are. But in ponds with no
predators, the reverse happened: fine gravel promoted larger spots and coarse gravel smaller. Again, this makes sense— the less camouflaged males stand out better to the females. Evolution in action? Belief in particles-to-people evolution is not necessary to understand real science, including experiments on natural and sexual selection. And clearly belief in creation does not ruin fascination for such science.Dawkins relates a story Endler told about an encounter with a fellow domestic airline passenger. This passenger showed much interest in Endler’s guppy research, and amiably asked what Endler himself calls “excellent questions … indicating that he was enthusiastically and intellectually following the argument.” Yet when this passenger asked what theory underlined the experiments, Endler replied, “It’s called Darwin’s theory of evolution by natural selection.” Then, by Endler’s account, this passenger quit the conversation, which Endler calls, “really tragic”. Dawkins calls this passenger “closed-minded” (p. 133).But even if this account is unspun, it doesn’t prove what they claim. This passenger might have been very annoyed at Endler’s cheap baitand-switch. Dawkins commits the same dishonest equivocation when he claims, “It is a spectacular example of evolution before our very eyes.” (p. 139). It might have been better to reply on the lines of, “Indeed, these are most ingenious experiments to support natural selection, a theory known to creationists before Darwin. But do guppies changing into guppies prove that fish evolved into fishermen? The changes don’t show any new features, just different expressions of the same ones.” Yet this type of change, which doesn’t add any new information, is usually the best “evidence” of evolution and alleged disproof of creation that evolutionists can come up with.Furthermore, it shows that belief in particles-to-people evolution is not necessary to understand real science, including experiments on natural and sexual selection. And clearly belief in creation does not ruin fascination for such science. So Dawkins’ scare-mongering about “history deniers” destroying science education is shown—even by his own account—to be wide of the mark. Molecular limits to natural variation by Alex Williams Darwin’s theory that species originate via the natural selection of natural variation is correct in principle but wrong in numerous aspects of application. Speciation is not the result of an unlimited naturalistic process but of an intelligently designed system of built-in variation that is limited in scope to switching ON and OFF permutations and combinations of the built-in components. Kirschner and Gerhart’s facilitated variation theory provides enormous potential for rearrangement of the built-in regulatory components but it cannot switch ON components that do not exist. When applied to the grass family, facilitated variation theory can account for the diversification of the whole family from a common ancestor—as baraminologists had previously proposed—but this cannot be extended to include all the flowering plants. Vast amounts of rapid differentiation and dispersal must have occurred in the post-Flood era, and facilitated variation theory can explain this. In contrast, because of genome depletion by selection and degradation by mutation, the potential for diversification that we see in species around us today is trivial. Darwinian evolution Figure 1. Potential for variation in modular regulatory control systems. The hair dryer (A) and the vacuum duster (B) consist of similar components, but one is wired up to blow air, the other is wired up to suck air. The axolotl (C) is an adult salamander that has retained its juvenile gills; if thyroxin is given at the right time, it develops into a normal salamander (D) with lungs.Charles Darwin will always be remembered for turning descriptive biology into a mechanistic science. His famous 1859 book The Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life argued persuasively that species are not immutable creations but have arisen from ancestral species via natural selection of natural variation. Two main points contributed to Darwin’s success:he presented a simple, testable, mechanical model that enabled other scientists to engage experimentally with the otherwise overwhelming and bewildering complexity of life;unlike others, Darwin approached the subject from many different angles, examined all the objections that had been raised against the theory, and provided many different lines of circumstantial evidence that all pointed in the same direction.He went wrong in four main areas, however. First, he proposed an entirely naturalistic 1 mechanism, but we now know that it must be intelligently designed. 2 Second, he extrapolated his mechanism to all forms of life, but we will soon see that this is not possible. Third, he went wrong in proposing that selection worked on every tiny advantageous variation, so it led to the continual ‘improvement of each creature in relation to its … conditions of life.’3 By implication, deleterious variations were eliminated. We now know from population biology that selective advantages only in the order of ≥10% have a reasonable chance of gaining fixation. 4 The vast majority of mutations are too insignificant to have any direct influence on reproductive fitness, so they are not eliminated and they accumulate relentlessly like rust in metal machine parts. The machine can continue to function while the rust accumulates, but there is no improvement in the long term, only certain extinction. 5Fourth, he proposed that reproductive success—producing more surviving offspring than competitors—was the primary driving force behind species diversification. If this were true, then highly diversified species in groups like the vertebrates, arthropods and flowering plants would produce more surviving offspring per unit time than simpler forms of life. This is not generally true—quite the opposite. The ratio of microbial offspring numbers per year compared with higher organisms is in the order of billions to one. Facilitated variation theory Kirschner and Gerhart’s facilitated variation theory provides a far better explanation of how life works. In a companion article,2 I showed that this requires an intelligent designer to create life with the built-in ability to vary and adapt to changing conditions, otherwise it could not survive. This leads us to the important question of the limits to natural variation.The limits of natural variation today are extremely narrow, being evident only at the variety and species level. History requires a far greater capacity for diversification in the ante-diluvian world to be available for rapidly repopulating the Flood-destroyed Earth, and quickly restoring the ecological balances crucial to human habitability. Baraminologists have identified created kinds that range from Tribe (a sub-family category, e.g. Helianthus and its cousins within the daisy family), 6 to Order (a super-family category, e.g. cetaceans—the whales and dolphins).7 Theoretical limits to natural variation Scope for change in core structure According to facilitated variation theory, the capacity to vary requires:
functional molecular architecture and machinery, a modular regulatory system that maintains cellular function but provides built-in capacity for variation through randomly rearranged circuit connections between machines and switches, a signaling network that coordinates everything. Most variation occurs between generations by rearrangement of ‘Lego-block-like’ regulatory modules. Over this timescale, we can emphatically say that no change at all occurs in the molecular architecture and machinery, because it is physically passed in toto from mother to offspring in the egg cell. Variation between generations must therefore be limited to the regulatory and signaling systems. Scope for change in regulatory modules The law of modules2 says that the basic module of information has to contain functionally integrated primary information plus the necessarymeta-information to implement the primary information. This information has to be kept together so that the module retains its functionality.Genes only operate when they are switched ON. Their default state is to remain OFF. Genes don’t usually work alone, but as part of one or more complexes. Even the several different exons (the protein-coding segments) within a gene can participate in different gene complexes, some being involved with up to 33 other exons on as many as 14 different chromosomes. 8 And genes are not just linear segments of DNA, but multiple overlapping structures, with component parts often separated by vast genomic distances.9Sean Carroll, a leading researcher in developmental biology says, ‘animal bodies [are] built—piece by piece, stripe by stripe, bone by bone—by constellations of switches distributed all over the genome.’10 Evolution, he believes, occurs primarily by adding or deleting switches for particular functions, for this is the only way to change the organism while leaving the gene itself undamaged by mutation so that it can continue to function normally in its many other roles. Carroll considers this concept to be ‘perhaps the most important, most fundamental insight from evolutionary developmental biology.’ 11Diversification via Carroll’s proposed mechanism consists of rearranging the signaling circuits that connect up genes, modules and switches, while retaining functionality of both the modules and the organism. Carroll tells us that gene switches are extremely complex, comparable to GPS satellite navigation devices, and easily disabled by mutations, so if switches can be spliced into and out of regulatory circuits, then it must happen via a cell-controlled process of natural genetic engineering (the law of code variation2).Regulatory areas within gene switches are hotspots for genetic change. An average gene switch will contain several hundred nucleotides, and within this region there will be 6 to 20 or more signature sequences. These signature sequences are similar to credit card PIN numbers—they allow the user to operate the bank account—and they are easy to change. The result of such change is that different signaling molecules will then be able to operate the ‘bank account’ of natural variation.There are about 500 or so ‘tool-kit proteins’ that are highly conserved across all forms of life and that carry out a wide range of basic life functions. For example, bone morphogenetic protein 5 (BMP5) regulates gastrulation and implantation of the embryo, and the size, shape and number of various organs including ribs, limbs, fingertips, outer ear, inner ear, vertebrae, thyroid cartilage, nasal sinuses, sternum, kneecap, jaw, long bones and stature in humans, and comparable processes in other animals including the beaks of Darwin’s Galápagos finches.The signature sequences recognized by such tool-kit proteins are usually about 6– 9 nucleotides long. A 6-nucleotide sequence can have 46 = 4096 different combinations of the nucleotides T, A, G and C, and a 9-nucleotide sequence can have 49 = 262,144 different combinations. But there are 6 to 20 or more signature sequences that can be recognized by the 500 different tool-kit proteins, which gives somewhere between 500 6 (~1016) to 50020 (~1054) different possible combinations.An obvious limitation to change in regulatory circuits is that switches can only switch ON functions thatalready exist. It is easy to switch OFF an existing function, but it is impossible to switch ON a function that does not exist.Two examples of regulatory variation are given in figure 1. The hair dryer and the vacuum duster both use similar materials—motorized fan, plastic housing, power circuit and switch. In one, the control circuit is wired up to blow air; in the other, the circuit is reversed, and the machine sucks air. A biological example is the axolotl, a salamander that has retained its juvenile gills into adulthood. This can happen if there is an iodine deficiency in the diet, or if a mutation disables thyroxin production. By adding thyroxin, the axolotl will develop into a normal salamander. Both these switch-and-circuit rearrangements seem to be simple changes, but they are possible only because complex mechanisms of operation already exist within the system. Scope for change in signaling networks While there is enormous potential for variation built-in to the circuitry that connects up regulatory modules, it is signals that trigger the switches and their functional modules. What scope is there for diversification in signal networks?Signal networks are compartmented. They operate as a cascade within each compartment—one signal triggers other signals, which trigger other signals etc. Each compartment cooperates with its adjacent compartments so that the unity and functionality of the organism is maintained, but they do not influence activities beyond their local neighbourhood. Figure 2. Embryonic switching cascades represented as a ‘domino cascade’. The domino cascade is set up on the left so that when the ‘Start’ domino is toppled, the sequential falling of dominoes will trigger the next activity in the series, but also trigger other developmental modules in the outer circles, until the ‘Stop button’ is hit. Once the cascade is complete, an organism does not need any of the sequence again so it is permanently shut down, as on the right where all the dominoes have fallen and will not get up again. There is no coded information in this signal network because everything that has to be done has been designed into the pattern of dominoes. With no coded information, no mutations or recombinations can occur, so this kind of signal network probably marks a limit to natural variation.The two examples I used to illustrate this point in the companion article ‘How Life Works’2 were the propagation of plants from cell culture, and the regeneration of double-headed and double-tailed planarian flatworms. In both these cases, a single signal molecule triggered a dramatic developmental cascade (shoot/root growth in the former, and head/tail growth in the latter) that was completely independent of, but cooperative with, the other half of the whole organism.Some signals are hard-wired into the cell, while others are soft-wired. An example of a hard-wired signal occurs within theapoptosis cascade for dismantling cells and recycling their parts. In a normal cell, apoptosis is extensively integrated with a wide range of functional systems and can be triggered by a variety of causes through a complex signaling network. However, in human blood platelets the system is isolated from its normal whole-cell environment and we can see it operating in a much simpler form.A complex of two proteins, Bcl-xL and Bak, performs the function of a molecular switch. When Bcl-xL breaks down, Baktriggers cell-death.12 In a normal whole cell, homeostasis maintains the
balance between Bcl-xL and Bak, but platelets are formed by the shedding of fragments from blood cells and there are no nuclei in them. Once the platelets are isolated from homeostatic control, Bcl-xLbreaks down faster than Bak, so the complex provides a molecular clock that determines platelet life span—usually about a week. No signal is sent or received in this hard-wired system, so there is no room for diversification.Hard-wired signaling networks are probably a major component of stasis. We can visualize them by using a domino cascade model, illustrated in figure 2. In this case, embryogenesis is symbolized as a series of events in the main circle, which trigger other peripheral cascades as they proceed. Each cascade continues until it meets a STOP signal, at which point the whole circuit is shut down. A similar thing happens in individual cells when they differentiate. Embryonic stem cells have the potential to become any cell in the body, but once the cascade is traversed, all options but one are shut down.In contrast, a soft-wired system sends actual signal molecules, raising the possibility of adaptive change—e.g. sending a different signal molecule. A recent study of red blood cells investigated cell fate decision making—whether to proliferate, to kill themselves or to call for help. This decision lies at the very heart of homeostasis because it determines the robustness and stability of the organism in the face of change and challenge. Figure 3. Grass flower (spikelet) structure and some common variations. A—conventional spikelet on the tip of a branch. B—exploded view of spikelet: a = lower glume; b = upper glume; c = lemma; d = palea; e = ovary (black oval) with bifid filamentous stigmas, surrounded by 2 or 3 translucent lodicules and 3 anthers. C—apex of lemma may elongate to produce a straight awn, or corkscrew several turns to produce a twisted column with a straight or curved terminal bristle.The researchers discovered that they did not need to know the detailedstructure of the decision-making system, just a knowledge of its network of signaling interactions was sufficient to identify which components were the most important.13 This finding was confirmed in another study in which a wide range of perturbations were applied to white blood cells and the effect upon the cell fate decision was examined. The decision came not from any particular target of perturbation, but as an integrated response from many different nodes of interaction in the signaling network. The authors suggested that computations were carried out within each node of the signaling network and the combination of all these computations determined what the level of response should be from any particular perturbation. 14Does this indicate a potential for adaptive change? Or does it suggest a system that is designed to resist change?The primary role of the signaling system is to coordinate everything towards the goal of survival. Life can survive only by maintaining a balance between contradictory objectives. On the one hand, it has to achieve remarkable results as accurately as possible—e.g. plants turning sunlight into food without the high energies involved killing the cell. On the other hand, it has to do it in an error-tolerant and constantly variable manner to maintain its adaptive potential and its robustness and stability.The solution to this dilemma is error minimization. All possible routes will involve risks of error, but the optimal solution will minimize those risks. A computer simulation study of regulatory networks found that using an error minimization strategy leads to the formation of control motifs (gene switching patterns) that are widely found in very different kinds of organisms and metabolic settings. 15 When applied to the ‘noise’ in yeast gene expression that results from the ON/OFF nature of signaling, it was found to also be the case in real life. Genes that were essential to survival exhibited the lowest expression-noise levels when compared with genes that were not directly essential. The author concluded that ‘there has probably been widespread selection to minimize noise in [essential] gene expression.’ But there is a down side—noise minimization probably limits adaptability.16 Figure 4. The grass inflorescence consists of (A) the basic unit of a single terminal flower (spikelet) on a short stalk (pedicel) which is repeated in a terminal group of branches (B). This terminal group structure is then repeated on side branches (C), with the lower branch(es) including further internal branching. This basic inflorescence type is called a panicle.Since the goal of signal coordination is survival, I suspect that the large, interconnected signaling networks in all forms of life contribute more to stasis than to change. Practical limits to natural variation It is impossible to describe the full range of natural variation across all life forms in a journal article, so I will focus just on variation within the grass family (Poaceae), and between it and other families of flowering plants (Angiosperms).The grass family comprises about 10,000 species in about 700 genera. Is it possible that maize, lawn grass and bamboo all arose from a common ancestor? Baraminologists believe so.17 Grass morphology The easiest way for us to conceptualize the extent of natural variation is through illustrations of morphological variations. We need to keep in mind that much more than morphological variation is involved in speciation, but it can serve as a convenient surrogate for our present purpose. The basic structure of a generalized grass flower (spikelet) is illustrated in figure 3. Figure 5. Ordination and classification of specimens of the three native Puccinellia species identified in Western Australia, based on 34 morphological characters. Principle Coordinates 1 and 2 provide a 2-dimensional representation of the differences between the specimens and a clustering algorithm identified groups of similar specimens (ellipses). A common variation on the standard structure is the development of an awn upon the apex of the lemma (or glume) in figure 1C. This transformation is fairly straightforward. The apex of the lemma is extended into a long straight awn, then a regulatory change causes the edges to grow faster than the centre, which causes the base part of the awn to spiral around into a twisted column, leaving a straight or curved bristle at the top.Grasses generally have a multitude of spikelets, arranged into a terminal structure called theinflorescence, as shown in figure 4.
Species-level variation in the Australian salt grass Puccinellia Salt grasses of the genus Puccinellia are distributed worldwide, from the Antarctic to the Arctic, and they occur right across southern Australasia (Australia and New Zealand) in marine salt marshes, around the edges of inland salt lakes and on salinised pasture lands. They have a quite generalized grass morphology, with no special adaptations for dispersal, as many other grasses do, so they may represent a typical primordial grass.The most widespread species, found right across Australasia, is Puccinellia stricta. When Edgar18 described the New Zealand species in 1996 she noted some differences between Australian and New Zealand populations of P. stricta and suggested that further detailed study was warranted. I was fortunately able to undertake that study,19 with results that are quite typical of many widespread plant genera. My study focused on the genus in Western Australia (WA), where three native species were identified—P. stricta, P. vassica and P. longior. An ordination and classification of specimens based on their morphological characteristics is shown in figure 5. Figure 6. Ordination and classification of specimens of Puccinellia stricta from across Australasia. The group labeled perlaxa had been identified as a subspecies of P. stricta. Four geographically isolated regions were sampled: WA = Western Australia, SE Aus = South East Australia (Victoria, South Australia and New South Wales), Tas = Tasmania, NZ = New Zealand. The axes of ordination and the ellipses of classification have the same meaning as Figure 3 and were based on the same 34 morphological characters.The plot shows that all three species are well separated from one another, with members of each species being more closely similar to members of their own species than to other species.I then needed to know how our specimens of Puccinellia stricta compared to specimens of the same species from right across Australasia. Loan specimens were obtained from other herbaria and the same analysis was carried out as for the WA specimens. A very different plot resulted, as shown in figure 6.In this case, a new species was clearly separated out from the rest, while the remainder spread broadly right across the ordination space. The group labeled perlaxa (occurring only in southeast Australia) had previously been identified as a subspecies of stricta, but from this analysis it was clear that it warranted species status, so we named it Puccinellia perlaxa.The big picture of the native Australasian species of Puccinellia that emerged from this study was of a single widespread species, P. stricta, that varied in a continuous manner right across the whole region, and then localized species with restricted distributions that could generally be explained in terms of local ecological and/or geographical factors.Historically, therefore, it is most likely that the widespread species was the progenitor of the all the other species. It has retained at least some of its capacity for variation, and certainly a greater capacity (wider dispersion in the ordination space) than any of the other species that I studied. Morphological variation in Australian Puccinellia Figure 7. Panicle variations within Australian species of Puccinellia. The contracted panicle with a variety of branch lengths at A is typical. B has numerous spikelets crowded along very short branches, while C has very few spikelets on very short branches, and D has few spikelets that are mainly on the ends of very long branches. Images were scanned from dried herbarium specimens; in life, D would have had straight branches and a more symmetrical shape. Figure 8. Variations in upper glume length (marked with black bars) in spikelets of some Australian species of Puccinellia. Figure 9. Paleas from five different Australian species of Puccinellia. Note the variation in hair development on the margins, ranging from glabrous (no hairs) on D, a few hairs near the apex of E, the top half of B with hairs and the lower region glabrous, with A and C having hairs extending into the
lower half.
Figure 10. Retrogression of Panicoid grass spikelets. The characteristic condition in the Tribe is to have one terminal fertile floret subtended by one sterile floret. The primordial condition at A has the sterile floret male. Condition B has lost the anthers of the sterile floret. Condition C has lost the palea of the sterile
floret. Condition D has lost the lower glume. The series E, F, G and H illustrate the same pattern of retrogression but with the spikelet axis rotated in relation to its adjoining branch. Figure 11. Transformation of a panicle into wheat. The side branches of A are eliminated to give B, the number of spikelets is increased to form C, then the pedicels are reduced to form D. Australian Puccinellia species vary most markedly in their panicle structure, a few of which are illustrated in figure 7. Puccinellias have multiple florets per spikelet, ranging from 3 or 4 up to 10 or more. One feature that varies significantly in spikelet structure is the length of the upper glume, illustrated in figure 8. The palea also varies significantly, particularly in the extent of hairs on the margins, as shown in figure 9. Genus-level variations in Tribe Paniceae The grass family is divided up into Tribes of genera that (ideally) reflect their common ancestry. The largest Tribe is Paniceae, and Häfliger and Scholz have suggested that the spikelet variations within this Tribe follow a fairly simple pattern of retrogression from the original Paniceae spikelet,20 as illustrated in figure 10. Sub-family variation within Poaceae Argentinian researchers Vegetti and Anton have shown that if we begin with a panicle as the primordial grass inflorescence, then every other generic form can be derived simply by adding, subtracting, shortening or lengthening the components of the panicle. 21 I will take just three types of transformations that represent different sub-family groups within Poaceae—wheat, maize and silkyhead lemon grass. Wheat The hypothesized transformation of a panicle structure into the reduced seedhead of a wheat plant via the Vegetti-Anton theory is illustrated in figure 11. Maize Figure 12. Transformation of a panicle into maize. The middle branches of the panicle A are replaced with leaves and leafy bracts, and the lower branches are transformed into a spike (like wheat, Figure 9) to form B. The upper spikelets lose their female parts, and the lateral spikelets lose their male parts to form C. The male spikelets multiply, and the female spikelets elongate their pollen receptors to form a tassel that emerges from the enveloping leafy bracts, to formD. Transformation of a panicle into the compact seedhead of maize is more complex, but still conceivable, as illustrated in figure 12. The primordial panicle could have been divided by the panicle branches being switched OFF in the midsection, and leaf modules being turned ON. A leaf within the inflorescence is called a ‘spathe’ leaf. Apical dominance is a common mechanism in all plants for repressing growth below the apex until conditions are appropriate. This normally controls the proliferation of fertile seeds within grass spikelets. It represses female organ development more strongly than the male parts, so in many grasses the apical florets within a spikelet will be either male or sterile, and only the lower florets (those furthest away from the dominating apex) will produce fertile seed. This mechanism is already in place to suppress female organ development in the top branches of the maize plant, making them all male. But the lower branches of the inflorescence are now far distant from the apex, so apical dominance is eliminated and the female organs grow uninhibitedly, perhaps out-competing the male organs and suppressing them altogether. Leaf and bract growth in the lower parts is stimulated and they cover the female spike entirely. This causes the female florets to lengthen their pollen receptors so that they can reach the open air and receive wind-dispersed pollen, making the silky tassel at the end of a corn-cob. Silkyhead lemon grass Figure 13. Transformation of a primordial panicle into the spatheate panicle of Cymbopogon obtectus. The branching pattern in A is reduced to a repeating set of branches in which a sessile fertile spikelet with an awn occurs at each secondary branch point, accompanied by a pedicellate awnless sterile spikelet (B). Pairs of these branched structures are subtended by a spathe leaf, from which they emerge at flowering time (C) to produce the complex mature panicle (D).Transformation of the panicle into silkyhead lemon grass (Cymbopogon obtectus) can be hypothesized by reducing the pedicel of alternate spikelets so that they occur in pairs—one pedicellate, the other sessile. The pedicellate spikelet retains apical dominance and is sterile or male, and the sessile spikelet is fully fertile, but it also develops an awn on its lemma (see figure 3). The paired branching structures occur also in pairs, and a leaf growth module is switched ON within the developing inflorescence to produce a spathe leaf surrounding each pair of branched structures. Hairs are normally present in many parts of the inflorescence, and are usually short, but in Cymbopogon obtectus, the hairs are abundant and long, producing a fluffy white ‘silkyhead’ at flowering time, as illustrated in figure 13. Origin of the angiospermsWithin the grass family, diversification from a common ancestor seems to be fairly straightforward, and could have occurred via numerous rearrangements of parts that were already present in the primordial grass ancestor. But can we continue this process back to a common ancestor with daisies, orchids and all other flowering plants?A recent review of the subject was entitled ‘After a dozen years of progress the origin of angiosperms is still a great mystery.’ 22 The ‘progress’ referred to was the enormous effort put into DNA sequence comparisons, in the belief that it would give us the ‘true’ story of life’s origin and history. While such comparisons have proved of great value in sorting out species and genus relationships, the results for family relationships and origin of the angiosperms has often been confusing and/or
contradictory—thus the remaining ‘mystery’.Recent discoveries of fossil flowers show that angiosperms were already well diversified when they first appeared in the fossil record. The ‘anthophyte theory’ of origin, the dominant concept of the 1980s and 1990s, has been eclipsed by new information. Gnetales (e.g. Ephedra, from which we get ephedrine), previously thought to be closest to the angiosperms, are now most closely related to pine trees. To fill the void, new theories of flower origins have had to be developed, and ‘Identification of fossils with morphologies that convincingly place them close to angiosperms could still revolutionize understanding of angiosperm origins.’22 Conclusions Theoretically, the greatest scope for natural variation appears to lie in the almost infinite possible permutations of the Kirschner–Gerhart ‘Lego-block’ regulatory module combinations, and these could rapidly produce the enormous diversification implied by the young age history. In contrast, there is no scope at all for change in the machinery of life from one generation to the next because it is passed on in toto from the mother in the egg cell. Signaling networks appear to be limited in their scope for diversification, particularly those that are hard-wired (designed into the system) into compartments and cascades that have symmetry and functional constraints. The elaborately interconnected signaling networks are very robust in the face of perturbation, and provide a crucial component of stasis. There is some potential for variation in the signaling molecules that are sent, but error minimization limits its functional scope.From a practical point of view, diversification of the whole grass family from a common ancestor is conceptually feasible via switching ON and OFF the original component structures within a primordial grass. It is not possible to switch ON components that don’t exist, however, so this mechanism cannot be extrapolated to include a common ancestor between grasses and other angiosperms such as daisies and orchids.Flowering plants display an enormous amount of differentiation and dispersal (between 250,000 and 400,000 species in 400 to 500 families worldwide) and appear only in the upper levels of the fossil record. Most of this diversification appears therefore to have happened rapidly, possibly in the post-Flood era. This is not Darwinian evolution. It is intelligently designed, built-in potential for variation in the face of anticipated environmental challenge and change. The word ‘evolution’ is still useful in describing processes of historical diversification, but its Darwinian component is now only a minor feature. In contrast to Darwin’s proposed slow development of variation, the evidence supports a vast amount of rapid differentiation in the past, degenerating into only trivial variations today—a far better fit to Kirschner–Gerhart theory and the young history. DO MUTATIONS THAT CONFER RESISTANCE TO ANTIBIOTICS,POISONS, ETC PROVE EVOLUTION Anthrax and antibiotics: Is evolution relevant? by Dr Jonathan Sarfati 15 November 2001; updated 8 April 2005 After the terrorist attack on 11 September, many people fear a new danger—biological warfare in the form ofanthrax. Perhaps understandably, many Americans are taking antibiotics such as Cipro (ciprofloxacin) as a preventative measure. Data from the pharmaceutical tracking company NDCHealth of Atlanta, Georgia, show that almost 63,000 more Cipro prescriptions have been issued in the third week of October alone than for the entire previous year. However, this has caused some concern in the medical profession that antibiotic overuse could result in antibiotic resistance in many types of bacteria. Not surprisingly, the humanist-dominated secular media has used phrases such as ‘Bacteria evolve drug resistance very quickly’. Fortunately, in the current round of articles, I haven’t seen repeated the hysterical outburst of one particular evolutionary propagandist who claimed that people will die because of creationists, because they will allegedly fail to understand this vital fact of evolution of drug resistance.We have covered antibiotic resistance in many articles on this website. So here it will suffice to summarize the main issues to enable people to assess critically any articles on this current scare. First some principles:Watch for equivocation, i.e. using the same term in different ways in the same article. It’s very common for evolutionary propagandists to define evolution as (1) simply ‘change in a population over time’, as well as (2) the idea that all life came from a single cell, which itself came from a chemical soup. Then they produce examples of ‘evolution’ (1) and use this to prove evolution (2), and then claim that the young age model is wrong! However the model does imply that organisms change over time—but these changes would always involve sorting or loss of already existing (created) genetic information, never the gain of new information. But evolution (2) requires the gain of new information. Even if information losing (or neutral) processes could continue for billions of years, they would never add up to a gain of information. Rather, to support evolution (2), evolutionists must demonstrate changes that increase information. If this theory were true, there should be plenty of examples, but we have yet to observe even one. Since evolution (2) is the only issue at stake in the creation/evolution controversy, we advise against referring to any mere change as ‘evolution’—not even ‘micro-evolution’—and reserving the term ‘evolution’ for (2). Natural selection is not evolution. This merely weeds out organisms and the information they contain; it doesn’t generate new information. The creationist Edward Blyth discussed natural selection 25 years before Darwin, but recognized that it was aconservative, not a creative, force. Mutations are not evolution. They are copying mistakes in the genes. No mutation is known to increase information content; every known mutation has either decreased information content or was informationally neutral. This applies even to the rare examples of beneficial mutations. To apply these principles to antibiotic resistance, there are several ways that germs can acquire resistance to drugs, none of which have anything to do with evolution from goo to you via the zoo: Natural selection: the drugs wipe out all the non-resistant germs, so the most resistant germs survive and multiply. This leads to a whole population that’s resistant to antibiotics. This is not evolution because the resistance already existed in the population. Despite this, the PBS Evolution propaganda series used selection of pre-existing antibiotic resistance in tuberculosis germs as a major ‘proof’. In fact, some bacteria revived from corpses frozen before the development of antibiotics have shown resistance. Selection for resistant bacteria is a real danger when a patient fails to complete a prescribed course of antibiotics (60 days for Cipro)—i.e. stops taking the drug when the symptoms ease, which just means that most germs have been destroyed. The remnants require the final doses of antibiotic to finish them off, but if the treatment stops, they are free to multiply. This time the drug is far less effective, since the remnant population will tend to be the more resistant ones.This problem of selection of resistant varieties applies not only to the targeted germ, but all the other types affected by the same antibiotic. This is the main reason that the medical profession is concerned with people taking Cipro for a few days because of the anthrax scare. Indeed the over-use of Cipro could result in many germs that are resistant to this drug, so the concern is very well founded. Antibiotics as a preventative measure are warranted only where there’s evidence that people were in a ‘breathing zone’ of the deadly airborne anthrax spores, not for the milder skin form of anthrax.Sometimes bacteria can pass on information to other bacteria, via loops of DNA called plasmids. Sometimes plasmids contain information for antibiotic
resistance. But here too, the information already existed, so this is not evolution.Information-losing mutations can confer resistance. Such mutations are often harmful in an ‘ordinary’ environment without antibiotics. It is well documented that many ‘superbugs’ are really ‘superwimps’ for this reason—see Superbugs not super after all . Also, some sorts of information-losing mutations evidently cause HIV resistance to antivirals, because the ‘wild’ types easily out-compete the resistant types when the drugs are removed. Despite this, this was promoted as another ‘proof’ of evolution by the PBS series.So, how can an information loss confer resistance? Here are some observed mechanisms: A pump in the cell wall takes in the antibiotic. A mutation disabling this pump will prevent the bacterium pumping in its own executioner. But in the wild, a bacterium with a disabled pump will be less fit than other bacteria because the pump also brings nutrients, etc., into the cell.A control gene regulates the production of an enzyme that destroys the antibiotic, e.g. penicillinase which destroys penicillin. A mutation disabling this gene destroys the regulation of the production, so far more enzyme is produced. Such a bacterium can cope with more antibiotic than others can, but in the wild, it would be less fit than normal because it’s wasting valuable resources producing more enzyme than is needed.An enzyme is highly specialized to break down one specific type of chemical very well, and hardly affect other chemicals. A mutation could reduce its specificity, i.e. it no longer does its main job so well, and affects other chemicals to some extent too. Normally, a biological system with such a mutation would not function as well, and reduced specificity is reduced information by definition. But sometimes the other affected chemicals happen to be antibiotics, so this type of mutation confers resistance. See further discussion in this refutation of a critic and Not By Chance (top right), ch. 5.The antibiotic streptomycin works by attaching onto a precisely matching site on the surface of a bacterium’s ribosome, where decoding of DNA information to proteins occurs. When the streptomycin attaches, it stops this machinery from producing the right proteins, and the bacterium dies. Resistance to the drug can be caused by an information-losing mutation that degrades the surface of a bacterium’s ribosome, which reduces the binding ability of the drug to the ribosome, preventing it from ruining the protein manufacturing machinery.More detail on information-losing resistance-increasing mutations can be found in the article Is bacterial resistance to antibiotics an appropriate example of evolutionary change?These principles should be enough to demonstrate that these latest claims about bacteria ‘evolving’ resistance are not a threat to the model. Despite all this, many evolutionists crow about antibiotic resistance as an amazing ‘prediction’ of evolution. Even aside from the above points, this is revisionist history. Historically, antibiotic resistance first took the medical profession by surprise—even as late as 1969, experts stated that ‘infectious diseases were a thing of the past’. I.e. antibiotic resistance was hardly a ‘prediction’ of evolution, but is really a phenomenon explained ‘after the fact’ by evolutionary language. But as shown, the young age model explains it better. Poison-resistant tomcods and the meaning of ‘evolution’ Published: 19 May 2011(GMT+10) The Atlantic tomcod only benefits from its information-losing mutation in the heavily polluted Hudson River. In response to the article on the mutated tomcod fish in the polluted Hudson River, evolution-defender Steven L. wrote in claiming that it contained “blatant mistakes” and gave substantial detail and detailed reasons. We first publish his email intact, then again with a point by point interspersed response by the article author, Dr Carl Wieland of CMIAustralia. Steven wrote: Your article on the evolution of the Tomcod possesses a few blatant mistakes. First of all, it assumes that mutations are some form of “damage”. That is not the case. Mutations are a fact of life (and are necessary for evolution to occur), and the vast majority of mutations are strictly neutral—that is, they are not expressed, or their expression has no effect on the life of the organism. Secondly, the article posits that information gain is a necessity of evolution. This is false—evolution is simply change, whether it be through the addition, deletion, or alteration of base pairs. While we tend to see a net gain of information as demonstrated by the increasing complexity of the fossil record over time, it is not a requirement. Third, the article references the deletion of the base pairs in the tomcod as a sort of “downhill damage”, but it is not taking the environment in to account with this assessment. In their current environment, the mutation is anything but. The overall cost/benefit analysis of a mutation has to be made within the context of the environment in which it occurs. Fourth, the article states as fact that the mutation happened in one generation. This is not necessarily the case, but the author has assumed it to be true and has stated as such without any evidence to back his position. Because the mutation also exists occasionally in the non-poisoned populations elsewhere, it suggests that the mutation already existed in the overall population of the animal. It is a similar situation to the 1952 Lederberg experiment. Further still, the continued existence of the mutation in roughly 5% of the population from uncontaminated waters shows that the relative cost of the mutation isn’t so large as to make it a major hindrance to reproductive success. Like any other healthy, genetically diverse population, we see a variety of different genes existing in greater or lesser numbers within the population. In summary, you should strive to have a bit more accuracy in your articles. Carl Wieland responds: Thank you for your email. You wrote: Your article on the evolution of the Tomcod possesses a few blatant mistakes. Well, it’s important to know of any mistakes, even in a brief item responding to a news article meant for the layperson; but let’s see how accurate this confident assertion of yours is. I would ask you to try to lay aside your presuppositions and [try] thinking the matter through carefully for yourself, because there is a lot at stake. My responses are interspersed with your email below.First though, note that the article was not on the ‘evolution’ of the tomcod, but on how it adapted to pollution. When people hear the word “evolution”, they assume it means the same sort of change as would, given time, turn protozoa into people, etc. The article was about demonstrating that this is an inappropriate description of what happened. First of all, it assumes that mutations are some form of “damage”. That is not the case. The article actually used the word “damage” in the specific context of those mutations that cause antibiotic resistance, and gave one such example of exactly that—damage to a functioning mechanism. It then indicated that mutations mostly damage existing structures. So that is not the same as your representation of the article’s claims.
Mutations are a fact of life Agreed. In this fallen world, such genetic copying mistake are exactly that—mistakes. What do we observe in the process of heredity in living things, if not a highly complex mechanism which functions to produce a letter-by-letter copy of the genetic information (DNA). Even those who deny purpose (teleology) in living things overall would have to agree that this machinery’s role is to produce such a copy. It even incorporates error-correcting and proof-reading machinery. Most mutations occur when, despite this, there is a deviation from an exact copy. Not surprisingly, then, the biological machinery that is coded for on the DNA that undergoes a mutation is generally not likely to result in an improvement, but the opposite— for the same reason that a random change in a software code that has a specific function is very, very unlikely to generate an improvement in that function, but more likely the opposite. So to say that mutations will mostly ‘damage’ things makes sense even at first glance—but see more shortly. The argument is one from probability; there are many more ways to break things than make them. (and are necessary for evolution to occur), You are right that ultimately mutations are the ‘only game in town’ for evolutionists as a theoretical source for the ‘raw material’ for ‘nature’ to ‘select from’. Natural selection (NS) in and of itself culls genes, gets rid of information. See Muddy waters: clarifying the confusion over natural selection. If copying were perfect, all the selection in the world could never generate any real evolutionary novelties, being restricted to differing combinations of what is already there. But the big question then is: are mutations capable of doing what they are supposed to have done over billions of years, i.e. generated all the information needed for all the biological machinery in all organisms on Earth? For those whose kneejerk, even socially conditioned, answer is ‘yes’, it’s interesting that the examples in textbooks of ‘evolution happening’ are either examples where there is not even demonstrable mutation involved (i.e. the selection which led to adaptation was from existing variety in the population, and involved a loss of genes or thinning of the gene pool). Or else, where a mutation was involved, the mutation was a definite loss or degradation of information. For example, wingless beetles on windy islands. and the vast majority of mutations are strictly neutral—that is, they are not expressed, or their expression has no effect on the life of the organism. In fact, it is nowadays more accurate to say that the vast majority of mutations are near-neutral; i.e. they are deleterious, but the effect is so small that it is to all intents and purposes just as you put it, that it has no discernible external effect and thus is transparent to selection (which simply means that NS has no way of eliminating these near-neutral mutations). This is actually a severe detriment to evolutionary theory, as former Cornell University (and still courtesy) professor, and genetic engineering pioneer Dr John Sanford has shown in his bookGenetic Entropy and the Mystery of the Genome (a good introduction to the subject is the DVD of an excellent presentation he gave on the subject to a conference involving both lay and professional folk.) To explain: the latest figures show that these near-neutral mutations are accumulating so rapidly that our human genome is actually facing a very serious decline, a situation worsening with every generation. Their nearneutrality is actually a detriment, precisely because of what was stated above, namely that NS can’t get rid of them individually fast enough. But their combined, cumulative effect is very deleterious, since they are so numerous. See this interview with Sanford for a foretaste of what the other items go into in more detail. It was this that helped bring Sanford around from his former position as an evolutionist to being not only a creationist, but a convinced believer in recent creation. The human genome simply can’t have been around for more than a few thousands of years at most, in order to have avoided what is known as ‘error catastrophe’. This reality has been backed up by sophisticated supercomputer modelling of the mutation-selection process (see http://mendelsaccountant.info/). Secondly, the article posits that information gain is a necessity of evolution. This is false—evolution is simply change, whether it be through the addition, deletion, or alteration of base pairs. While we tend to see a net gain of information as demonstrated by the increasing complexity of the fossil record over time, it is not a requirement. With respect, the last sentence of the above paragraph reveals the flaw in the reasoning of the entire paragraph. If we define evolution as ‘genetic change’, then that change can be in any direction. But that would be a self-serving, question-begging definition, since a Creation-Fall model would also expect ‘genetic change’, but in a net downhill direction. To put it very simply—an evolution model would expect change happening in all directions, so downhill change per se does not falsify the idea of evolution by any means, nor was that claimed in the article. However, we need to remember that I’m defining ‘evolution’ in the way most people understand it—and the way Darwin proposed, not mere ‘genetic change’, but, as the article stated, a process that has allegedly turned microbes into magnolias, mosquitoes and microbiologists. So to demonstrate that a particular proposed mechanism (neo-Darwinism) is able to produce genetic change adds no credibility to that mechanism [as a driver of evolution, and a demonstration of ‘evolution happening’] if it seems to mostly, if not exclusively, lead to ‘downhill’ change.To focus once again on your last sentence—a “net gain of information” is not what “we tend to see”. It is, however, what you must believe has occurred, since you believe that a microbe with ~0.5 million base pairs on its DNA did eventually turn into a microbiologist with 3,000 million base pairs. We can also think of the traits that humans have that microbes don’t: muscle, skeleton, blood vessels, nerves, skin, hair, etc. These traits require new specifications to be added to the DNA (a minimalist microbe has a few hundred proteins, but humans can make over 100,000 different ones). So by definition, there must have been a huge “net gain of information”. Which means that gain of information has to be a major part of the alleged evolutionary process (especially since it has to overcome the overwhelming tendency of mutations to destroy the information). A businessman making lots of $10 sales cannot make a net profit on all of them combined unless most of them make an actual profit. Do you see the point? By you conceding, in effect, that a “net gain” had to have happened to turn microbes into mudskippers, you are reinforcing the fact that there needs to have been a lot of actual gain by mutation. And in fact, if we saw lots of information-gaining mutations in the process of building new structures and functions all around us, it would be legitimate for an evolutionist to take this as a positive and strong support for his proposal. However, if virtually all known mutations associated with adaptive change are in this opposite direction, then wouldn’t you agree that it is misleading to use such adaptive change as an example of ‘evolution happening’? That was the point of the Tomcod article. Indeed, your definition of evolution as merely ‘change’ can be shown to be an extraordinarily lame one, since it makes all and any genetic change ‘evolution’. So if every type of genetic change in the world were to be such as to lead to extinction, by your definition that would still be ‘evolution’. Third, the article references the deletion of the base pairs in the tomcod as a sort of “downhill damage”, but it is not taking the environment in to account with this assessment. First, a description like ‘downhill damage’ is never going to be a rigorous statement, but it makes a valid point nonetheless, and second, the article most definitely took the environment into account. To clarify: as our article on wingless beetles points out, a defect can have a survival advantage in a particular environment. A beetle having a mutation that in its offspring destroys the ability to produce normal wings is better able to survive and have offspring on a windy island, as it is less likely to be blown into the sea and drown. So in time, all those beetles on that island are likely to be of the wingless variety. But
this shows us a complex information-transfer and construction system (the machinery by which the genetic information in beetles gives rise to wings, with their specific function able to be defined in engineering terms) and how this system is then subject to corruption, loss of function, etc. This can hardly of itself give any clues as to how such a process of random change could have led to that complex system in the first place. Sheep with crippled legs might be better able to survive because they are less likely to jump over a fence into the jaws of a hungry dingo, so in that environment, once again, a defect is a survival advantage, but is still a clear defect. The neo-Darwinian mechanism could gain some credibility if Darwinists could point to hundreds of mutations (among the vast numbers occurring constantly) that can be seen to be building structures, adding functional complexity, etc. (in a complex world, one would expect the occasional tiny bit of information to arise by chance, and that may have occurred with bacterial ability to digest nylon, though note the careful analysis in our article on this). But that is simply not what happens in the real world. In their current environment, the mutation is anything but. The overall cost/benefit analysis of a mutation has to be made within the context of the environment in which it occurs. Of course. That’s simple population genetics, which is quite independent of the truth or otherwise of the neo-Darwinian postulate. The issue still remains this: there has to have been a massive net gain of information if ‘evolution’ has actually happened in history. Such a net gain requires substantial amounts of informationally ‘uphill’ change, no matter how much downwards or sideways movement may have occurred along the way.It is the extreme paucity of any informationally uphill changes by mutation (virtual absence), which is actually expected on probabilistic grounds, that justifies extreme scepticism about neo-Darwinism as a credible mechanism for any ‘evolution’, and to call downhill change “evolution” is only convincing if there is already a prior belief that evolution has happened. Fourth, the article states as fact that the mutation happened in one generation. This is not necessarily the case, but the author has assumed it to be true and has stated as such without any evidence to back his position. I find it hard to see why it’s not obvious that mutation, by definition, always happens in one generation. It may take time to spread through the population, but a mutation is a one-time event (though it can sometimes occur more than once, i.e. the same mistake can just happen to be repeated in another individual). The relevant sentence in the article started with “Mutation happens in one generation,” which by both the absence of either ‘the’ or ‘this’ in front of it, as well as by the use of the present continuous tense should, I would have thought, made it clear that this was a statement about mutation in general, and not just about this mutation. It then went on to talk about the expected rapidity of spread of “the mutated gene” after that initial event (obviously now referring to the tomcod one in question, i.e. in this “poison-rich environment”). It specifically said that this took “just a few decades”. Since this is obviously a lot more than one generation, it’s obvious that your comment here substantially misrepresents the article. I presume you have simply misunderstood. Because the mutation also exists occasionally in the non-poisoned populations elsewhere, it suggests that the mutation already existed in the overall population of the animal. It is a similar situation to the 1952 Lederberg experiment. I have no problem with the possibility that the same mutation may exist in non-poison-exposed populations, though note that in the case of antibiotic resistance to penicillin studied by Lederberg in his classic experiment, it was not necessarily the case that the resistance that was already in the population had itself arisen by mutation, i.e. the experiment itself did not demonstrate that. But my question to you is: Why would that affect any point in the article, and in this reply, in the slightest? I could have just as easily said (and maybe should have, for clarity) that the mutation arose at some point in one generation and then took only a few decades to spread in that poison-rich environment. But see my next point for what may be a better explanation for the low level of the mutation “in the non-poisoned populations elsewhere”. Further still, the continued existence of the mutation in roughly 5% of the population from uncontaminated waters shows that the relative cost of the mutation isn’t so large as to make it a major hindrance to reproductive success. That’s possible, but given the comments about the disadvantages to the organism that were reported from this mutation, it is not likely. A major point you seem to have overlooked when referring to the 5% from my article is that these waters were “nearby”. So that allows for a ‘supply’ of mutated fish to these less contaminated waters (which may in any case have previously been contaminated, but cleaned up relatively recently, for all I know) from the Hudson where the gene is kept at a high frequency. Thus, as the Hudson contamination presumably declines from legislative efforts, etc., one would expect a decline of the gene’s frequency not only in the Hudson, but also to much lower levels than the current 5% in nearby waters. A gene with such effects as mentioned in the article would be expected to approach zero frequency in due course in waters with no such poisons and no nearby ‘feeder’ source of this mutation. Like any other healthy, genetically diverse population, we see a variety of different genes existing in greater or lesser numbers within the population. This benign-sounding description makes it sounds as if these fish are ‘as healthy as any other’. It ignores the fact that the researchers themselves concede that the fish carrying this mutation are not as ‘healthy’ as those without it—to use their words again, these fish have “suffered in other ways”. In summary, you should strive to have a bit more accuracy in your articles. We strive for accuracy at all times, and are grateful when people point out perceived inaccuracies, as sometimes they are correct, of course. It seems though that in this case a commitment to evolution as ‘established fact’ may have detracted from what I think might otherwise have been a careful reading of the article.I hope that you will understand a little more where the creationist argument is coming from via this exchange, including following the links provided (and those provided on those linked articles). Superbugs not super after all by Carl Wieland After over 12 years as a medical practitioner, I suddenly found myself an avid consumer, rather than a provider, of medical care. Involved in a serious road accident in 1986, I spent many months in hospital, including weeks in an intensive care unit. While in intensive care, I became infected with one of the varieties of so-called ‘supergerms’, which are the scourge of modern hospitals. These are strains of bacteria which are resistant to almost every (and in some cases every) type of antibiotic known to man.Several others in the same unit with me died as a result of infection by the same bacterial strain. The germs overwhelmed their immune systems and invaded their bloodstream, untouched by the most expensive and sophisticated antibiotics available.This ‘supergerm’ problem 1 is an increasingly serious concern in Western countries. It strikes precisely those hospitals which are more ‘high-tech’, and handle more serious illnesses. Applying more disinfectant is not the answer; some strains of germs have actually been found thriving in bottles of hospital disinfectant! The more antibacterial chemical ‘weapons’ are being used, the more bacteria are becoming resistant to them.The reality of increasing bacterial resistance seems at first to be an obvious example of onwards and upwards evolution. But the facts, when carefully examined, show otherwise. Natural selection, but not evolution
Evolution is basically the belief that everything has made itself—that natural processes (over millions of years, without miraculous, divine input of intelligence) have created an increasingly complex array of creatures. According to evolution, there was once a time when none of the creatures in the world had lungs. This means that there was no genetic information (the ‘blueprint’ for living things, carried on the molecule DNA) for lungs—anywhere. Then, at a later time, ‘lung information’ arose and was added to the world, but no ‘feather information’ as yet—feathers evolved later.In other words, for every feature which arises by evolution, there would need to be new genetic information added to the total information in the biosphere (i.e., all the information in all creatures on earth). Some features could be lost subsequently, of course, so there will not always be a gain, but if microbes turned into magpies, maple trees and musicians, there must have been a massive net increase in information. This is not just any jumble of chemical sequences, but meaningful information, since it codes for complex structures which have purposeful functions.So if new information, new functional complexity, can be shown to be arising by itself where previously there was none, this would give some credibility to the idea of molecules-to-man evolution, although it would not strictly prove that it had occurred. However, it can be shown that in every situation where populations of living things change, they do so without increase (and often with a decrease) of information. Thus, it is completely illegitimate for anyone to claim that such changes show ‘evolution happening’. Let’s look at what is known about how the ‘superbugs’ became resistant, and ask—did any new structures or functions arise in the process (which is another way of asking whether there was any evidence of evolution)?There are a number of different ways in which germs can become resistant to these poisons. A ‘superbug’ is, by definition, resistant to many different antibiotics. It may have become resistant to antibiotic A in one way, to antibiotic B in a completely different way, and to antibiotic C in another way again. So if we look at all the known ways of resistance arising in a population of germs, we will see if any of them are uphill, information-adding processes. 1. Some germs already had the resistance. If out of a million bacteria, five already have a feature which makes them resistant (however that arose) to, say, penicillin, then soaking them in penicillin will kill all of them except for the five. Now the body’s natural defences will often ‘mop up’ such a small population before it can multiply and cause harm, so resistance will not become a problem. However, if that doesn’t happen, then those five germs can multiply, and their offspring will obviously also be resistant. So within a short time, there will be millions of germs resistant to penicillin. Notice that: (i) This is why multiple resistance to major antibiotics is more common in hospitals which treat more serious conditions— these are the hospitals which will frequently be using the sophisticated, expensive ‘heavy artillery’ antibiotics, so this sort of ‘natural selection’ will happen more often. (ii) In this kind of instance, the information to resist the antibiotic was already there in the bacterial population—it did not arise by itself, or in response to the antibiotic. That some germs were already resistant to man-made antibiotics before these were invented is common knowledge to microbiologists. Soil samples from villages where modern antibiotics had never been used show that some of the germs are already resistant to drugs like methicillin which have never existed in nature. Bacteria revived from the frozen intestines of explorers who died in polar expeditions carried resistance to several modern antibiotics, which had not been invented when the explorers died.2 2. Some germs directly transfer their resistance to others. In an amazing process, the closest thing to sex in bacteria, one germ inserts a tiny tube into another, and a little loop of DNA called a ‘plasmid’ transfers from one to another. This sort of gene transfer, which can obviously pass on information for resistance to a drug, can even happen between different species of bacteria.Notice, again, that the information for the resistance must already exist in nature before it can be passed on. There is no evidence of anything totally new arising which was not there before. This is information transfer, not information creation.So far, we have dealt with situations in which resistance was obviously already there. Evolutionists would claim, of course, that such resistance evolved originally in the (unobservable) past. However, if observed changes in the present do not show us new information, what support is there for the idea that such information arose in the past? The mechanism that is put forward for this past evolution is invariably mutation—a copying mistake, an accidental change in the DNA code passed on to the offspring. So that brings us to the final way in which bacteria can become resistant. 3. Some germs become resistant through mutation. Interestingly, where this happens, there is no clearcut evidence of information arising. All such mutations appear to be losses of information, degenerative changes. For example, loss of a control gene may enhance resistance to penicillin.3Some antibiotics need to be taken into the bacterium to do their work. There are sophisticated chemical pumps in bacteria which can actively pump nutrients from the outside through the cell wall into the germ’s interior. Those germs which do this efficiently, when in the presence of one of these antibiotics, will therefore efficiently pump into themselves their own executioner.However, what if one of these bacteria inherits a defective gene, by way of a DNA copying mistake (mutation) which will interfere with the efficiency of this chemical pumping mechanism? Although this bacterium will not be as good at surviving in normal circumstances, this defect actually gives it a survival advantage in the presence of the man-made poison.4 Once again, we see that information has been lost/corrupted, not gained. Superwimps It is precisely because the mutations which give rise to resistance are in some form or another defects, that so-called supergerms are not really ‘super’ at all—they are actually rather ‘wimpy’ compared to their close cousins. When I was finally discharged from hospital, I still had a strain of supergerm colonizing my body. Nothing had been able to get rid of it, after months in hospital. However, I was told that all I had to do on going home was to ‘get outdoors a lot, occasionally even roll in the dirt, and wait.’ In less than two weeks of this advice, the supergerms were gone. Why? The reason is that supergerms are actually defective in other ways, as explained. Therefore, when they are forced to compete with the ordinary bacteria which normally thrive on our skin, they do not have a chance. They thrive in hospital because all the antibiotics and antiseptics being used there keep wiping out the ordinary bacteria which would normally outcompete, wipe out and otherwise keep in check these ‘superwimps’. 5If they are ‘weaker’, then why do they cause so much death and misery in hospitals? These bacteria are not more aggressive than their colleagues, it is only that doctors have less power to stop them. Also, those environments which will tend to ‘select’ such resistant germs, like intensive care units, are precisely the places where there will be critically injured people, physically weakened and often with open wounds.This is why more than one microbiologist concerned about these super-infections has mused (only partly tongue in cheek) that the best thing to happen in major hospitals might be to dump truckloads of germ-laden dirt into the corridors, rather than keep on applying more and more chemicals in a never-ending ‘arms race’ against the bacteria. In other words, stop using the antibiotics (which of course is hardly feasible), and all this ‘evolution’ will reverse itself, as the bacterial populations shift back again to favour the more hardy, less resistant varieties. Summary and Conclusion 1. ‘Supergerms’ are actually not ‘super’ at all. They are generally less hardy, and less fit to survive outside of the special conditions in hospitals.
2. There are many instances in which germs become resistant by simple selection of resistance which already existed (including that ‘imported’ from other bacteria). 3. Where a mutational defect causes resistance, the survival advantage is almost always caused by a loss of information. In no case is there any evidence of an information-adding, ‘uphill’ change. 4. ‘Supergerms’ give no evidence to sustain the claim that living things evolved from simple to complex, by adding information progressively over millions of years. Postscript Death, suffering and disease (including infection) are part of the curse which came upon a once-perfect world through the rebellion of our original ancestor, Adam, against his Maker.Bacteria actually provide evidence against evolution. Bacterial populations multiply at incredibly high rates. In only a matter of a few years, bacteria can go through a massive number of generations, equivalent to millions of years in human terms. Therefore, since we see mutation and natural selection in bacterial populations happening all the time, we should see tremendous amounts of real evolution happening. However, the bacteria we have with us today are essentially the same as those described by Robert Koch a century ago. In fact, there are bacteria found fossilised in rock layers, claimed by evolutionists to be millions of years old, which as far as one can tell are the same as bacteria living today.The famous French biologist Pièrre Grassé, who held the chair of evolution at the Sorbonne for many years, admitted that mutations in bacteria simply showed shifts back and forth around a mean, but no net effect. Overall, he said, ‘mutations do not produce any kind of evolution.’6 Patterns of change over time: organophosphorus resistance in the Australian sheep blowfly, Lucilia cuprina by Jean K. Lightner A deeper understanding of patterns of change in creatures over time is necessary to advance the creationary view of biology. While much research has been done at a molecular level with bacteria, there is a need to evaluate changes in sexually reproducing organisms. The development of insecticide resistance in insect populations has been studied in considerable detail. A literature review focusing on insecticide resistance inLucilia cuprina, the Australian sheep blowfly, was conducted. While the development of resistance to malathion can be easily explained by natural selection, resistance to diazinon is not so easily explained. It is suggested here that diazinon resistance and multiple resistance from gene duplication may be the result of designed mechanisms that allow for adaptation in created life. It is pointed out that evolutionists are increasingly discussing genetic and metabolic systems within the context of computer programming. A deeper understanding of the underlying mechanisms involved in genetic changes may explain the considerable variation within created kinds (baramins) and the ability of these creatures to adapt to changing environments. In other words, we can gain a deeper understanding about the world. Figure 1. Lucilia cuprina, the Australian sheep blowfly, is an introduced pest that costs the Australian wool industry over $160 million a year. Eggs laid on living sheep hatch and the maggots eat through the animal’s flesh in what is called flystrike. To further develop a creationist view of biology, it is necessary to more fully understand patterns of change within creatures and the likely role of these types of changes during history. Unfortunately, since evolution is sometimes defined as ‘change through time’, creationary apologists have sometimes responded with vague arguments that creatures don’t really change much. It is not so much the amount (very small genetic changes can result in large phenotypic changes) as the pattern of the changes that is important. The evolutionary model predicts an overall upward trend from chance processes to account for the origin and subsequent major restructuring of well integrated morphology and biochemical pathways. This trend should be obvious since this model claims to be able to account for the diversity of extant kingdoms and phyla. The young age model may include providential changes or degenerative changes (since the world was cursed as a result of mankind’s rebellion2 ), but not the overall ‘creative’ changes by purely random processes that characterize the evolutionary model.Considerable research has been done describing changes in different life forms. Much research has been done at the molecular level in bacteria since they are so convenient to study in the laboratory. It is interesting that researchers in this field who are not part of the creation or intelligent design movements have pointed out that many changes in the genetic code appear as a result of far more complex mechanisms than just random, chance processes. 3 For example, when bacteria are starved, directed mutations may occur to alleviate the stress. It is unclear if similar directed mutations occur in sexually reproducing life forms. 4 One issue is that there must be a mechanism for introducing these mutations into the germline. Insects as models for studying adaptive genetic change in sexually reproducing organisms Insects cause tremendous damage to crops and livestock. Numerous insecticides have been developed to control or eliminate these pests. Much to the dismay of those involved in agriculture, insect populations regularly develop resistance to insecticides. Due to its economic impact on agriculture, this resistance has been fairly well studied and provides a logical place to look for patterns of change in sexually reproducing animals. Emphasis will be placed here on a specific pest, Lucilia cuprina, the Australian sheep blowfly (figure 1).There are several popular organophosphorus insecticides (OPs) used to control ectoparasites in sheep. These poisons target acetylcholinesterase, a product of the Ace gene. Normally this enzyme breaks down acetylcholine after it has been used to transmit nerve impulses (figure 2). The OPs inactivate acetylcholinesterase so it cannot break down acetylcholine. This results in a build up of acetylcholine at the nerve synapse and a hyperexcited central nervous system which kills the insect. While some insects (e.g. Drosophila melanogaster5and Musca domestica6 ) have developed OP resistance through mutations in the Ace gene, L. cuprina has not, despite the fact that it has a highly homologous gene in which ‘All major structural and functional features of the protein are conserved.’7 Further study indicates that the product of the Ace gene in L. cuprina does not interact as readily with OPs as does the product of another gene (αE7). The reverse situation occurs in Drosophila. Malathion resistance and natural selection Malathion is an OP often used to control lice in sheep. L. cuprina has developed resistance to this pesticide through a point mutation in theLcαE7 gene which results in a Trp251Leu substitution. The LcαE7 (sometimes known as Rop-1 or Rmal) gene normally produces a carboxylesterase, E3. The mutation decreases the carboxylesterase activity while improving the enzyme’s ability to break down dimethyl OPs, particularly malathion.8 In an attempt to determine if this variant was present prior to selection by OP use, pinned specimens were sampled. It was found that this particular mutation was fairly
widespread prior to the introduction of OPs.9 Thus, the development of resistant L. cuprinapopulations appears to be a classic case of natural selection. It is not that the data precludes the possibility of directed mutations playing a role, but such an explanation appears unnecessary. Diazinon resistance Diazinon is an OP that is used to directly control the sheep blowfly. Resistance to this OP is associated with a separate point mutation in theLcαE7 gene that results in a Gly137Asp substitution. In this case the carboxylesterase activity is abolished and a new OP hydrolase activity is conferred on the enzyme, making it more effective against diethyl OPs such as diazinon.10 Initially this was associated with significant asymmetry and fitness costs in the absence of the insecticide. Eventually, a mutation appeared in a modifier gene which ameliorated these deleterious effects. 11 Since diazinon is used widely in sheep producing countries such as Australia, this mutation is present in the majority ofL. cuprina sampled in these areas. However, this polymorphism has not been detected in any of the pinned specimens collected prior to OP use. 9The development of diazinon resistance has been cited as evidence for evolution. 12 Clearly this research has advanced our understanding of the molecular mechanisms of adaptation, but it sheds no light on the origin of molecular systems. Genetic changes which result in a shift of an enzyme’s substrate hardly explain the origin of the gene for the enzyme. 13There are still many unanswered questions. For example, it could be argued that diazinon resistance was present in the population prior to the use of this OP, but was not detected due to low frequency in the population and the small sample size of pinned specimens. However, if this is true, it seems odd that natural selection would not have effectively eliminated it given the significant fitness costs associated with the loss of carboxylesterase activity. Conversely, it could also be argued that both the appearance of the resistant mutation and of the subsequent modifier mutation were the result of directed mutations resulting from the selection pressure. Interestingly, the same mutation conferring diazinon resistance has been found in a sister species, L. sericata,9 and in the housefly M. domestica.14 This has been interpreted as ‘suggesting convergent evolution around a finite set of resistance options.’ 9 Evolutionists have yet to provide credible explanation of how molecular systems that putatively originated by random, chance processes come equipped with ‘options’ that allow for adaptation. It appears that evolutionists generally accept that this mutation arose independently in separate species. The fortuitous timing of the appearance of this mutation that corresponds with OP use suggests something more than just random processes at work to allow for such dramatic adaptation. Gene duplications No variants have been found where both mutations occur together within the same gene. Moreover, it is predicted that if both mutations existed within a single gene, it would not confer effective resistance against both these OPs. This is because effective malathion resistance appears to require the presence of some carboxylesterase activity, and the mutation which confers diazinon resistance abolishes this.15However some isogenic strains of L. cuprina are resistant to these two OPs as a result of gene duplication. Intriguingly, three different gene duplications were identified and each involved a resistant form of the gene. No gene duplications were identified with any of the various susceptible alleles.8 This suggests that gene duplication may be a designed adaptive mechanism, rather than just an accidental occurrence as the standard evolutionary paradigm predicts.Recently, there have been articles in the scientific literature that seem to confirm this idea. For example, in humans differences in the copy number of genes are a significant source of variation. 16 Researchers examining gene duplications in fungal genomes concluded,‘ … that gene duplication and loss is highly constrained by the functional properties and interacting partners of genes. In particular, stress-related genes exhibit many duplications and losses, whereas growth-related genes show selection against such changes. … By characterizing the functional fate of duplicate genes we show that duplicated genes rarely diverge with respect to biochemical function, but typically diverge with respect to regulatory control. Surprisingly, paralogous modules of genes rarely arise, even after whole-genome duplication. Rather, gene duplication may drive the modularization of functional networks through specialization, thereby disentangling cellular systems.’17 Laboratory development of resistance Figure 2. Acetylcholine is used to transmit nerve impulses. Acetylcholinesterase normally breaks down acetylcholine so the signal doesn’t last indefinitely. Organophosphates bind acetylcholinesterase so it is unavailable resulting in a hyperexcited nervous system and, if the dose is high enough, death. At least one study has been done attempting to develop strains resistant to diazinon in the laboratory. Some of the blowfly males were mutagenized using ethyl methanesulfonate (EMS). When both susceptible and mutagenized strains were selected with a diazinon concentration that kills 100% of susceptible flies (0.0004% w/v), the LC100, no susceptible flies survived. Some of the mutagenized flies survived and appeared indistinguishable from natural populations carrying the LcαE7 resistant allele. In contrast, when susceptible and mutagenized strains were selected on low doses of diazinon (0.0001% w/v), there was no significant difference in the responses between strains. The insect populations developed a low level, polygenic resistance. The specific genes involved varied with each trial. However, none of these insects survived a challenge of diazinon at the LC100 concentration which discriminates between susceptible flies and heterozygotes for the LcαE7 resistant allele.18 It is intriguing that mutagenesis resulted in LcαE7 resistant phenotypes with selection above the LC100 , but not in selection significantly below this concentration. Perhaps some resistant insects were generated in both cases, but the selection with low levels of diazinon did not favour them significantly enough for that genotype to remain in the population. Alternatively, perhaps EMS did not directly generate the resistant allele, but instead affected the genetic stability which resulted in the resistant phenotype when significant pressure was applied.A study attempting to induce particular mutations in bacteria found that low exposure times to radiation that killed roughly half the population failed to produce the desired mutants. As the exposure time increased killing 93% of the population, some mutants were found. Further increasing the time until there was a 96–99% mortality left only the desired mutants. 19 In both the bacteria and diazinon resistance in blowflies, the mutations are costly in terms of loss of normal function. Thus from a creationary viewpoint, it is not surprising that these changes are generally resisted. The example in bacteria suggests that selecting diazinon mutants might be most effective
just below the LC100. It would be interesting to see if the mutation can be induced in susceptible flies under these circumstances without the aid of EMS. In any case, there are many questions waiting to be answered to gain a deeper understanding of how, when and why these changes occur. Evolving ideas of evolutionists The neo-Darwinian view of random mutations driving variability is increasingly seen by evolutionists as inadequate to account for observational data. Recent theories have been advanced including natural genetic engineering 3 and facilitated variation.20 Both these views encourage an understanding of genetic and metabolic systems within organisms in terms of computer programming. The properties of modularity, reusability and robustness presented in the theory of facilitated variation correlate with well thought out, good design patterns in computer engineering.21 These and several other properties are combined in a way which allows for genetic variation and adaptation.‘These special properties reduce the number of genetic changes needed for phenotypic change, increase the number of targets for regulatory change, reduce lethality, and increase genetic variation retained in the population. Although the core processes are constrained in their own change of function, they deconstrain regulatory change.’22The authors assume a naturalistic explanation for the origin of these properties; they never attempt to explain their origin. Nevertheless, many of these concepts may prove useful for creationists to explain the remarkable variation that occurs within created kinds (baramins) and the ability of creatures to adapt to changing environments. Conclusions Although the study of the development of insecticide resistance is often considered a topic in evolutionary biology, this type of research is essential for understanding the types of changes which occur in living things. The information derived from observations in this area are critical to further development of our understanding of the world. It is fascinating that evolutionists are increasingly describing living things in terms of programming. The notion that genetic changes are always from chance processes should be rejected by creationists. Instead, evaluation of conditions surrounding the appearance of particular changes can help elucidate what underlying mechanisms may be involved. Scientific research continues to reveal the amazing complexity and design of creatures as well as their astounding ability to overcome immense environmental challenges; facts inconsistent with naïve naturalistic explanations of the origin of life. This area holds great promise as a fertile field for creationary researchers. Creationist article ‘saved my favourite cow’ A Dr T.W. (his doctorate is not to do with medical or veterinary sciences) wrote saying : I was travelling in New Zealand and met a man (he was a farmer)who said that an article by CMI’s Carl Wieland about ‘superbugs’ [ Supergerms not super after all—Ed] saved his favourite cow. This cow apparently had mastitis and the vet had tried a whole range of antibiotics and nothing worked. [Mastitis is an inflammation of the mammary gland or udder, the part designed to suckle its calf. The bacteria normally enter through the teat opening —Ed] They tested to find a suitable antibiotic but could find nothing, he said. So the vet suggested they put the cow down. The farmer had just read Carl’s article which explained how superbugs (those which are resistant to many antibiotics) said that the superbugs were less able to compete with normal bacteria and he wondered where he could get normal bacteria. He got some dirty water from the ground with cow manure in it and he injected some of the liquid (filtered, I assume) into the cow’s udder. The vet was furious. But the mastitis cleared up and the cow survived. A few days later the cow got mastitis again but this time the normal antibiotics fixed it. The cow is still alive and well after several years. He told me that he was always intending to tell Carl about it if he had the chance. I thought you would like to know. The author of the article, Carl Wieland (who used to practice as a medical doctor) replies, along with a very important caution towards the end: Dear Dr T.W. Thank you for letting me know of that. It’s encouraging, of course, and given the way many evolutionists claim that their belief system, not creationism, gives rise to practical results, I can see how one might want to use it as an example of creationist principles at work in a practical setting. Is evolution really necessary for biology? The challenges one hears from many evolutionists about such matters are in any case mostly wrongheaded. See for example this feedback I wrote in 2002, or this section in the response to recent National Academy of Sciences evolutionary agitprop. Most medical and scientific advances, even in biology, have had little to do with evolution (see this feedback). We have also noted that evolutionary theory has held back science, e.g.: The notion of useless ‘vestigial organs’ has hindered discoveries of their important functions. This applies to the notion of ‘junk DNA’, a notion which one geneticist called the biggest mistake in the history of molecular biology; science belately discovered functions for at least 93% of our DNA. Conversely, creationists have predicted functions for this ‘junk’ for a long time, e.g. writing in 1994: ‘Creationists have long suspected that this “junk DNA” will turn out to have a function. In fact, junk DNA research is now a hot topic; not only are more functions being detected, but it is suspected that junk DNA is full of yet-to-be-discovered “intellectual riches”.’1 The faulty naturalism-motivated ‘big bang’ theory is held with such dogmatism that even secular cosmologists charge that fudge factors are required to prop it up. These include dark matter, dark energy and inflation. Conversely, the CMI speaker and physics professor Dr John Hartnett has proposed an alternative cosmology using Moshe Carmeli’s physical model. This explains many vexing problems in astrophysics without needing to fudge with dark matter or dark energy. The big bang is likewise unable to explain the Pioneer anomaly, yet CMI physicist Dr Russell Humphreys’ cosmological model does so. The faulty ‘dynamo theory’ of planetary magnetism, proposed to preserve the magnetic field for billions of years, led to hopeless predictions for the fields of Mercury, Uranus and Neptune. Conversely, Russell Humphreys proposed a creationist model that predicted the fields correctly, and which has been strongly supported by recent Messenger satellite measurements of Mercury’s field.
What happened with the cow’s superbugs? In this case of the cow, if one were to assume that the farmer’s ‘treatment’ actually caused the cure (and I’ll return to that question shortly), one could rightly say that it would not have been thought of without first demolishing the standard belief that superbugs really are ‘super’ (stronger, better), a belief which best fits the evolutionary notion.But the real facts about superbugs can still be held to by evolutionist ‘true believers’, i.e. fitted into their framework. Indeed, evolutionists didpromote a similar therapy to cure antiviral resistant HIV, which evolutionists crowed about, but of course it was also consistent with the creation model, as my colleague Dr Sarfati wrote: HIV resistance to drugs This episode claims that Darwin didn’t really see evolution in action, but now we do. Supposedly the HIV, the cause of AIDS, evolves resistance to drugs faster than we can make them. Because the virus can produce billions of copies per day, it can ‘evolve’ in minutes to hours. One researcher said that this rapid change would be a ‘surprise’ if we didn’t have the concept of evolution. There were also attempts to tug heartstrings, by portraying AIDS patients as ‘victims of evolution’.The major error in much evolutionary propaganda is equating natural selection with evolution. In reality, natural selection was discovered by creationists before Darwin, is an important part of the young age model, and is a culling rather than a creative force.First, we see the equivocation—HIV producing HIV is supposed to show that particles could turn into people; but they’re still HIV— they haven’t changed into something else. Second, in Episode 4, it’s made clear that the related phenomenon of antibiotic resistance in bacteria took the medical community by surprise—this means that it wasn’t a prediction of evolution, except after the fact. Third, they fail to demonstrate that new information is involved, and the next segment shows that the opposite is true:Veronica Miller of Goethe University in Germany experimented by ceasing all antiviral drug treatments to a patient. Then the few surviving original (‘wild’) types easily out-competed the vast numbers of resistant forms. She said this was a risk, because the wild types were also more dangerous, more efficient. The superior efficiency and reproductive success of the wild type implies that the others have acquired resistance due to a loss of information somewhere. This should not be surprising, because the same is true of many examples of antibiotic resistance in bacteria. E.g. the bacterium has an enzyme that usually has a useful purpose, but it also turns an antibiotic into a poison. So a mutation disabling this enzyme would render the antibiotic harmless. But this bacterium is still disabled, because the useful process the enzyme usually enables is now hindered, so it would be unable to compete in the wild with non-resistant ones. The information loss in both HIV and the bacterium is the opposite of what evolution requires. CMI has already explained antibiotic resistance in Superbugs: Not super after all, and answers the question Has AIDS evolved?This shows that such experiments neither prove creation nor disprove evolution as such. The major error in much evolutionary propaganda is equating natural selection with evolution. In reality, natural selection was discovered by creationists before Darwin, is an important part of theyoung age model, and is a culling rather than a creative force.An interesting question, though, is whether the farmer’s initiative (certainly worth a try for him, seeing as he was told the cow was otherwise doomed) was actually what led to the cure. In the clinical sciences, isolated reports of cures (as opposed to larger-scale controlled trials) are of very limited value, especially when they are anecdotal. I’m sure that all of us have heard of sensational cures, where someone you know took wonder pill X or magic herb Y and, lo and behold, whatever it was all went away. There is a well known fallacy in formal logic called thepost hoc ergo propter hoc fallacy (Latin for ‘after this, therefore because of this’). Sometimes shortened to be called simply the ‘post hoc’ fallacy, it’s easy to understand. Someone may have been eating a carrot two minutes before having a heart attack, but it doesn’t follow that therefore eating carrots causes heart attacks. See more in the article Logic and Creation. Would the recovery have happened anyway? The short answer is that there is no way of knowing. Cows as well as humans have amazingly designed mechanisms for repair and recovery. Spontaneous cures do occur, even in situations where one’s normal clinical judgment, based on what ‘usually happens’ and ‘should happen’, says otherwise. In my own former medical life, for instance, had I accepted the same cause and effect reasoning, I would have had to share the beliefs of the patients in question that:Epsom salts cured severe arthritis in someone whose joints were so deformed and inflamed they could not even walk.A pencillin injection cured a viral illness (penicillin targets bacteria, not viruses).Rubbing a mixture of kerosene and violets picked at midnight onto the chest reversed advanced secondary lung cancer.And several more.One should also not overlook the possibility that the simple act of injecting the udder might have contributed to the cow’s natural defences being able to overcome this, perhaps by relieving pressure or allowing builtup infection to drain in some way. Warning–don’t try this at home! Most importantly of all, I would give a major caution, before anyone decides to ignore antibiotics and inject themselves with dirty water! When my article on superbugs referred to rolling in the dirt as a way of more rapidly overcoming the ‘superbugs’ on my skin, this was notin the context of treatment for an established infection. As the article indicated, these bugs were passively colonizing my skin, so the ‘roll in the dirt’ advice I received from a specialist was to ensure that the population on the skin shifted progressively in favour of the more ‘home-brand-normal-variety’ germs. But that is not the same as having a raging infection, and then injecting one type of germ to somehow ‘fight’ another. To inject such ‘homeboy germs’ in any situation would be inviting potential disaster. As I said before in this feedback to someone,‘a raging infection with a superbug is regarded as more ‘serious’ than one of the same species that is not multiply resistant only because of the fact that the usual antibiotics don’t work. The ‘ordinary’ Staph. aureus that are not multiply resistant are very capable of causing very serious infection, it’s only that antibiotics are effective against such infections. In fact, as pointed out, the nonresistant ones are if anything more capable of causing such infection; they are more virulent, if anything, i.e. ‘stronger’ than the socalled ‘supergerms’.And of course, there are many different types of bacteria. To inject oneself with something derived from ‘garden dirt’ is particularly serious, because this often contains the spores of the germs that cause tetanus and gas gangrene. These types of bugs love to multiply in an environment with little oxygen. That is why a seemingly insignificant puncture wound by a contaminated nail or thorn is far more likely to have a fatal outcome with one of these diseases than if the injury were a slash with a razor, for instance, with profuse bleeding; the oxygen in the blood saturating the area would be unfavourable to these particular bugs. Whereas a puncture wound with no bleeding means that the very small blood vessels feeding an area of tissue will have been crushed, rather than cut. Even a tiny amount of ‘dead’ tissue with no blood supply carrying oxygen to the area will be a fertile breeding ground for these sorts of deadly germs, especially if the individual is unvaccinated.In short, while it is possible that the treatment attempted on this cow was the cause of its recovery, it is by no
means certain. (The fact that the recurrent infection a few days later seems to have been by antibiotic-sensitive bacteria, seemingly a different type to the original infection gives a little bit of support to the hypothesis, but does not prove it.)As much as one would love to use this interesting incident to answer the common objection that evolution, not creation, leads to scientific advances, I would resist it. Especially since it is quite unnecessary. As Dr Marc Kirschner, founding chair of the Department of Systems Biology at Harvard Medical School, said:‘In fact, over the last 100 years, almost all of biology has proceeded independent of evolution, except evolutionary biology itself. Molecular biology, biochemistry, physiology, have not taken evolution into account at all.’2 Has AIDS evolved? by Carl Wieland They can conquer smallpox, so why not AIDS? Indeed, why not the common cold? Smallpox was (hopefully) overcome by vaccines. These are specific substances which are used to trigger the body’s ‘soldier factories’ into making lots of ‘soldiers’ (antibodies) which are designed to kill only a specific, particular type of virus before it can do much damage. (Smallpox, AIDS and the common cold are caused by various types of viruses—AIDS is caused by a virus called HIV, Human Immunodeficiency Virus.)The reason why vaccines have not succeeded in eliminating influenza, for example, is because the viruses change. Soldiers trained to attack only enemies in grey uniforms will be useless if the enemy changes into blue uniforms. Effective vaccines against particular strains of flu virus constantly need to be updated for this reason.The same potential problem plagues the development of an effective vaccine against HIV. As the virus multiplies, the ‘copies’ which are made of it often have copying mistakes (mutations) which can change those parts of the virus that your body’s defences are geared to recognize. Only a very small change may be enough—a change which otherwise is completely irrelevant to the structure or function of the virus. So a ‘new strain’ emerges, and although you were able to fight off the first one, now you can’t. World Health Problem It is thought that HIV may have arisen as a problem for humans by just such changes. From a fairly harmless virus infecting the green monkey population in Africa, it has now become a major world health problem for humans. 1Well then, do viruses ‘evolve’? Has HIV evolved? If you define evolution simply as genetic change, the answer would seem to be yes. But does this give us evidence for the evolution of all living things on earth from humble beginnings (e.g. an amoeba) to man and other organisms living today, which are therefore all related by common descent? After all, this is what people mean by the word ‘evolution’.This issue is important when considering all types of observed changes in living things, including speciation in fruit flies, for example.Are the observed changes, on analysis, heading in the ‘right direction’? That is, are they the type of changes which, given enough time, would be capable of producing a massively complex organism like a horse from a onecelled creature? If they are not, it is misleading to call such changes ‘evolution’. Should we call them ‘micro-evolution’? This may be technically correct, and a proper term for creation scientists to use. However, at the risk of semantic hair-splitting, I suggest that what most people understand by the word ‘micro-evolution’ is ‘a little bit of that which would, given enough time, cause real macro-evolution’. Horizontal Hopping A small example may help here. Let’s say that you are on the first floor of a building and you find there is a baby kangaroo on the same floor. You and a friend are arguing as to whether he could have come up via the stairs. To obtain evidence to make this explanation plausible, it would certainly help if you could demonstrate the animal’s ability to hop from one step to the next higher one. But to observe its ability to hop horizontally across the room tells you nothing at all about the question being contemplated. ‘Evolution’ to most people means ‘hopping up the stairs’. So if hopping across the room and down the stairs is labelled ‘micro’ or ‘mini’ evolution or whatever, it risks being misleading.Observed changes in viruses, even if these involve the conversion of a harmless virus into, say, the deadly AIDS virus, cannot, in terms of the above discussion, be called ‘evolution’, as we will see.To understand why, we first need to look into what a virus really is. We may regard a living cell (for example, a cell in your skin or liver or other tissue, or a bacterial cell) as a very, very complex chemical factory. This factory is capable of many functions, including that of reproducing itself. Directing all this machinery is a blueprint, which is the coded information contained in the molecule, DNA. A virus is very different—it consists of a small amount of this ‘blueprint’ material (DNA or RNA). Note that it has no ‘factory’ of its own—it cannot move itself, it has no power source, and it has no machinery with which to duplicate itself.By means of simple chemical programming, it’s able to latch on to a cell wall. The material it contains is automatically released into the cell, and the information on the ‘blueprint’ takes over and starts to direct the cell’s factory, which starts to manufacture many copies of the virus. Package with a Code The cell eventually swells and bursts, releasing lots of new viruses to start the process all over again. 2 So we see that a virus is nothing much more than a package containing a code, which takes over from the cell’s code so that the cell then makes more code-containing packages. The cell is destroyed in the process.Many semantic arguments have raged over whether a virus can be called a living thing or not. This is one reason why many people feel it is sort of ‘half and half’— therefore a good candidate for a kind of transitional stage between life and non-life.Whether you call it living or not is a matter of definition, but I hope to demonstrate that however you define life, the virus can in no way be used as an evolutionary ‘intermediate’. The reason is simple—it needs to have all the complex machinery of a living cellular organism available to it! Without a fully functioning, living cell, the virus cannot reproduce (or should we say, arrange its own reproduction).So, regardless of your ideas about either evolution or creation, a virus will not be able to exist before a cellular creature is on the scene. Viruses do not really fit anywhere on the evolutionary ‘tree of life’. They cannot represent ‘early forms of life’ because they can only multiply within living cells. This ‘chicken and egg’ problem is often overlooked. They obviously could not, therefore, have been the ancestors of one-celled creatures, and it is difficult to see how they can be their evolutionary descendants. Little Value So we see, then, that any changes which might occur in viruses have very little, if any, apologetic value for evolutionists trying to show us how a fish supposedly changed into an amphibian, for instance.Wouldn’t a change in a disease-causing agent, converting it from a minor nuisance to a serious health threat, be a major evolutionary step? Surely, say some, this could not be labelled ‘horizontal change’ or ‘change within the kind’? Once again, though, we will see that this has little relevance to evolutionary apologetics.To assess the significance of any genetic change (real or proposed) as an argument for the idea of ‘vertical evolution’ (that is, change to a higher overall level of complexity) we must look at the informational change required. Thus, for evolution to have converted a reptile into a bird, we can tell by looking at the gross morphological and physiological differences that the amount of new highly ordered genetic information required would be incredibly large.The same would be true of every significant step along the way—it requires the addition of new, teleonomic (project-oriented) genetic information. Such information would reflect the required increase in functional complexity. When we discuss disease-causing agents, we need to remember a few things about the ability of such an agent
(not just viruses) to infect. These include its ability to withstand host defences—for example, immunologic mechanisms, antibiotics and antisepsis. Thus, the informational change required may be very small, ‘horizontal’ if you like, even though it has a major impact on us as sufferers of disease. Life and Death For example, the bacterium Staphylococcus aureus may exist as penicillin-sensitive and penicillin-resistant strains. From all other standpoints, they are identical—such as their morphology. They are even classified as the same species. But to a human being suffering from a Staphinfection who has access only to penicillin, the difference may be one of life or death.Someone may say at this point—isn’t there a vast informational difference between the two? After all, the resistant strain has the genetic information necessary to produce penicillinase, which is a complex chemical.However, the sensitive strain may have this same information, only that it has not been ‘switched on’, or else the resistant strain has gained its information in toto by a special transfer process from an already resistant one. Here also, the complex information has not ‘evolved’, but was already there.Incidentally, the reason why it is much easier to have an antibiotic against a bacterium than against a virus is because it is possible to find or design a chemical which throws a ‘spanner’ in the machinery of a bacterium without doing the same for the machinery of the human cells it infects. Because, as we have seen, a virus uses the human’s machinery, it is extremely hard to do anything to destroy viruses without at the same time destroying the cells of the human host. Alteration To Coat Returning to our main point about viruses, a virus may need only a slight variation in its protein coat to alter the way it is recognized by the body’s defence mechanisms. Consider a population immunized against an otherwise deadly virus, which we will call ‘V1’. Now suppose that a mutation manages to cause a slight transformation in the protein coat of one of these viruses by interfering with the sequence of letters in the alphabet of the genetic code. Let’s call the new virus strain ‘V2’. In all other respects, these two are identical. Nothing new in the way of complexity has been added, but this minor structural change causes the body’s immune defence mechanism not to recognize it as V1. Before a new vaccine has been developed and put into use, it wipes out millions of people. Emotionally, people would assess this as a change of major proportions.Therefore we see that in micro-infective agents, minor genetic shifts can easily have catastrophic consequences out of proportion to the actual change in informational content. When compared to the usual, supposed evolutionary transformations in ‘higher’ creatures we can easily see that there is no comparison left at all, in spite of the obvious favourable selection which occurs. To Summarize Viruses can have no evolutionary relationship to any other form, and so whatever may have happened to say, the AIDS virus, has no relevance to the supposed history of truly living organisms in any case.An apparently major effect is probably caused by only a horizontal or even a negative change in informational content, and therefore does not relate to the sort of evolution postulated generally. It certainly does not involve any increase in functional complexity.So to answer the question posed by the title of this article, while viruses may change considerably, and while the AIDS virus may have changed its infectivity, it is certainly not the type of change, in quality or direction, which would or could cause that virus to become a totally new, more complex type of living organism. In that sense, AIDS has not evolved. Addendum Long after this article was published, the PBS/SBS Evolution series used HIV/AIDS as ‘proof’ of evolution. Yet the new data has done nothing to make the principles in this article obsolete. Rather, in one case, HIV resistance to drugs was clearly caused by a deleterious mutation, as shown by their inability to cope with the ‘wild’ type when the drugs were removed; and immunity to AIDS can be conferred by a mutation that causes loss of certain receptors on the immune cells preventing the HIV from docking on them. HOW DOES NATURAL SELECTION FIT INTO A CREATIONISTS PARADIGM Natural selection ≠ evolution by Marc Ambler
This is an important ‘equation’1 that all people should be aware of, namely ‘Natural Selection does not equal (≠) Evolution’.2 People should know it so they do not get conned, and evolutionists should know it as a reminder that they still have lots of work to do to be able to claim that they have a mechanism for evolution.How often we hear an example of natural selection being used as proof of evolution. Changing sizes, colours, skin patterns and shapes are often paraded as evolution’s honour roll. This bait-and-switch tactic has been so often exposed for what it is, it’s a wonder that it is still used, or that people are still taken in by it. The very term should put people on their guard that something is missing. If we think of the word ‘selection’, in our common, daily experience, we select from something pre-existing. Think of being asked to select cards from a pack. You could select cards from a pack every second for the rest of your life and all you would only ever produce is different groups of the same cards. You would not have created anything new—only re-arranged cards, or removed cards or added cards from another pack. If we think of the word ‘selection’, in our common, daily experience, we select from something pre-existing.
If an illusionist asks you to select a card from a pack, and surprises you with something new, you know it is an illusion, a sleight of hand. We need to learn to see the evolutionists’ sleight of hand when they claim to have pulled something ‘new’ out of the pack. Selection is always from a pre-existing series or range; it creates nothing new.This illustration applies equally to ‘selection’ in the biological context. Those features that would interact with the environment: the overall size of a plant, animal or person; the size of individual organs or limbs such as beaks and noses, leaf sizes, skin colours, hair and feather lengths, textures and colours. All of these and many more variations were programmed into the DNA of the creatures in order that as populations of the various kinds moved into new environments, expression of those variations enabled individuals to survive those environments. Individuals with those variations then passed them on to their young. When these variations and the habitat of the population expressing that variation are distinct enough, we might distinguish different ‘species’. In all of this selection process, new information is never added. It can be conserved or lost, but never gained. The creationist chemist/zoologist Edward Blyth (1810–1873) wrote about natural selection about 25 years before Darwin misappropriated it to support his theory of evolution. But whether variation is selected naturally by the environment, or artificially by breeders for a particular trait, it remains just that, ‘selection’ from existing genetic information. Nothing new is created. Evolution desperately needs ‘Natural Invention’, ‘Natural Novelty’ and ‘Natural Creation’. Patent law calls for a product to have an ‘inventive step’ in order for it to be patented. Mere changes in design of an existing product cannot be patented. Many legal battles over patent rights have been waged over this point. Evolution requires the same thing—an ‘inventive step’, a novel organ or body part, facilitated by new information in the DNA that wasn’t there before. Despite the huge resources thrown at evolution in universities and research institutions, natural selection has never been shown to bring about this type of ‘inventive step’.Today’s Darwinists point to mutations as the mechanism which provides this novelty from which ‘Natural Selection’ selects. Evolutionists should then focus on mutations to defend their theory, instead of ‘Natural Selection’. When pressed for examples of novel genetic information or body organs created by mutation, they typically point to instances such as wingless beetles4 on islands, or the flightless cormorant on the Galapagos islands. 5 The problem with these examples is obvious. While they may confer a benefit to the creatures in a specific, very unusual environment, nothing ‘new’ is added to the DNA or creatures’ body parts. They actually involve a loss or corruption of existing genetic information.6 Evolution desperately needs ‘Natural Invention’, ‘Natural Novelty’ and ‘Natural Creation’. ‘Natural Selection’ just does not pass muster as exhibit A for evolution.. Natural Selection ≠ Evolution. Darwin’s finches Evidence supporting rapid post-Flood adaptation by Carl Wieland Thirteen species of finches live on the Galápagos, the famous island group visited by Charles Darwin in the 1830s. The finches have a variety of bill shapes and sizes, all suited to their varying diets and lifestyles. The explanation given by Darwin was that they are all the offspring of an original pair of finches, and that natural selection is responsible for the differences.Surprisingly to some, this is the explanation now held by most modern creationists. It would not need to be an ‘evolutionary’ change at all, in the sense of giving any evidence for amoeba-to-man transformation. No new genetic information would have been introduced. If the parent population has sufficient created variability (genetic potential) to account for these varied features in its descendants, natural selection could take care of the resulting adaptation, as a simplistic example will show.Say some finches ended up on islands in which there was a shortage of seeds, but many grubs were living under tree bark. In a population with much variation, some will have longer, some shorter, beaks than average. Those birds carrying more of the ‘long-beak’ information could survive on those grubs, and thus would be more likely to pass the information on to their descendants, while the others would die out. In this way, with selection acting on other characters as well, a ‘woodpecker finch’ could arise.The same thing is seen in artificial selection, with all the various modern breeds of dogs being more specialized than the parent (mongrel) population, but carrying less information—and thus less potential for further selection (you can’t breed Great Danes from Chihuahuas). In all these sorts of changes, finches are still finches and dogs are dogs. The limits to change are set by the amount of information originally present from which to select.Creationists have long proposed such ‘splitting under selection’ from the original kinds, explaining for example wolves, coyotes, dingoes and other wild dogs . The question of time has, however, been seized upon by anti-creationists. They insist that it would take a much longer time. Artificial selection is quick, they admit, but that is because breeders are deliberately acting on each generation. The usual ‘guesstimate’ of how long it took for Darwin’s finches to radiate from their parent population ranges from one million to five million years.However, Princeton zoology professor Peter Grant recently released some results of an intensive 18-year study of all the Galápagos finches during which natural selection was observed in action. 1 For example, during drought years, as finches depleted the supply of small seeds, selection favoured those with larger, deeper beaks capable of getting at the remaining large seeds and thus surviving, which shifted the population in that direction.While that is not very surprising, nor profound, the speed at which these changes took places was most interesting. At that observed rate, Grant estimates, it would take only 1,200 years to transform the medium ground finch into the cactus finch, for example. To convert it into the more similar large ground finch would take only some 200 years.Notice that (although the article fails to mention it) such speedy changes can have nothing to do with the production of any new genes by mutation, but are based upon the process described, that is, choosing from what is already there. It therefore fails to qualify as evidence for real, uphill (macro) evolution — though many starry-eyed students will doubtless be taught it as ‘evolution in action’.Instead, it is real, observed evidence that such (downhill) adaptive formation of several species from the one created kind can easily take
place in a few centuries. It doesn't need millions of years. The argument is strengthened by the fact that, after the Flood, selection pressure would have been much more intense — with rapid migration into new, empty niches, residual catastrophism and changing climate as the Earth was settling down and drying out, and simultaneous adaptive radiation of differing food species. DOES IT TAKE LONG PERIODS OF TIME FOR NATURAL SELECTION TO OCCURE Brisk biters Fast changes in mosquitoes astonish evolutionists, delight creationists. by Carl Wieland About 100 years ago, bird-biting mosquitoes called Culex pipiens entered the tunnels then being dug for the London Underground (the ‘Tube’). Cut off from their normal diet, they changed their habits to feed on rats and, when available, human beings. During WW2, they attacked Londoners seeking refuge from Hitler’s bombs. Their plaguing of maintenance workers may be the reason the underground variety has been dubbed molestus.British scientists have now found that it is almost impossible to mate those in the Tube with the ones still living above ground, thus suggesting that they have become a new species1 (or almost so). This has ‘astonished’ evolutionary scientists, who thought that such changes must take many times longer than this.2 Informed creationists have long pointed out that the yong age model of earth history would not only allow for the possibility of one species splitting into several 3 (without the addition of new information, thus not ‘evolution’ as commonly understood), but would actually require that it must have happened much faster than evolutionists would expect. The thousands of vertebrate species 4 emerged into a world with large numbers of empty ecological niches, often as varied as the two worlds of our mosquito example here. They must have split many times into new species in the first few centuries thereafter, as the bear population, for example, gave rise to polar bears, grizzlies, giant pandas and more.5 The observations on these underground mosquitoes are thus exciting news.Actually, creationists have long suspected that organisms had ‘built-in’ genetic mechanisms for rapid variation—even beyond the normal processes of adaptation where genes, reshuffled by sexual reproduction, are selected in various environments. 6 Thus, recent discoveries of such mechanisms being still viable today are of very great interest.For example, there are genes which can ‘jump’ around the chromosome. These are normally kept in check, but Drs Jenny Graves and Rachel O’Neill of La Trobe University in Melbourne, Australia, have found that in hybrids, these can undergo ‘rampant’ changes.This may even be ‘the general mechanism for speciation in all multi-cellular creatures’ (by making it impossible to ‘back-breed’ with a parent population). Graves says, ‘We thought it took millions of years of long-term selection for a jumping gene to be activated. We’ve now shown that it can happen maybe in five minutes after fertilization.’7 These are exciting times to be a creationist.We think that expanding genetic research will likely reveal even more examples of built-in, ‘pre-fab’ mechanisms for rapid change in response to environmental pressures. Ironically, as more such created mechanisms (very far from normal Darwinian ideas) are discovered, they will probably be misconstrued as support for evolution Book review: The Beak of the Finch Evolution in Real Time by Jonathan Weiner, Random House, 1994. by Carl Wieland Some years back, I was due to have a creation/evolution debate with a university academic in South Australia. Just before the event, I happened to be part of the crowd standing next to my opponent-to-be, a population biologist. Unaware that his creationist opponent was standing close by, he was busily expounding his bewilderment about having to defend what he ‘knew’ to be Figure 2. The Linnaean ‘lawn’—the ‘kinds’ were the same as today's true.He explained that he felt like an species. astronaut who had just returned from observing the earth from space, only to have to defend the planet’s sphericity in public debate. After all, biologists like himself routinely ‘see evolution’, so what is there to debate?By ‘seeing evolution’, he meant seeing examples of inherited changes in populations— but this demonstrates evolution only if Figure 3. The creationist ‘orchard’—diversity has occurred with time within the old straw-man argument is the original ‘kinds.’ accepted that any such heritable change is fatal to the young age model. Using the evolutionary ‘tree’ metaphor, demonstrating genetic change (even to the extent of speciation) is only fatal to the old idea of the ‘Linnaean lawn’, not the ‘creationist orchard’, which has been a part of the modern scientific creation movement since its inception.1,2,3 There is a very heavy burden of proof on those propounding the doctrine that bacteria have self-transformed into palm trees and fish, and the latter turned into tigers and nuclear scientists. For one thing, it demands a natural process capable of generating vast amounts of new, bio-functionally significant, coded information. To watch natural selection sifting and sorting through existing information, deleting chunks of it, begs the question of the origin of all that information. Of course adaptation will occur in variable populations subjected to selection pressure. Plants with a mixture of genes coding for deep roots and shallow roots, if growing in an area where the climate is becoming more arid, will show this phenomenon. Those members of the population with naturally deeper roots will be more likely to survive to pass on their deeper-rooted genes, so in time the population will adapt to its conditions by ‘becoming deeper-rooted’—utilizing the store of information already present in that population.However, this process will occur regardless of whether the genetic information (variability) needed for it to take place arose in the first place by creation, or by some process of mutation/selection over countless ages. So a demonstration of such changes can of itself have no real apologetic value for the evolutionist.The anecdote at the beginning relates very much to the subject of this book review. I can identify (in reverse) with the evolutionist’s sense of bewilderment—how is it that, so many years on in the modern creation/evolution debate, intelligent,
educated evolutionists have not grasped this simple point? How can they keep resurrecting the same straw-man (‘any inherited change due to selection proves that the young age model is wrong, Darwin was right—particles did become people’)? Seeing evolution? The Beak of the Finch: Evolution in Real Time is consciously and deliberately a hymn of praise to evolution, a drawn-out celebration of what the author perceives as a logical deathblow to creationists, Figure 1. The evolutionary ‘tree’—all today’s species are descended from who are represented (I should say the one common ancestor (which itself evolved from non-living chemicals). misrepresented) smugly and patronisingly. Without detracting from the author’s brilliant and readable style, I believe that this is the key reason why the book has received near-religious adulation by science journalists and other reviewers.The message is that now, for the first time, those foolish, bigoted creationists have no leg left to stand on— Weiner’s book:‘tells the extraordinary story of two scientists, Peter and Rosemary Grant, whose ingenious, meticulous and extended work in the Galápagos has culminated in the sight of evolution occurring before their eyes—not in fossils but in living, breathing creatures, Darwin’s own famous finches’.We are told this book ‘permanently alters one’s view of nature and even of life and death’.None of what follows is meant to detract from the dedicated fieldwork of the Grants, whose incredibly detailed measurements of thousands of birds over a 20-year period on the small island of Daphne Major are a major contribution to the study of population dynamics and ecology. Others have demonstrated natural selection occurring before (although you might not think it from the hyperbole and fervour accompanying this book), but never with such precision and clarity. I think that their observations of sexual selection are of great importance, also. Evolution: more than selection What a pity that neither the researchers nor Weiner appear to understand the logical fact that, while natural selection may be an intrinsic part of a particular evolutionary model, demonstrating it does not of itself demonstrate the ‘fact’ of evolution— if by that you mean a one-celled organism becoming today’s complex biosphere. This fact was apparently grasped by the renowned biologist L. Harrison Matthews F.R.S. writing in the foreword to the 1971 edition of Darwin’s The Origin of Species. Discussing Kettlewell’s experimental observations on the famous peppered moths, Matthews pointed out that while this beautifully demonstrated natural selection, or survival of the fittest, it did not show evolution in action.The book has much of interest for creationist readers. It makes it clear, for instance, that despite the common myth, Darwin did not deduce his theory under the eureka-like inspiration of seeing the finches on the Galápagos. In fact, as Gould has pointed out,4 Darwin did not know at the time that they were finches. I was also interested to read again of Darwin’s experimental finding (with its implications for post-Flood biogeography) that garden seeds still sprouted after 42 days soaking in seawater. Weiner recounts how Darwin was able to apply selection to breed pigeons so different from each other that if found by biologists in the wild, they would not only have been categorized as separate species, but even separate genera. This is of course a marvellous demonstration of the amount of variability built into each created kind, allowing it to respond to changing environmental pressures and thus conserve the kind. It also opens a window of understanding into how the intense selection pressures after the Flood could have acted on gene pools of rich variability to allow rapid speciation/adaptive radiation from the restricted number of land-dwelling kinds. No new information Not only are all the varieties of pigeons still pigeons, however, but if allowed to interbreed they will revert to the common wild-type rock pigeon. There is no evidence that any truly novel, functional information arises de novo in such artificial selection—nor, one finds after reading this book, is there any evidence for this from the Grants’ observations of natural selection, either.Darwin’s finches exhibit an unusually high degree of variability. This, coupled with the fact that the Grants and their co-workers were fortunate enough during their 20-year vigil to experience a severe drought and the very opposite, means that it is no surprise that they were able to document some quite rapid changes under selection. When the drought brought a shortage of easily available small seeds, is it any wonder that the birds with big beaks survived better because they were the only ones to be able to crack big seeds, and so on?In fact, as a 1992 article in Creation magazine (actually based on the Grants’ work on the Galápagos finches) emphasized, observations showing rapid selection/speciation are helpful to the creation model, which has only a relatively short time in which post-Flood adaptive radiation/speciation must have occurred (see Darwin’s Finches).5 Finches: no net change! After all the ‘hype’ about watching ‘evolution’, one reads with amazement that the selection events observed actually turned out to have no net long-term effect. For example, for a while selection drove the finch populations towards larger birds, then when the environment changed, it headed them in the opposite direction. The author says concerning this sort of effect (also seen in sparrows) that ‘Summed over years, the effects of natural selection were invisible’ (p. 108). So that when Darwin looked at the fossil record and found it ‘static and frozen for long stretches’ (p. 109), this was the reason. Consider, he says: ‘how much less visible these [natural selection] events will be in the strata of rock beneath our feet, in which the generations have been summed for many millions of generations.’Evolutionists have long argued the opposite—that evolution is invisible in the short term, but would become visible if we had enough time. Yet according to Weiner, we can see evolution happening in the (very) short term, but any longer and it becomes ‘invisible’! The mind boggles at how evolutionists can be blind to this inconsistency.Weiner quotes a researcher as saying that:‘A species looks steady when you look at it over the years—but when you actually get out the magnifying glass you see that it’s wobbling constantly.’Obviously, since macroevolution is supposed to be about long-term, directional change (even the creation/Flood model requires more directional change than the Grants documented) such ‘wobbling back and forth’ (fluctuation around a mean) over short time-spans, with no net change over longer time periods, is hardly supportive of the case for evolution. Yet instead of acknowledging this, the researcher goes on to say, ‘So I guess that’s evolution in action.’Most creationists would agree that Darwin’s finches probably came from an ancestral pair or two (which were themselves finches), so the idea that some of the descendant species might hybridize, even to the extent of leading to a new species, is hardly threatening. The Grants not only observed such hybridization between species of finches which did not interbreed as a rule, but that under certain conditions the hybrids appeared to be fitter than either of the parent populations. I was surprised when the book hinted that here we were
approaching the answer to the mystery of the origin of species. Perhaps the obvious needs to be restated; the mingling of two sets of pre-existing information can scarcely tell one anything about the ultimate origin of that information. There is a particularly misleading sideswipe at creationists on page 216 in the section on DNA and genetics; we are told that if species were created as functional entities, the genes in each species would not change. We are then told that the genes in each generation are ‘shuffled and cut … like a mammoth deck of cards’—ergo, creation is wrong. Of course, the reshuffling of pre-existent information by such recombination neither denies original creation of that information nor confirms its naturalistic origins by Darwinian mechanisms. From a creation viewpoint, the ‘deck-shuffling’ achieved in this way by sexual recombination is an amazingly effective mechanism for maximizing variability (without any de novo information having to arise post-creation). It enhances the ability of species to avoid or postpone extinction in changing environments, and assists the rapid filling of empty ecological niches (adaptive radiation), such as after the Flood. Mutations The real key to the credibility or otherwise of macroevolutionism is not natural selection, but the question of the origin of the information on which natural selection may act. In the current materialist paradigm, the only conceivable source of such information is mutation (random mistakes as the information on DNA is copied). Yet information theory, common sense and observation unite to indicate that randomness fails as a source of functional information. Thus it is no wonder that the section on mutations/DNA is markedly fuzzy—almost skipped over in haste. A casual reader could gain the impression that random mutations have been involved in the changes observed by the Grants, but close reading reveals that there is no evidence for this at all. Nor is it likely in view of the rapidity of the changes, and the lack of net effect already discussed. The‘storehouse’ of variation is already there, allowing the populations to shift this way and that, as required.What about the observation on page 217 that three out of three hundred bases (‘letters’) of the cytochrome c sequence are different in two of the finch species? I think these differences are indeed the result of mutations. However, such mutations are unlikely to have, historically, generated the raw material for the differences in the two finch species. They are almost certainly functionally meaningless or ‘neutral’ mutations, not expressed in the phenotype, and thus transparent to selection. Why? Cytochrome c is a crucial enzyme for life; any copying errors of functional significance (that is, in those stretches of gene critical to the function of the resultant enzyme) are likely to be lethal.The probable course of events which gave rise to the current base-pair differences (which, because of the redundancy of the code may not have resulted in an amino-acid substitution, or if so, this has been in a non-critical segment of the enzyme, not altering its function) is this: selection operating on existing, functionally significant (created) genetic variation gave rise to the initial divergence of the populations. Because of their reproductive isolation, the populations were free to independently accumulate such ‘neutral’ mutations in the cytochrome cgene at varying rates and loci.Towards the end of the book, the author seeks to cement his imagined Darwinian triumph with other examples of ‘evolution’ such as antibiotic and pesticide resistance. Farmers in US would oppose evolution, yet at the same time are spending increasing amounts on spraying their crops as insects become more resistant to pesticides, are treated with the bemused contempt deserved by such ‘closed-minded fundamentalists’. Yet his attempts to provide further observations which deal death-blows to the creation have the same logical and scientific weaknesses as the beak arguments. The reader is referred to a recent article in this journal on the subject. 6 Interestingly, Weiner shows in some detail how a mutational change in one particular bacterium (p. 260) gives a survival advantage—but the enhanced survival comes via a loss of information/function. Conclusion In summary, this book will reinforce the prejudices of the evolutionary faithful; it will delight the shallow-thinking evolutionist who has not bothered to think through or become informed about the matters raised by creationist biologists such as Lester and Bohlin, in their classic The Natural Limits to Biological Change.7 Careful reading of The Beak of the Finch: Evolution in Real Time will reveal much to support the creation model, and nothing to dismay the discerning creationist— except frustration at the continuing, seeming ‘wilful ignorance’ displayed towards creationist biological arguments.As a very polished, readable account of a piece of classic fieldwork demonstrating natural selection in the wild, the book is noteworthy. As an alleged empirical proof that Darwin was right about the origin of all things, it is easy to show that it fails completely. It never once comes to grips with the crucial question of the origin of biological information. No doubt creationists confronted by bright-eyed evolutionary disciples inspired by this tale of finches’ beaks and straw-men will end up feeling like astronauts debating flat-earthers all over again. Do toads goad snake evolution? David Catchpoole 18 April 2006 When leading public institutions repeatedly broadcast as fact that ‘we see evolution happening today’, 1 it’s not surprising that many people believe it.One example is a recent prime-time breakfast radio segment on Australia’s national broadcaster, ABC Radio National. The University of Sydney’s Professor Richard Shine told the presenter Fran Kelly that he and his coresearchers studying snakes have observed ‘genuine evolutionary changes’. 2What were they? Allegedly snakes are evolving to cope with the spread of cane toads across the Australian continent. (Cane toads were introduced to north Queensland in the 1930s, and have steadily expanded their range, moving south into New South Wales and west into the Northern Territory.) The changes are making snakes ‘much less vulnerable’ to the toxin in the toad’s skin. (One reason that the cane toad has spread so rapidly is its toxic gland that can kill native predators that eat it.)But as the interview progressed, the discerning listener would have picked up from Professor Shine’s own words that he and his colleagues had not observed evolution at all. Rather, it was an example of natural selection acting to favour certain already-existing genetically determined traits in the snake populations. Creationists do not dispute natural selection—indeed it is an important part of the young age model, and was theorized by creationists even before Darwin!The researchers had firstly been able to rule out learned behaviour as a factor in this case. ‘We’ve done a bunch of trials to see if it could just be that the snakes are learning and so forth but they seem to be remarkably stupid …’, said Professor Shine, going on to emphasize the genetic basis to snake behaviour:‘Basically you’ve got a strong genetic component to feeding responses, and some snakes really go mad on eating frogs and others really want to eat nothing but mammals and so forth, and it’s actually pretty sophisticated. And there’s a lot of work overseas showing that even within a single litter of baby snakes you’ve got genetic variation in what kinds of things they treat as prey. And it’s just that the only snakes that survive after the toads arrive are the ones that happen to be born with a set of genes saying: “If it looks and smells like a cane toad, don’t eat it.”’And genetically-determined physical attributes such as the snake’s head dimensions and body size are key factors too. ‘Essentially the size of the toad you can eat depends on the size of your head, so if you’ve got a small head you can’t eat a very big toad.’So, if you’re a snake, having a small head stops you eating big toads, which have more poison, therefore helps you to survive. And having a big body helps as well:‘The size of toad it takes to kill you depends on the size of your body. So if you’ve got a really big body, it takes more poison. So, basically, the right shape to be when the toads arrive is to be a big snake with a small head and that’s exactly the evolutionary change that we’re seeing in a couple of species of snakes, through the history of the toad’s invasion in Queensland.’But the toad-goaded natural selection favouring large-
bodied, small-headed snakes and/or snakes with an apparently genetically-predetermined aversion to eating cane toads is not ‘evolutionary change’. To get from pond scum to snakes requires an increase in genetic information but all that Professor Shine and his colleagues have observed is a culling of genetic information. Genes that code for large heads, small bodies and an urge to swallow a cane toad are being removed from snake populations, no doubt reducing the aforenoted existing ‘genetic variation’. See also The evolution train’s a-comin’ (Sorry, a-goin’—in the wrong direction). And you’d expect it to happen quickly—i.e. in just one generation you’d expect to see, in a population of snakes, an increase in the numbers of snakes with large bodies, small heads, and a decided lack of interest in hunting cane toads. But evolutionists, used to thinking that slow-and-gradual evolution is how we got here, and that change through natural selection is evolutionary, are often caught by surprise at the rapidity of such changes.When ABC presenter Fran Kelly put it to Professor Shine that what he’d observed was ‘pretty quick for evolutionary changes, physical changes like this, isn’t it?’ Professor Shine responded:‘Yes, look, I’m amazed at the speed that it’s all happening. I mean, we’re used to antibiotics eliciting very rapid change in microbes, and insects evolving to pesticides and so on, but these are pretty big vertebrates that take a couple of years to mature and so on. So you would have expected that evolutionary change would be fairly slow. But of course the toads are a massive selective force in evolutionary terms. The only way to make a living as a black snake, once the toads have arrived is to somehow have a trick that makes you invulnerable, and that seems to be exactly what’s happened.’Toads are indeed a ‘massive selective force’, but not ‘in evolutionary terms’. The gene-coded ‘trick’ favouring snake survival when cane toads are present did not ‘evolve’ out of nowhere—it was already present in the snake population. But such is the ruling evolutionary paradigm that many people can’t (or won’t?) see this point. (A New Zealand atheistic evolutionist writing in Wellington’s main newspaper has likewise invoked this natural selection in Queensland toad-eating snakes as ‘proof’ of evolution in action; see CMI refutation published in the same paper.)If only Professor Shine and his colleagues knew that the antibiotic-elicited rapid change in microbes (see also here and here) and pesticide’s selective culling of insects do not show any evidence of evolution either, it would put what they really observed in a whole new light, as was the case for the former evolutionist who gave his testimony on this DVD. Rapid tomcod ‘evolution by pollution’? Yeah, right … and wrong by Carl Wieland Published: 22 February 2011(GMT+10) The Atlantic tomcod only benefits from its informationlosing mutation in the heavily polluted Hudson River. Headlines have screamed that fish in New York’s Hudson River have ‘evolved’ into ‘super mutants’, able to resist the toxic effects of PCBs (polychlorinated biphenyls) in that heavily polluted waterway. And all this ‘evolution’ has happened in less than 50 years.1 As reported in the respected journal Science,2 researchers have indeed shown that some 95% of the Hudson’s bottom-feeding Atlantic tomcod have become resistant to these poisons. It is the first recorded case of poison resistance (similar to antibiotic resistance or pesticide resistance) developing in vertebrates (creatures with backbones). And this is almost certainly via mutation, which is then favoured by natural selection. Why would the same article that made those frank admissions about these damaged, weakened fish have a headline that referred to them as having ‘evolved’ into ‘super mutants’? So the fish have adapted to this new environment by a Darwinian mechanism. But as we have already extensively shown in detail (for example, in this article on supergerms), such resistance to poisons in bacteria, for instance, most definitely does notdemonstrate the sort of biological change required to have turned microbes into magnolias, mosquitoes and microbiologists. It is in fact demonstrating the opposite, if anything, especially in those cases of antibiotic resistance where mutations have generated the resistance.This is something that is simple to understand and demonstrate; the germs become resistant due to various forms of damage (which is what mutations—inherited genetic copying mistakes—mostly do) to their internal engineering. A good example is where a germ that uses biological pumps to draw in its nutrition has a mutation that damages the pumps. That makes it harder for it to pump in not just nutrients, but also antibiotics when these are in its environment—in short, it is no longer as good at sucking in the poison that kills it.So the ones that have this defect do better when there are such poisons around (natural selection—a fact of life). But they are ‘damaged goods’, unable to pump in nutrients as efficiently—so, once the poison is removed from their surroundings, they don’t do as well as the normal, undamaged germs. So the ‘normal’ type of germ will come to dominate the population once more, because it is more efficient at what it needs to do.This is not ‘evolution’ (as most people understand that word to mean) at all, since that requires a net uphill gain of information, improvements giving greater viability and efficiency, building new and improved biological machinery, not damaging that which exists. In short, even a committed evolutionist should concede that this sort of mutation that ‘breaks things’ is not the sort that he would like to see to demonstrate the viability of his belief in ‘uphill’ evolution.And—surprise, surprise—despite the media hype, all indications are that the same sort of downhill damage as in the bacterial example just given has taken place in the case of the Hudson tomcod. All such Atlantic tomcod fish have a gene called AHR2. This codes for a receptor protein which in its normal state allows PCBs to bind to it, causing severe problems (some 30 years ago, 94% of Hudson tomcods were found to have a PCB-induced liver tumour, for instance). The Hudson River variety, according to one of the researchers, Dr Mark Hahn of the Woods Hole Oceanographic Research Institution, “appear to be missing two of the 1,104 amino acids normally found in this protein”. This is apparently the result of six of the bases in the gene’s DNA sequence having been deleted (two lots of three bases, each coding for one amino acid). This loss mutation has damaged the receptor such that PCBs and dioxins cannot bind as readily to it. Mutation happens in one generation, and since in such a poison-rich environment the non-damaged fish would be rapidly eliminated, it’s no wonder (and in keeping with other instances in non-vertebrates of poison resistance) that the mutated gene would spread quickly enough to dominate the population in just a few decades.Given that these mutant fish are ‘damaged goods’, and in keeping with our comments earlier, it’s also no surprise to read about the Hudson tomcod that “the fish have suffered in other ways. They likely grow slower than other tomcod, and they may have reduced resistance to other dangers.” 3One would therefore expect that these genetically damaged fish would not do as well in less polluted areas, and so again it’s no
surprise to read that only “5% of the fish in the nearby, relatively clean waters off Connecticut and Long Island possess the mutated gene.”Of course. About the only surprise is, why would the same article that made those frank admissions about these damaged, weakened fish have a headline that referred to them as having “evolved” into “super mutants”? But then, maybe one shouldn’t be surprised there, either. It seems that in this day and age sensationalist headlines that keep reinforcing the idea that there is all this ‘evidence’ of ‘evolution happening’ are just par for the course. If anything, it should encourage us all to get involved much more with passing on the sort of information that can counter this ‘propaganda war’; tell your friends and acquaintances about this site; subscribe to our free email newsletter; give them gift subscriptions to Creation magazine, hand out books and DVDs of quality creation information. And keep yourself informed. Yes, it helps us to keep going and growing, but it is also one way in which all of us can ‘do our thing’ to help combat this relentless onslaught of misinformation. As you get behind us, we can ‘make the bullets’ in this spiritual war, but we need you to help fire them. DOES SEXUAL SELECTION EXPLAIN HOW FEATUERS LIKE PEACOCK`S TAIL DEVELOPED The beauty of the peacock tail and the problems with the theory of sexual selection by Stuart Burgess The peacock tail contains spectacular beauty because of the large feathers, bright, iridescent colours and intricate patterns. The colours in the tail feathers are produced by an optical effect called thin-film interference. The eye pattern has a high degree of brightness and precision because the colour-producing mechanisms contain an extremely high level of optimum design. According to the theory of sexual selection, the peacock tail has gradually evolved because the peahen selects beautiful males for mating. However, there is no satisfactory explanation of how the sexual selection cycle can start or why the peahen should prefer beautiful features. In addition, there is irreducible complexity in both the physical structure of the feather and in the beautiful patterns. Figure 1. Peacock with tail feathers displayed. Most birds have two types of tail feather: flight feathers and tail-coverts. The flight feathers provide stability during flight, while the tailcoverts ‘cover’ and protect the tail region. In the vast majority of birds, the tail-coverts are small feathers, just a few centimetres long. However, some birds like the peacock have very large tail-coverts for decorative purposes. These decorative feathers are also referred to as ornamental feathers, or display feathers. 1 It should be noted that a peacock is a male peafowl and a peahen is a female peafowl. The peahen does not have any decorative feathers.When a peacock displays his tail feathers during courtship, a magnificent ‘fan formation’ of feathers forms a beautiful backdrop to the body of the peacock as shown in Figure 1 (below). An adult peacock has an average of 200 tail feathers and these are shed and re-grown annually. Of the 200 or so feathers, about 170 are ‘eye’ feathers and 30 are ‘T’ feathers. The ‘eyes’ are sometimes referred to as ocellations.This paper describes some of the complex structures that are responsible for producing the beautiful features and why the beauty of the peacock is evidence for intelligent design. The paper also describes the theory of sexual selection and shows that there are serious problems with the theory. Fan formation of displayed feathers When the peacock feathers are displayed there are several beautiful features that can be seen: Fan formation of feathers Uniform distribution of ‘eyes’ Intricate ‘eye’ feathers Intricate ‘T’ feathers One reason for the beauty of the displayed feathers is that they form a semi-circular fan over an angle of more than 180 degrees. The fan formation is very even because the axis of every feather can be projected back to an approximately common geometrical center. The radial alignment of feathers requires the root of each feather to be pointed with a remarkable degree of accuracy. Another remarkable feature of the displayed feathers is that they are ‘deployed’ into position by muscles in the peacock’s tail. Not only can the peacock deploy the feathers, but he can also make them vibrate and produce a characteristic hum.Another beautiful feature of the displayed feathers is the uniform spacing of the eyes. Even though the display contains around 170 eye feathers, they are all visible and all spaced apart with a remarkable degree of uniformity. All the eyes are visible because the feathers are layered with the short feathers at the front and the longer feathers at the back. The eyes have an even spacing because each feather has the right length.Each ‘eye’ feather and ‘T’ feather is an object of outstanding beauty in itself. The eyes contain beautiful patterns, and the ‘T’shaped feathers form a beautiful border to the fan. The eye feather Figure 2. Structure of the eye feather. Figure 2 (right) shows a sketch of the top section of the eye feather. There are several beautiful features to the feather: Bright colours Intricate eye pattern Loose barbs below the eye pattern Absence of stem in the top half of eye pattern
Narrow stem in the bottom half of eye pattern Brown coating of the stem near the eye pattern The bright colours and intricate shapes of the eye pattern are the most striking aesthetic features. The loose barbs on the lower part of the feather are beautiful because they make a contrast with the neatness and precision of the barbs in the eye pattern. The last three features in the list above are usually only noticed by very careful observers. However they represent important ‘finishing touches’ which make an important contribution to the beauty of the feather. The absence of a stem in the top half of the eye is an important detail because it prevents the pattern from being divided into two sections. The stem is not needed because the barbs fan out around the top of the feather. The narrowness of the stem in the bottom half of the eye pattern is important because this makes the stem fairly obscure. The stem can be narrow because it has a deep section in the area of the eye pattern. The brown coating of the stem in the area of the eye pattern is very important because the stem is a natural white colour and this would be too conspicuous for the eye pattern. It is interesting to note that the stem is white everywhere except local to the eye pattern. This strongly indicates that the brown coating near the eye pattern is a deliberate feature. A large eye feather has been examined at Bristol University to determine the number and size of each part of the feather. The number and size of barbules was estimated by examining sample sections of barbs with a microscope. The data for the feather are summarized as follows: Length of feather = 1.3 m Number of barbs = 290 Maximum length of barbs = 200 mm Average length of barbs = 105 mm Barbules per mm on one barb = 32 (16 each side) Length of barbules in eye pattern = 0.8 to 1 mm Length of barbules below eye pattern = 2 to 3 mm Total number of barbules in feather = nearly 1 million The results show that a large peacock tail feather is very large both in terms of size and number of barbules. The unique length and structure of the peacock display feathers is acknowledged by bird experts.2,3 The colours in the eye feather The colours in the peacock tail are particularly beautiful because they are bright and iridescent. An iridescent colour is a colour that changes with the angle of view. The colours are not produced by pigments but by an optical effect called thin-film interference that takes place in the barbules.4 In technical terms, the peacock has ‘structural colours’. In the eye pattern, the barbules appear bronze, blue, dark purple and green. Away from the eye region, the barbules are uniformly green. The colours in the eye feather can only be seen on the front surface of the feather because this is where the barbules are positioned. The back of the feather is uniformly brown because the barbs contain a brown pigment. To understand how thin-film interference is produced in the peacock tail, it is first necessary to understand the detailed structure of the feather. Structure of the barbules Figure 3. Peacock barbules. The basic structure of the peacock tail feather in the eye region is shown in Figure 3(a) (right). For comparison, the structure of a typical flight feather is shown in Figure 3(b) (right). Like the flight feather, the peacock tail feather has a central stem with an array of barbs on each side. Also, individual barbs have an array of barbules on each side of the barb. Even though there is a basic similarity with a flight feather, the peacock tail feather has an unusual barbule structure. The barbules are like long flat ribbons that overlap to form a flat surface on top of the barbs. (Under a microscope the barbules are actually slightly curved and segmented and the surface has a bubbly appearance). In contrast, a flight feather has narrow barbules which do not cover the barbs. Other types of birds such as hummingbirds, pigeons and kingfishers have some patches of flat iridescent barbules, but the peacock has the largest iridescent barbules of any known bird. 5The colours of the barbules dominate the front face of the tail feather because they completely cover the barbs. The barbules are not very visible from the back of the feather because the barbs are quite close together. Thin-film interference in the barbules Figure 4. Cross-section of peacock barbule. Thin-film interference can be produced in one or more layers of a very thin and transparent material. Usually the thin film is placed on a dark surface. The thickness of the transparent material must be close to the wavelengths of visible light. Visible colours have wavelengths between 0.4 and 0.8 µm and thin films typically have a thickness of between 0.3 and 1.5 µm. Another requirement for thin-film interference is that the thin film must have a refractive index that differs from air so that the light is retarded when it passes through the thin film. Thin-film interference commonly occurs in oil slicks on a wet road. The oil will often form a thin layer on the wet surface of the road or on the surface of a puddle, the thin-film producing blue and green colours.In the case of the peacock, thin film interference takes place in three layers of keratin which cover the barbules as
shown in Figure 4. Each barbule is about 60 µm wide and 5 µm thick. 6 The barbules have a foam core that is 2 µm thick and this is covered with three layers of keratin on each side, as shown in Figure 4. The keratin layers are very thin, being about 0.4–0.5 µm thick.7The principle of thin-film interference in a single layer of keratin is shown in Figure 4. White light is reflected off the front and back surfaces of the thin film. The light which passes through the keratin is retarded and therefore when it emerges from the keratin, some of the colour components of white light are out of phase with the light-waves that were reflected from the front surface. When two wave trains of the same colour are out of phase, destructive interference removes the colour. In the case of white light, the result of the interference is a reflected colour due to the remaining colour components of white light. In practice, interference occurs simultaneously in all three thin films.The only pigment in the peacock tail is melanin, which gives the barbs a uniform brown colour. This provides a dark background colour for the thinfilm interference in the keratin layers. The different colours in the eye pattern result from minute changes in the depth of thickness of the keratin layers. 8 In order to produce a particular colour, the keratin thickness must be accurate to within about 0.05 µm (one twenty thousandth of one millimetre!).The barbules in the peacock feather contain a high degree of optimum design. The thickness of the keratin layers is optimal for producing the brightest thin-film colours. The dark brown background colouring is optimal because it prevents light shining through the back of the feather. The three layers add to the brilliance of the colours in the feather by adding multiple components of light. The barbules are also slightly curved in the longitudinal direction.9 This curvature causes a mingling of slightly different colours, which produces a softening of the colours seen in the keratin layers.9 The eye pattern Figure 5. Mathematical curves in the eye pattern. The particular beauty of the eye pattern comes from the rounded shapes that have a high degree of resolution as shown in Figure 5 (below). The ‘pupil’ of the eye is formed by a dark purple cardioid and the ‘iris’ is formed by a blue ellipsoid. These shapes are located within a pointed bronze ellipsoid that is surrounded by one or two green fringes. A very important feature of the eye pattern is that it is a digital pattern which is formed by the combined effect of many thousands of individual barbules. Some patterns in nature are formed by natural growth mechanisms, as with the spiral shape of the nautilus shell. However, the eye pattern in the peacock tail requires the precise coordination of independent barbs and this cannot be achieved by a simple growth mechanism. Barbules on adjacent barbs coordinate perfectly with each other to produce the eye pattern.The spacing of colours on each barb must be specified by instructions in the genetic code. To specify the pattern, there must be timing or positional instructions in the DNA which causes the right thickness of keratin to be grown on the right barbule and on the right barb. To help appreciate the precise nature of the information in the genetic code, it is helpful to consider the mathematical complexity involved in calculating the required spacing of colours on each barb. Required colour spacing on barbs Figure 6. Intersection points on barbs. Figure 6 (right) shows the colour spacing on a single barb. Along the first part of barb ‘n’, the thickness of the keratin films on the barbules gives a bronze colour. Then an abrupt and minute change in thickness of the keratin films produces a blue colour. Another abrupt and minute change in thickness of the keratin films so produces a bronze colour. The abrupt nature of the changes in thickness is important because if the changes were gradual then there would be a gradual change in colour.10 The abrupt changes in thickness of keratin along a barb are an amazing feature because it involves sudden and precise changes in the dimensions of the barbule. Even more amazingly, along the length of the barb the thickness of the keratin does not continually get thicker and thicker (or thinner and thinner) but it involves both increases and decreases in thickness.The required length of the colour sections on each barb can be determined mathematically by finding the points where the barbs intersect with the curves as shown in Figure 6. For example, to find the positions of the points Bn and Cn the following procedure can be followed. Firstly the equation for the ellipsoid (conic function) can be written as:
(1) Then the equation for the straight line of barb n can be written as: (2) By taking the equation for the ellipsoid (1) and substituting it into the equation for a straight line (2) and eliminating y we get an equation forx as follows:
(3) This equation can be solved as a quadratic to get two solutions for x, the two intersection points xB(n) and xC(n). The y coordinates of these points then can be found from either (1) or (2). Then, the length of the first section of bronze colour on barb n can be found by geometry:
(4) A similar procedure can be used for the intersection points on the cardioid shape and the outer green fringes. For each barb there are on average about four points at which colour changes and so there are on average four positions to calculate. Since there are around 50 barbs on each side of the pattern and since every one of these barbs has a unique spacing of colour, it is necessary to calculate 200 intersection points in order to construct the whole eye pattern. ‘T’ border feathers The long ‘T’ border feathers provide a beautiful border to the tail feathers because they form an inverse shape to the peacock eye as shown in Figure 7 (below). An inverse shape is beautiful because the inside profile of the T feather follows the outline of the eye pattern. The T feathers often form an ‘ogee’ curve on each side of the feather as shown in Figure 7. An ogee curve is beautiful because it is both concave and convex. For this reason, ogee curves are used in architecture in structures such as arches. The formation of an ogee curve from individual barbs is yet another remarkable feature of the peacock tail. Each barb at the end of the T feather has a unique length and curvature and all the barbs coordinate exactly with each other to form the curved T. Information content in the genetic code Figure 7. The ‘T’ feathers and ‘eye’ feathers. Every detail in the peacock tail must be defined by genes in the genetic code of the peafowl. Since the tail feathers have very complicated structures and colour-producing mechanisms, there must be a large amount of design information in the genetic code.It is difficult to determine how many genes would be required to specify the aesthetic features of a peacock tail feather because it is not known how the tail feather grows. However, a conservative estimate can be made by assuming that each separate aesthetic feature is specified by one gene. By assuming that each colour and each shape within the eye pattern represents a separate feature, and taking into account the other features discussed in this paper, the total number of aesthetic features in a single feather comes to about 20. Therefore an estimated 20 genes are required for the peacock tail. This may be a very conservative estimate. In particular, it may be that many genes are required to produce each shape in the eye pattern since the eye pattern is formed from the coordinated arrangement of over 100 barbs. In addition, the fanning-out of barbs in the top of the feather, where there is no stem, is a complex feature that may well need several controlling genes.Even if only 20 genes are required to specify the beautiful features of the peacock tail, this still amounts to a lot of genetic information. A gene typically consists of 1,000 chemical units of information (base pairs). Therefore, 20 genes would contain many thousands of chemical units of information. According to evolutionists, all of this information has appeared gradually by genetic mistakes and by sexual selection. The theory of sexual selection The theory of sexual selection was first proposed by Charles Darwin in The Descent of Man.11 Even though this theory has always been controversial, most evolutionists now believe that it can explain how beautiful features could evolve from nothing.12According to sexual selection, a female can have a preference for a mate with a feature such as a long tail. Over a long period of time, sexual selection is believed to be able to develop a particular feature to a great extent. For selection to work, a number of things are thought to be typically required. Firstly, the male must have an aesthetic feature. Secondly, the female must have a preference for that particular aesthetic feature. Thirdly, the female must be able to have the opportunity to view a number of different males before mating. Fourthly, the female must be able to have some control over which male mates with her.Sexual selection is a circular process based on a particular fashion. When females have a preference for a long tail, the selection of a male with a long tail is an advantage because the male offspring will have long tails and therefore be more successful at mating. A key aspect of sexual selection is that ‘fitness’ is not measured in ability to escape from predators but in ability to produce offspring. Evolutionists fully recognize that sexual selection would often produce features that reduce the ability to escape from predators because aesthetic features often make a creature more conspicuous and slower. However, if females prefer beautiful males for mating, then the advantage of beauty can outweigh the advantages of camouflage and maneuverability. According to the theory of sexual selection, ornamental features will develop to the point at which the disadvantages of being caught by a predator outweigh the advantages of being selected by a female.13Evolutionists recognize that a female such as a peahen does not have aesthetic appreciation and that the preference of the female is based on an instinctive response. In addition, it is recognized that the instinctive response needs to be specified by one or more genes in the genetic code14 called preference genes. Do the peacock tail feathers play a role in the courtship ritual? There is no doubt that the peacock tail feathers do play a role in the courtship ritual of peafowl. Many creatures have a courtship ritual that acts as a cue for mating. In the case of the peafowl, the peacock shows his intention to the peahen by displaying his feathers. However, even though the display feathers have a role in the courtship ritual, this does not necessarily mean that the female is ‘attracted’ to the feathers. When the peahen observes the feathers of the peacock, it may be that her only reaction is to understand that the peacock is ready for mating.Of course, the beauty of the peacock tail display is vastly beyond what is required to make a cue for the peahen. Do preference genes exist in the peahen? Biologists have carried out studies on the behavior of peafowl during courtship to try to determine if the peahen is really attracted to particular features of the peacock. One study has revealed that peahens do recognize obvious features in the
peacock such as the number of eye feathers. 15 The results of this study indicated that the peahen prefers males with a greater number of eyes. However, other studies have indicated that the peahen has little or no interest in the appearance of the peacock.16 There is no evidence that peahens can recognize subtle aesthetic features.If there is a preference gene for aesthetic features, this does not prove that the sexual selection theory is true. The reason for this is that a preference gene were installed as a means of ‘maintaining’ beautiful features. Beauty generally gives a disadvantage in terms of escaping from predators. If a peacock lost its colours due to a gene mutation, it would suddenly find itself more protected from predators. This is an example of where a loss of information could be a great advantage in terms of survival. Even in the case of subtle aesthetic features, it is conceivable that a intelligent designer may have created preference genes in order to root out genetic mistakes. However, there would be less selective pressure for subtle features to be lost since they do not affect the ability of the peacock to escape from predators.At present, there is no conclusive evidence about the existence of preference genes. Future experiments in this area should be very interesting, especially if a preference gene could be directly identified in the genetic code. It is possible, though, that the peahen does have preference genes for obvious features like colour. However, it is unlikely that preference genes exist for subtle features like the brown coating of the stem near the eye pattern. Problems with the theory of sexual selection If future experiments show that there are no preference genes in the peahen, then the theory of sexual selection would absolutely collapse. However, even if future studies do reveal a preference gene for obvious aesthetic features, there are still some very serious problems with the theory of sexual selection. Five of the problems are: (i) Why should the female select a ‘beautiful’ feature? When females have a preference, that preference becomes self-perpetuating. 14 However, there is no reason a fashion should always be a ‘beautiful’ fashion. According to evolution, preference genes appear by totally random processes and therefore there could be a fashion for all kinds of features including ugly features. In reality, where males have decorative features, such as the birds of paradise and the peafowl, it is clear that every aesthetic feature contains a very high degree of aesthetic merit. To overcome the problem that females always prefer beautiful features, evolutionists have proposed the ‘good genes’ theory that proposes that beauty is directly related to health and fitness. 17 However, the decorative features found in nature are so overwhelmingly beautiful that it would require an extremely strong correlation between beauty and health and there is no evidence for such a strong correlation. (ii) How can the sexual selection cycle start by chance? Another big problem with the theory of sexual selection is the question of how the sexual selection cycle can start by chance. The cycle cannot start until there is both a trait gene and a preference gene. Therefore for a sexual selection cycle to get started there must be the appearance of two new genes in the DNA. Since genes contain complex information and since the preference gene and trait gene are useless on their own, it must be concluded that sexual selection could never spontaneously commence on the basis of incremental changes to the DNA.To overcome the problem of the simultaneous appearance of two new genes, evolutionists have proposed that the two genes appear at different places and different times in the following way.18 First, a female spontaneously produces a preference gene for a male with, say, a long tail. This gene lies dormant for perhaps many generations without any opportunity to be expressed. Then one day, a male spontaneously generates a gene which produces a longer tail. The female then selects that male and some of their offspring have both the trait gene and the preference gene. Therefore, the cycle is in place and ready to develop and perpetuate long tails.At first, this scenario may seem plausible. However, it still relies on simultaneous chance events. Firstly, there must be a preference gene thatmatches a trait gene. Secondly, there must be a chance meeting between the right female and male. The first gene to arise also has to survive genetic drift until the male gene arises. Therefore, even with the scenario given by the evolutionists, it is clear that the sexual selection cycle is extremely unlikely to get started. (iii) How can multiple aesthetic features start by chance? The starting of one sexual selection cycle is difficult to explain by chance. However, when a creature contains many separate aesthetic features, the problem becomes even more pronounced because many cycles must be started. In the case of the peacock, there are many aesthetic features in the tail. In addition, the peacock also has several aesthetic features in the rest of its body. For example, it has a bright blue neck, patterns around the eyes, a crown on the head and speckled contour feathers. This array of features would probably require many sets of preference genes and trait genes. (iv) How can the female appreciate subtle features? It may well be possible that a peahen has a preference for obvious features such as a long tail. However, there are some extremely subtle features in the peacock which are not easy to recognize. These subtle features include an absence of a stem in the upper part of the eye pattern, the brown colouring of the stem near to the eye pattern and the intricate shape of the ‘T’ feathers. It may be reasonable to argue that a peahen could recognize whether a peacock had lost its eye feathers or T feathers. However, to discern subtle changes in these feathers would require tremendously detailed observation.The above features are so subtle that many people do not notice them. In addition, it is necessary to get quite close to the feather to recognize such features. Since peahens do not undertake close visual inspections of the peacock, they would have to have a much better eye for detail than a human being in order to recognize the subtle features of the peacock tail.Darwin himself recognized the problem of subtle aesthetic features. Darwin said, ‘Many will declare that it is utterly incredible that a female bird should be able to appreciate fine shading and exquisite patterns. It is undoubtedly a marvellous fact that she should possess this almost human degree of taste’.19 What is really incredible is that evolutionists really believe that a peahen is able to recognize fine shading and exquisite patterns. There is no evidence that the peahen can recognize such subtle aesthetic features. (v) Some features contain irreducible mechanisms Some of the structures that produce the aesthetic features in the peacock tail are irreducible. This means that they require several features to be simultaneously present in order for the structure to function. One example of an irreducible structure is the thin-film interference. Thin-film interference in a feather requires all of the following features to be simultaneously present: 1. Flat barbule(s) 2. Keratin layer(s) 3. Correct thickness of keratin layer(s) Since evolution is supposed to work by changing one parameter at a time, thin-film interference cannot be produced by a process of evolution. For example, if there was a random gene mutation that suddenly caused a barbule to become flat, this change would not be enough to cause thin-film interference. Even if a barbule were to become flat and acquire a layer of keratin, this would still not produce a thin-film colour unless the keratin was the right thickness.Getting the right thickness of keratin by chance is very difficult because the keratin thickness has to be within a very narrow range for thin-film interference to work. For thin-film interference to work, the thickness of keratin normally has to be within a range of 0.4–1.5
µm. However, keratin can be formed in thicknesses from 0.2 µm up to 1 mm. For example, nails and feather stems have keratin with a thickness of around 1 mm. If one considers 1,000 different layers of keratin which all have a different thickness ranging from 1 µm, 2 µm, 3 µm, etc., all the way to 1,000 µm (1 mm), only one or two out of the thousand thicknesses would produce thin-film interference. Therefore, it is inconceivable that a peacock could acquire a flat barbule and exactly the right thickness of keratin simultaneously. The only way to produce iridescent feathers is to make a fully functioning flat thin-film barbule from the beginning.The fact that thin-film interference is a delicate and sophisticated mechanism is fully acknowledged by evolutionists. For example, Mason says the following:‘The theory of thin films as the cause of iridescence, although it fits all the observed facts, cannot but inspire one to marvel at the perfection of nature’s method of producing these colours with such uniformity through successive generations, especially when a slight general variation in thickness of the films of the feathers of a bird, such as a peacock, would be enough to alter its coloration completely.’ 20This is an important quote because Mason’s studies on the colour of peacock feathers are referred to by most modern texts on bird coloration. Notice how the author refers to the ‘perfection of nature’s method’, and marvels at how the thin-film is maintained in successive generations. If it is hard to understand how the peacock ‘maintains’ its delicate structures through successive generations then how does the evolutionist explain how it could have evolved in the first place? (vi) Some features contain irreducible beauty According to evolution, a complex pattern like the eye pattern in the peacock’s feather has evolved by the accumulation of hundreds of genetic mistakes occurring over vast periods of time. However, patterns like the blue ellipsoid in the eye are irreducible, i.e. they require several features to be simultaneously present in order for there to be a clear pattern. If only one barb in a peacock tail feather was to have a patch of blue colour this would not produce a beautiful pattern. Such a random change would arguably cause the peahen to deselect, not select the pattern. Since evolution requires every step change to have a selective advantage, the eye pattern cannot evolve but must be designed complete from the beginning. Alternative theories for the existence of beauty The difficulties with the theory of sexual selection have led some evolutionists to develop alternative theories for the origin of beauty. The existence of these alternative theories suggests that the theory of sexual selection is not sound. The main alternative theories are: (i) Male pecking order Some evolutionists believe that males like the peacock compete with other males in order to win a privilege of mating with a female.21 It is believed that the competition can be based on the beauty of a display. The idea is that the male with the most impressive display frightens the other males into submission. A major problem with this theory is that it cannot explain why there should be subtle aesthetic features. (Ii) Camouflage Some evolutionists claim that the peacock tail gives a camouflage advantage. 22 The reason they believe that camouflage plays a role is that the peacock train (i.e. undeployed tail feathers) is mostly green and supposedly provides camouflage when it hides in trees. However, the theory of camouflage also has serious problems. Firstly, the tail makes the peacock more conspicuous on the ground, which is arguably where the greatest danger is to be found. Secondly, camouflage does not explain how the subtle eye patterns could have evolved. Thirdly, if the function of camouflage were really effective then the peahen should also have such a tail. (Iii) Recognition Some evolutionists believe that the colour and pattern of the peacock tail has the sole function of making the peacock recognizable to the peahen.23 However, this theory cannot begin to explain the origin of the subtle aesthetic features of the peacock. Added beauty Figure 8. Added beauty in a column. The beauty of the peacock tail can be termed ‘added beauty’ because it appears to be surplus to that necessary to survive. In other words, the beauty of the peacock tail is not a by-product of the function of the tail. Added beauty can be a powerful evidence of design because it is a common hallmark of an intelligent designer. The hallmark of added beauty can be seen in all kinds of human design. For example, an architect often adds decorative features to the different parts of a building. The adding of beauty to a column is illustrated in Figure 8 (left), which compares a classical column with a plain functional cylinder. The decorative features of the classical column have the sole function of providing a beautiful spectacle. But they also present evidence that an intelligent designer has designed the column. So also the added beauty of a peacock tail reveals an intelligent designer.Most evolutionists accept that creatures like the peacock have added beauty. This is why the peacock tail feathers are referred to as decorative feathers in standard biology textbooks. Darwin said this about beauty in nature: ‘A great number of male animals … have been rendered beautiful for beauty’s sake’; ‘the most refined beauty may serve as a charm for the female, and for no other purpose.’ 24 Considering that evolutionists recognize added beauty in nature, and considering that added beauty is very much a hallmark of an intelligent designer, beauty in nature must be seen as an important evidence of design. A study of added beauty in nature has been described in my bookHallmarks of Design.25 Conclusion There are many beautiful features in the peacock tail such as bright iridescent colours, intricate patterns and the fanformation of the displayed feathers. The mechanisms that are responsible for producing these beautiful features are very sophisticated. In particular, the barbules contain an astounding level of precision design in order to produce optimum thinfilm interference.There are several serious problems with the evolutionary theory of sexual selection. There is no satisfactory explanation of how the sexual selection cycle can start or why the peahen should prefer beautiful features. In addition, there is irreducible complexity in both the physical structure of the feather and in the beautiful patterns. Darwin once said, ‘The sight of a feather in a peacock’s tail, whenever I gaze at it, makes me sick!’26 If Darwin knew about the modern discoveries re the complexities of the peacock tail, he would have even greater reason to feel sick. WHAT ABOUT PEPPERED MOTHS?WHY ARE THEY FREQUENTLY USED TO SUPPORT EVOLUTION.
Goodbye, peppered moths A classic evolutionary story comes unstuck by Carl Wieland The ‘textbook story’ of England’s famous peppered moths (Biston betularia) goes like this. The moth comes in light and dark (melanic) forms. Pollution from the Industrial Revolution darkened the tree trunks, mostly by killing the light-coloured covering lichen (plus soot).The lighter forms, which had been well camouflaged against the light background, now ‘stood out,’ and so birds more readily ate them. Therefore, the proportion of dark moths increased dramatically. Later, as pollution was cleaned up, the light moth became predominant again.The shift in moth numbers was carefully documented through catching them in traps. Release-recapture experiments confirmed that in polluted forests, more of the dark form survived for recapture, and vice versa. In addition, birds were filmed preferentially eating the less camouflaged moths off tree trunks.The story has generated boundless evolutionary enthusiasm. H.B. Kettlewell, who performed most of the classic experiments, said that if Darwin had seen this, ‘He would have witnessed the consummation and confirmation of his life’s work.’ 1Actually, even as it stands, the textbook story demonstrates nothing more than gene frequencies shifting back and forth, by natural selection, within one created kind. It offers nothing which, even given millions of years, could add the sort of complex design information needed for ameba-to-man evolution.Even L. Harrison Matthews, a biologist so distinguished he was asked to write the foreword for the 1971 edition of Darwin’s Origin of Species, said therein that the peppered moth example showed natural selection, but not ‘evolution in action.’However, it turns out that this classic story is full of holes anyway. Peppered moths don’t even rest on tree trunks during the day.Kettlewell and others attracted the moths into traps in the forest either with light, or by releasing female pheromones—in each case, they only flew in at night. So where do they spend the day? British scientist Cyril Clarke, who investigated the peppered moth extensively, wrote:‘But the problem is that we do not know the resting sites of the moth during the day time. … In 25 years we have found only two betularia on the tree trunks or walls adjacent to our traps (one on an appropriate background and one not), and none elsewhere.’ 2The moths filmed being eaten by the birds were laboratory-bred ones placed onto tree trunks by Kettlewell; they were so languid that he once had to warm them up on his car bonnet (hood).3And all those still photos of moths on tree trunks? One paper described how it was done —dead moths were glued to the tree.4 University of Massachusetts biologist Theodore Sargent helped glue moths onto trees for a NOVA documentary. He says textbooks and films have featured ‘a lot of fraudulent photographs.’ 5,6Other studies have shown a very poor correlation between the lichen covering and the respective moth populations. And when one group of researchers glued dead moths onto trunks in an unpolluted forest, the birds took more of the dark (less camouflaged) ones, as expected. But their traps captured four times as many dark moths as light ones—the opposite of textbook predictions! 7 University of Chicago evolutionary biologist Jerry Coyne agrees that the peppered moth story, which was ‘the prize horse in our stable,’ has to be thrown out.He says the realization gave him the same feeling as when he found out that Santa Claus was not real.5Regrettably, hundreds of millions of students have once more been indoctrinated with a ‘proof’ of evolution which is riddled with error, fraud and half-truths.8 The Moth Files An UPDATE on the Peppered Moth fiasco by Carl Wieland Most people learned about these little moths in school as the ultimate triumph of Darwinism—evolution ‘captured in action’. Creation magazine reported (21(3):56) how the Peppered Moth story has fallen apart, with revelations of faked photos and more. So now that much of the dust has settled, what is the latest concerning this sensational debunking? Background The story concerning England’s Peppered Moths (Biston betularia) originally seemed very straightforward. The research is attributed to one H.B. Kettlewell, who is reported to have said that Darwin would be overjoyed to see the vindication of his theory. The insects used to be mostly of a light form, with occasional darker (melanic) forms. Light-coloured lichen growing on tree trunks meant that the light forms were very well camouflaged, while the dark ones would ‘stand out’ to the eyes of hungry birds.Pollution from the Industrial Revolution is said to have killed off much of the pale lichen covering the tree trunks, thus darkening them, so that now the dark forms were better camouflaged. Therefore, it made sense that hungry birds would eat more of the lighter ones, so the dark ones would become the dominant form.Kettlewell’s experimental observations were supposed to have shown that this is indeed what happened. Then, as pollution began to be cleaned up, the tree trunks became lighter again, so light moths resting on the tree trunks would now be less easily seen, thus the ratio shifted the other way.Photographs were taken of the dark and the light forms resting on the tree trunks, showing how obvious the camouflage differences were. To further ‘clinch’ the case, birds were filmed preferentially ‘picking off’ the less camouflaged forms. Selection, not evolution As we reported, the whole issue—ratios of dark to light moths shifting back and forth in response to their environment—is no big deal in the creation/evolution argument anyway. The famous evolutionary biologist L. Harrison Matthews, writing in the foreword to the 1971 edition of Darwin’s Origin of Species, pointed out that the Peppered Moths observations showed natural selection, but not evolution in action. Selection is an important part of evolutionary theory, but it is not the same thing. However, most evolutionists, including H.B. Kettlewell, write as if they were the same thing, muddying the waters for the lay public.1 Natural selection is also an important part of the Creation/Fall model, and was even discussed by the creationist Edward Blyth, 25 years before Darwin.Since there is that confusion, and since the moth story is so easy to understand and explain, it is not surprising that evolution’s apostles were motivated to ‘push’ the Peppered Moth scenario as hard as possible in educational and media circles. This made it doubly embarrassing for them when key elements of the story fell apart. The whistle blows The bubble started to burst as people finally faced the awkward fact that Peppered Moths do not rest on tree trunks in the daytime. Instead, they hide under leaves in treetops. As the story unravelled, it turned out that:The famous photos of light and dark moths resting on a lichen-covered tree trunk were faked by pinning and/or gluing dead moths onto logs or trunks.The filmed ‘experiments’ involved either dead moths, or laboratory moths (so stuporous they had to be warmed up first), placed on tree trunks in the daytime.We reported the reaction of evolutionist Jerry Coyne of the University of Chicago. He said that finding out the moth story was wrong was like when he found out at age six that it was actually his father who was bringing the Christmas presents.So what has happened since this story (which should never have been seen as proof of evolution anyway) collapsed so badly for evolutionists?The author of the main book that revealed the flaws, Michael Majerus, still defends the basic textbook story. He and other defenders admit, however, that there are serious problems with Kettlewell’s experiments, and that Kettlewell’s successors tested the bird’s feeding behaviour using dead moths.The previously mentioned Dr Jerry Coyne, apparently furious that creationists are making good use of his comments, seems to be hastily backpedaling, saying that the moths are still a good example of ‘evolution’.Others, like the University of
Massachusetts’ Theodore Sargent, are less forgiving, pointing out that the situation was totally artificial. The birds would have quickly learnt of a ‘free lunch in the woods’.Judith Hooper, the author of a just-released book 2 on the moth saga points out the serious clouds over some of Kettlewell’s results, which others have not been able to confirm. Noting that his field notes have conveniently disappeared, she says, ‘The unspoken possibility of fraud hangs in the air.’3The consensus appears to be, however, that the proportion of dark to light moths did indeed rise and fall in concert with the rise of (and subsequent decline in) industrial pollution. The main argument concerns whether this was due to differential predation by birds. (Even if it was, most now agree that Kettlewell’s lichen story may have had less to do with it than simple discolouration of the trunks by soot.)Whether or not it turns out that the moth population change was due to bird predation, two issues stand out. The first is the way in which evolutionists eagerly seized upon and promoted a story reeking with incompetence,naïveté and outright fraud. How come it took 50 years to wake up to the fact that no-one had ever actually seen Peppered Moths on tree trunks? (Why should moths of any colour spend their sleep time sitting in the open, anyway?) More importantly, this saga gives us the opportunity to repeatedly point out to an indoctrinated public the difference between natural selection as an observable, logical fact, and goo-to-you evolution. The evolutionary story demands creative additions of new information. Natural selection merely filters information by culling it; it can never add anything new.4 The bottom line Three statements sum up the biological reality about this issue. Before the industrial revolution, there was genetic information for dark and light moths. During the worst days of pollution, there was genetic information for dark and light moths. Today, there is genetic information for dark and light moths. In other words, the only thing that’s happened is that the relative numbers of each have gone up and down. What do I think should be the real take-home lesson of the Peppered Moth saga? The fact that this amazingly banal set of events has been hammered worldwide as ‘ultimate proof’ for a belief that microbes originally turned into moths (and moth researchers)! This is far more stupefying to contemplate than even all the faked photos and talk of fraudulent experiments. More about moths A recent attempt to restore the reputation of the peppered moth as an evolutionary icon falls flat T.F. writes: To Dr Carl—I read your stuff a while back where you claimed that the peppered moth stuff was based on fraud. I was disturbed when someone showed me a recent science article that unfortunately for you undermines this claim. It shows that the moths are a classic example of evolution after all. I hope you will retract your claims now in the light of this new evidence. Carl Wieland replies: Thanks for your email. By our ‘stuff’ on the peppered moths, I presume you are referring to one section of our tract, ‘Frauds used to support evolution’, or most likely to my 1999 article in Creation magazine on which it was based,Goodbye Peppered Moths. And/or to the follow-up Creation article in 2002, The Moth Files.And I presume that the recent evolutionist article you refer to would almost certainly be ‘The Moths at War’ in New Scientist.1 Your comment comes at a convenient time, as I had already started writing about this rather bald-faced attempt to falsely smear creationists. Rebutting it will be helpful to others, too, so please excuse if I am overly detailed in my reply.If one reads both our items and the New Scientist article carefully, it becomes clear that far from our comments having to be retracted, this latest story seems to be a classic case of misleading ‘evolution-spin’, trying to convert a public embarrassment into a PR victory against creationists.This concerns the classic example of ‘evolution in action’, England’s peppered moth, Biston betularia. The story in brief: The moth comes in two forms, light and dark. After the industrial revolution, pollution darkened England’s tree trunks.2 The Darwinian enthusiast H.B. Kettlewell claimed to have shown that after the industrial revolution, the darker moths predominated, and that this was the result of birds preferentially picking off the lighter forms on the now darkened tree trunks. This example became known as ‘industrial melanism’.3Our items highlighted the comments of other evolutionists that indicated that this example could no longer be regarded as proof positive of Darwinism—and that its ‘iconic’ status for evolution was based on some rather dubious practices. The key points in our items: That biologists have noted that it is extremely hard to find moths resting on tree trunks during the day—their favoured place appears to be in hiding under leaves. That Kettlewell released lab moths onto tree trunks that were in a state such that they may not have naturally rested on the tree trunks. Classic ‘textbook’ photos of the moths resting on tree trunks were faked, as dead moths were pinned or glued to the tree trunks. The ‘teaching’ film of the moths being eaten by birds was also ‘staged’ and not a true natural situation. That such ‘industrial melanism’ type of natural selection due to differential predation could easily be real, but would be trivial anyway. As we have pointed out countless times in our articles, natural selection is fact, and does not equal ‘evolution’ of itself. (Whether by differential reproduction or differential survival, it occurs via culling or loss of genetic information, not its creation.)That evolutionists were misrepresenting natural selection as ‘evolution in action’ was a secondary point; the main one was that there was so much seeming desperation to convince students of evolution that its proponents were willing to overlook these serious flaws, and even use fake photographs to buttress the point. The New Scientist article claims: That creationists have exploited ‘legitimate scientific debate over the fine details’ concerning these moths to unfairly attack the whole example, and with it, evolution itself.That when Chicago evolutionist Jerry Coyne said, ‘For the time being we must discard Biston as a well-understood example of natural selection in action’, he was taken out of context, selectively quoted, was unfortunately ‘unclear’, etc.That non-creationist journalist Judith Hooper, who in her book Of Moths and Men not only highlighted what even this New Scientistarticle agrees is the ‘flawed’ nature of Kettlewell’s experiments, but also accused him, without adequate evidence, of fraud (which was unfairly seized upon by creationists). 4That one of the biologists who had raised some of the initial issues about the moth observations, Michael Majerus, has ‘finished an exhaustive experiment … to reverse the creationists’ advances’ and that his preliminary results are ‘enough to fully reinstate the moth as the prime example of Darwinian evolution in action.’Importantly, the article does not even attempt to refute what we reported about the fakery involved in pinning dead moths to tree trunks. And the article itself concedes that Kettlewell’s
procedures were substantially flawed.Instead, it pushes the ‘strawman’ premise (so far as CMI’s articles are concerned, anyway) that the creationist articles were attacking natural selection as such, or at any rate were gloating that natural selection had been seen to fail precisely in the situation where it was touted the most. 5 But, as shown, our items made it clear that the validity of natural selection as such was never in doubt and not the issue at all.What about Majerus’s ‘exhaustive experiment’ that has allegedly triumphantly restored the moth’s trophy status for Darwinists? Well, let me say once again that if it had been convincing, one would have said, ‘Big deal—what’s surprising about that?’ But ironically, what we see once more is the desperation of Darwinists in the propaganda war, as well as a total misunderstanding/misrepresentation of the creationist position on natural selection. Majerus spent seven years releasing moths (overcoming the procedural flaws in Kettlewell’s experiments) such that some came to rest on light-coloured trunks, and he watched birds eat some of them. His earth-shaking results?Birds found it easier to spot (and hence eat) darker moths on light surfaces than their lighter counterparts. (One finds it hard to resist a ‘duh … ’)This accounts for the fact that the ones he released that went missing (thus presumably eaten) were 29% of the dark ones compared to 22% of the light ones.As if that were not trivial enough, even this article attempting to present the experiment as a ‘coup de grace’ for evolution makes it plain that it ‘doesn’t satisfy all evolutionary biologists’. Some of these evolutionist critics point out that other animals also eat moths in nature, and may have different preferences for light and dark moths. And, most significantly of all, the article points out that the frequencies of light and dark moths ‘do not always correlate with the level of pollution’ anyway. But one can overlook all the frantic arm-waving and trumpet-blowing over whether the article demonstrates natural selection, (which is a process we don’t think needs to be demonstrated anyway—it is a self-evident logical deduction, as well as having been amply observed elsewhere). What is truly disturbing is the way in which the leap is made from an observed change of gene frequencies (which is what industrial melanism, if adequately demonstrated, would be) to, in Majerus’s quoted words, ‘the proof of evolution’. The word ‘evolution’, of course, means in most people’s minds the whole notion that particles have turned into people.To say that because evolution requires a change in gene frequencies, demonstrating such a change demonstrates evolution is a logical fallacy of the following type (technically called affirming the consequent): For me to be a good driver requires that I have good eyesight. I can demonstrate that I have good eyesight. Therefore I am a good driver. That should be amply clear from such articles on this site as Muddy Waters, The Evolution Train’s A-comin , and Beetle Bloopers. A young age model would also predict changing gene frequencies with time, but within the limits of the original kind plus the addition of (mostly information-losing) mutations. Even as renowned an evolutionist as Pièrre-Paul Grassé, holder of the Chair of Evolution at the Sorbonne, made it clear that one can have mutations and selection in bacteria, for example, changing gene frequencies, but that this is a shift to the left, a shift to the right, with no net long-term result. Equally, the moths have shifted with pollution towards darker forms, then as the air has cleared up over the decades, the moth population has generally headed back again towards the situation where the lighter forms predominate once more. Where, then, is the net evolutionary change, the generation of novelty that is required by the theory?The biologist L. Harrison Matthews was prominent enough to be asked to provide the foreword to the 1971 edition of Darwin’s Origin of Species. He was at the time clearly also quite happy to see the moths, as does Majerus, as an example of selection in action (which would be no big deal to us, too). So it’s worth noting what he says in that foreword (emphasis added):‘The experiments beautifully demonstrate natural selection—or survival of the fittest—in action, but they do not show evolution in progress, for however the populations may alter in their content of light, intermediate or dark forms, all the moths remain from beginning to end Biston betularia.’Towards the end of the article, Majerus is cited as making a revealing statement. He says that the birds-eatingmoths story is ‘easy to understand because it involves things we are familiar with’. Exactly. It makes it easy to indoctrinate students with an example that makes sense, and then have them thinking that they have seen a process that somehow creates new things in biology. It is all part of the passion for the moth story, a story that evolutionists bolstered with not only inadequate procedures, but faked photographs. (And this passion has ensured that some major noses got out of joint when creationists made legitimate use of the revelations.) 6 This is the reason why, to ensure it was understood and ingrained in students, some evolutionists faked/staged photographs in the first place. And it is clearly the reason for this article, to try to rehabilitate at all costs the idea (which may be true, it’s just that there is so little evidence for it) that the birds are definitely responsible for the changes in frequencies. Which makes it all the more ironic that the same article cites other evolutionists as saying that the jury is still out, even on that aspect of it.And what about the alleged out-of-context (a politician’s favourite ruse) quotation of Jerry Coyne? In reality, as our articles show, it was never just a matter of him ‘pointing out some cautions’. We cited him from an article in his own hand in Nature magazine as indicating that the revelations about the moth story gave him the same feeling he had when he found out that Santa Claus was not real, and it was his father bringing the presents.7 As we said in the 2002 article mentioned earlier, ‘Three statements sum up the biological reality about this issue. Before the industrial revolution, there was genetic information for dark and light moths. During the worst days of pollution, there was genetic information for dark and light moths. Today, there is genetic information for dark and light moths. ‘In other words, the only thing that’s happened is that the relative numbers of each have gone up and down. What do I think should be the real take-home lesson of the Peppered Moth saga? The fact that this amazingly banal set of events has been hammered worldwide as “ultimate proof” for a belief that microbes originally turned into moths (and moth researchers)! This is far more stupefying to contemplate than even all the faked photos and talk of fraudulent experiments.’ Thank you once again—I have truly appreciated the opportunity to draw attention to this astonishing New Scientist article. If anything, the ‘beatups’ and ‘spin’ it so obviously utilizes strengthen the point about how desperate evolutionists are not to have this particular ‘icon’ exposed for what it is—at best, an extremely trivial example of natural selection (not ‘the proof of evolution’). WHAT ABOUT COMPTER SIMULATIONS ALLEGEDLY PROVING EVOLUTION BY CUMULATIVE SELECTION Weasel, a flexible program for investigating deterministic computer ‘demonstrations’ of evolution
by Les Ey and Don Batten Summary In his book, The Blind Watchmaker, Richard Dawkins described a computer program and the results that he claimed demonstrated that evolution by random changes, combined with selection, was virtually inevitable.The program described herein mimics Dawkins’ program, but also provides the user with the opportunity to explore different values for the parameters such as the mutation rate, number of offspring, the selection coefficient, and the ‘genome’ size. Varying the values for these parameters shows that Dawkins chose his values carefully to get the result he wanted. Furthermore, the user can see that, with realistic values for the parameters, the number of generations needed to achieve convergence increases to such an extent that it shows that evolution of organisms with long generation times and small numbers of offspring is not possible even with a uniformitarian time-frame. And this is with a deterministic exercise, which cannot be a simulation of real-world evolution anyway. The program also allows the user to set up a target amino acid sequence with the mutations occurring in the DNA base pair order. Since there is redundancy in the triplet codons, the dynamics of the convergence are different to a simple alphabetical letter sequence. The program also allows for the user to include deletions and additions, as well as substitutions, as well as variable length in the ‘evolving’ sequence.Cosmologist Sir Fred Hoyle (1915–2001) said the probability of the formation of just one of the many proteins on which life depends is comparable to that of the solar system packed full of blind people randomly shuffling Rubik’s cubes all arriving at the solution at the same time.1 In others words, it is impossible. In response to this huge problem for their naturalistic scenario, many evolutionists try to avoid the issue by breaking the evolution of proteins down into small and gradual steps. Richard Dawkins, a prominent atheist, is one such apologist.Many introductory courses in biology at universities have The Blind Watchmaker, by Dawkins,2 as required reading. The title, a play on William Paleys’ watchmaker analogy, wherein Paley (1743–1805) argued that the complexity of living things demanded an intelligent creator, reveals Dawkins’ aim—to rid his readers of any sense of a need for a Creator. The blind watchmaker is purely natural—mutation and natural selection. Dawkins’ book is an undisguised polemic for atheism.In this book, Dawkins presents a description of a computer program that generated the sequence of letters, ‘METHINKS IT IS LIKE A WEASEL’3from a starting sequence of random letters. The process involves randomly changing letters in each ‘generation’ and selecting the ‘offspring’ closest to the target sequence. The mutation and selection process is repeated until the sequence is arrived at. This supposedly showed that evolution by cumulative selection of favourable random changes was inevitable, easy and fast.At the time (1986) it was fairly showy to have a computer program to demonstrate something and many readers were duped into thinking that the program had proved something, not realizing that a program will do whatever its programmer designs it to do. Because of the deceptive nature of Dawkins’ demonstration, several creationist authors saw the need to counter Dawkins’ dupe. 4–6 These authors have pointed out reasons why Dawkins’ program does not ‘prove evolution’. It should be fairly obvious that any program that sets a target sequence of letters and then achieves it, by whatever means, has not demonstrated that the information in the sequence has arisen by some natural process not involving intelligence. The programmer specified the information; it did not arise from a ‘simulation’ of evolution.Dawkins’ program has apparently been lost. Evolutionist David Wise wrote a program that gave similar results to Dawkins’ program.7 CreationistRoyal Truman created an Excel spreadsheet program that generated similar results to Dawkins’ program.8In this paper we describe a stand-alone program, Weasel, that closely mimics the one Dawkins describes, as well as providing a range of options for the user to explore—such as user-defined mutation rate, offspring number and selection coefficient. The program also provides for a peptide sequence target, with mutations occurring in the base sequence of a randomly generated DNA segment. How Dawkins’ program worked To begin with, a target string of letters was chosen. Dawkins chose, ‘METHINKS IT IS LIKE A WEASEL’. Next, the computer generated a sequence of random uppercase letters to represent the original ‘organism’. So, there were only 26 letters, plus a space, to choose from to generate the starting organism. This sequence always contained exactly the same number of letters as the target phrase—28 letters and spaces. The parent sequence would be copied, probably about 100 times (how many is not stated, but it must be a large number to get the results obtained), to represent reproduction. With each copy there would be a chance of a random error, a mutation, in the copying. Now for what was supposedly analogous to selection, each copy would now be tested to determine which copy was most like the target string ‘METHINKS IT IS LIKE A WEASEL’. A copy would be chosen even if only one letter matched the target in the correct place, so long as it happened to be the best match.The chosen copy would then be copied several times, again with introduced errors in the copying. In turn this ‘progeny’ was also tested to find the best match. This process would be repeated until a copy was found that matched the target exactly. Weasel Weasel was written in Borland Delphi by LE. It is a freeware, but copyrighted, Windows program and you can click here to download. (895 kB zip file) Standard models available in Weasel: Under the Models menu item within Weasel, four models are available: Dawkins (default), error catastrophe, realistic mutation rates and DNA model. Dawkins model (default) In the Dawkins model (Figure 1), the target sequence and parameters are set as per Dawkins’ original exercise. Running the model will show convergence on the target usually in 30 to 60 generations (iterations). Since this is a probabilistic exercise involving a random starting sequence and random mutations, the result will vary with each run. The only addition to the original program concept here is the ‘generation time’. Here the years for a generation can be entered and the program then calculates the time taken for the convergence on the target (obviously if your imaginary organism has a generation time of hours, then read the Figure 1: A screen shot at the end of run of output bar at the bottom left as hours, not years). the Dawkins model, showing the user Error Catastrophe model interface, the output window and status Error catastrophe occurs when genetic information is destroyed by bars. Click on image above to see a higher mutations at such a rate that all progeny are less fit than the parent/s so resolution screen shot. that selection cannot maintain the integrity of the genome and, in a Dawkinsian-type model, a target sequence cannot be achieved.In the Error Catastrophe model, the offspring number is simply reduced from 100 to 10; all other parameters remain as in the Dawkins model. Because the number of offspring is low, the chances of a desirable mutation occurring in at least one offspring are reduced. Furthermore, as the model moves towards convergence,
the probability of a mutation undoing what has been achieved rises to the point where it equals the probability of adding a desirable new mutation. So the model fails to converge.The user can also induce error catastrophe by increasing the mutation rate after selecting the option for . One mutation in six letters per generation is about the error catastrophe point with 100 offspring. With 10 offspring the error catastrophe mutation rate drops to about 1 in 18. Increasing the length of the target letter sequence shows that the mutation rate has to be decreased in proportion to avoid error catastrophe.To avoid error catastrophe, the mutation rate (per letter or base per generation) has to be inversely proportional to the size of the genome. That is, the larger the genome, the lower the mutation rate. Once this is factored into the theory, ‘evolution’ slows down to such a slow pace that it could never account for the amount of biological information in existence (the basic point of ‘Haldane’s Dilemma’, which Walter ReMine spells out in his book 9).With an amino acid sequence (‘DNA model’ under the menu item), with a small offspring number of say 10, the substitution mutation rate cannot be much more than one in the length of the target sequence. E.g., if the target is 33 amino acids (99 base pairs), a mutation rate of 1 in 50 produces error catastrophe. So the Dawkins model will converge with a mutation rate of 1 in 28 with a target of 28 letters, but not on a genome just a little bit bigger and certainly not with a human-sized genome of 3x109 nucleotides. Adjusted mutation rate model In effect, the mutation rate cannot be much greater than one per genome per generation. This then severely limits the rate of progress from a chimp-like species to human, if this were possible, even with perfect selection and all the other assumptions.Real-world mutation rates are many orders of magnitude less than used in Dawkins’ model, or others supposed simulations of evolution for that matter. Spetner, in his book (right), summarizes the knowledge on actual rates of mutation as follows:‘In bacteria the mutation rate per nucleotide is between 0.1 and 10 per billion transcriptions [refs]. But in all other forms of life the rate is smaller. For organisms other than bacteria, the mutation rate is between 0.01 and 1 per billion [ref.].’10We expect that the reason for this difference between bacteria and other organisms relates to genome size: bacteria have the smaller genomes and can therefore sustain higher mutation rates without error catastrophe.Biological replication is extremely accurate. This level of accuracy is due to the processes of proof reading and error correction. This is vital since mutations disorder existing functional DNA sequences, and are therefore overwhelmingly harmful (and even rare beneficial mutations are the result of information loss).The Adjusted Mutation Rate model shows what happens when a more realistic mutation rate is applied to Dawkins’ model. A mutation rate of 1 in 100,000,000 (10 per billion letters) means that the model takes a long time to run. It could take a few weeks on a typical slower PC. Of course the Adjusted Mutation Rate model is still somewhat unrealistic, being the upper limit estimated for bacteria, but it helps to illustrate the point that real life is nothing like the Dawkins model.To cope with realistically low mutation rates, a suitable pseudo random number generator had to be found to replace the one provided in Delphi, which started to repeat the pattern before the end of a typical run. The Mersenne Twister pseudo-random number algorithm 11generates a pattern that repeats every 2 19937 numbers and distributes the numbers more evenly than Delphi’s internal generator. This makes it possible for mutation rates down to 1 in 1010 to be resolved. DNA Model Any standard biochemistry text would describe how proteins are made from the information contained in the base sequences on DNA. We have provided a brief tutorial provided with the program (under ). An important difference between the DNA model and Dawkins’ Model, or any alphabet model, is that the DNA of an organism is not compared directly with the target as it is in alphabetical model. Another important factor is redundancy, some of the amino acids can be coded by different codons. With some codons, only the first two base pairs are needed to determine which amino acid is produced. This gives the genetic code some resistance to change. In some cases you would require more than one mutation to convert the code of one expressed amino acid into the code for another.In running the DNA model, even though there are only four possible ‘letters’ compared to 27 in the Dawkins model, a target requiring 30 base pairs takes close to twice the number of generations to be reached compared to Dawkins’ target of 28 letters.The user can enter their own amino acid sequence—the program has an editor to assist in this—and adjust the various parameters to see what happens. One of the big differences in DNA mutations is that stop codons can be generated. These effectively truncate the sequence if occurring within the sequence rather than at the end. Irreducible Complexity Behe, in his book (right), uses a mousetrap to illustrate the concept of irreducible complexity.12 He points out that the individual parts of a mousetrap cannot function independently of each other. If you remove a single part or change its dimensions to a significant degree, the mousetrap will fail to function at all. This (among other issues) makes a mousetrap resistant to any step-wise explanation of its origin; that, of course, is without the aid of an intelligent designer. Dawkins’ weasel analogy, and all other evolutionary story telling, fails to address this issue. It does not demonstrate how a suite of interdependent proteins can evolve in parallel to a point where functionality appears.In Part II of his book, Behe discusses several irreducibly complex systems, such as blood clotting, where there is no conceivable gradual build up of functionality. For example, the proteins involved in blood clotting are required to act in unison. It’s not just a case of a slight lack of functionality if an essential protein is missing because the whole system is finely balanced. On the one hand, if one component is missing an animal could bleed to death; on the other hand, all of the animal’s blood could become one massive blood clot. These kinds of systems are all-or-nothing systems. Dawkins’ weasel model assumes functionality for any and every step in the run of the model with the only requirement for selection being greater likeness to the pre-specified goal.Michael Behe addresses Dawkins’ response to Paley’s argument for the irreducible complexity of a watch and the need for an intelligent designer:‘Neither Darwin nor Dawkins, neither science nor philosophy, has explained how an irreducibly complex system such as a watch might be produced without a designer.’ 13Dawkins’ concept of a slow, gradual build up of functionality is not valid for a system of proteins that have no function at all until all the proteins are present in the correct amounts and at the same time. Indeed almost every biochemical pathway is irreducibly complex. There is hardly a trait in a living organism that is independent of other traits for its function.The option in the program allows the user to specify how many of the target letters or amino acids have to be present together for an increase in ‘fitness’. This enables some recognition of the fact that not every point mutation can be adaptive in the change from one sequence to another. It does not address irreducible complexity at the system level. With set at three, for example, a mutant with one of the target letters added could not be selected against one without the letter. Nor would another mutant with two letters. Only if three new target letters were present together would the mutant be selected. With a setting of three, the number of generations for convergence for Dawkins’ model blows out to about 30,000, or about 600,000 years for human generation times—and this is with perfect selection, high mutation rate and 100 offspring!The option allows the user to specify that insertions and deletions are allowed, and the rates of occurrence per mutation event. For example, a deletion rate of 1 in 3 means that one in three mutations will be deletions. If four is then entered for insertions, then the rate for substitutions has to be 1:2.4, because a mutation can only be a substitution, deletion or an insertion. This option only applies to the adjusted mutation rate and DNA models (where is set to ‘No’), not the
basic Dawkins model. The user has to be a little judicious in selection of values for each these rates. For example, if a high insertion rate is used with a low deletion rate, at a high mutation rate, the sequence can diverge further and further away from the target as the lengths of the genomes of the offspring get longer and longer. This is another cause of error catastrophe.Other buttons on the user interface merely underline other limitations of this computer modelling of ‘evolution’: Fitness plateaus? For forelimbs to change into wings, for example, there would have to be a decrease in the functionality as legs prior to there being any increase in functionality as wings. Consequently, evolution from a tetrapod to a bird would require that the transitional animal would have to move from a fitness peak as a functional tetrapod into a fitness valley (less fit to survive) at some stage during the transition. This is a huge problem for evolutionary scenarios (ReMine discusses this14).Single parent? The Dawkins’ model, and ours, assumes asexual reproduction. This makes the offspring number in Dawkins’ model even more unrealistic, because the offspring number per generation for one bacterium is one. Sexual reproduction introduces other problems for evolutionary scenarios. These include genetic drift, wherein because only half the genetic information in a parent is passed onto each offspring, there is a significant likelihood of a given informationadding mutation being lost from a population. The other problem relates to recessive traits, where two copies of a gene need to be present for it to be expressed. Even if a male and female having one copy of the recessive gene happen to find each other to mate, the chances of an offspring receiving two copies is only one in four. This greatly slows down the rate of substitution of a new trait into a population—this is part of ‘Haldane’s Dilemma’ mentioned earlier. Fixed/average count? Is the offspring count exactly that specified for every generation, or does it vary with a mean of the set value?Guarantee mutation? In Dawkins’ model, there was apparently one mutation per offspring, and only one, in every offspring. The only random factor was the choice of which letter position would be changed and what it would be changed to. This is not the real world. A given offspring might actually receive two mutations, or none at all. When the mutation rate is not fixed, the number of generations needed for convergence increases. For example, with guaranteed mutation, 15 runs of the Dawkins model took an average of 46 generations to converge, whereas without guaranteed mutation, it took an average of 82 runs.Eliminate all but the best? This states that the selection coefficient is 1.0 in each and every generation. In other words, perfect selection operates. The sequence closest to the target is 100% fit to survive and all the others have 0% fitness—none of them survive. This is not the real world. A more typical real-world generous selection coefficient would be 0.01. If this could be factored in, the number of generations would multiply enormously.Accidental death? No allowance is made for the accidental death of the surviving organism in each generation. There is of course also no allowance made for lethal mutations. The exercise assumes that in every generation, one offspring will have 100% fitness.There are other limitations to this approach; limitations because it is a computer programming exercise. One area not covered is that mutations and selection occur in populations, not just in one individual’s offspring in each generation. This aspect introduces the whole area of population genetics. With a large population, desirable mutations are more likely—this can be seen by increasing the number of in the different models. However, the larger the population, the longer it takes for the new gene variant to take over the population, where all the individuals without the mutation have to die off (this is with realistic selection coefficients), and the more likely that it will be lost through genetic drift, etc.Other problems for simplistic models of gene evolution are also ignored: issues such as pleiotropy (one gene affecting several different traits) and polygeny (two or more genes working together to affect a trait). Another problem is multiple-coding genes, where the same sequence of DNA can be read using different frames, or the complementary strand read, or read backwards, or the messenger RNA edited (alternative splicing), to produce different proteins.15 Evolving a gene for one protein with one function is difficult enough; evolving one that can produce several different functional proteins would have to be completely out of the question. Following are some other problems that are ignored: the complexities of gene control (producing a new protein without control over the amount would not be very helpful), mutation hotspots (many base sequences are quite resistant to mutations; others are quite prone), the intron / exon structure of many eukaryotic genes (where introns are removed from the messenger RNA before protein synthesis—signals have to be coded into the DNA to control this editing) and the necessity of new control systems to destroy the new proteins when their job is finished.6 Conclusion Dawkins’ weasel program does not generate any new information—the information was completely specified in the target phrase. The target phrase is effectively a mould that is used to shape the virtual species. Perfect selection that is goal-based hammers this ‘species’ until it is forged into the likeness of the predetermined target. There is no mould that natural selection can use. The program uses many such unrealistic assumptions that all contribute to making evolution look easy, even inevitable. When the parameters of Dawkins’ weasel analogy are modified, it can be seen how carefully Dawkins chose the values for the parameters. Far from demonstrating how inevitable evolution is, the program presented here can be used to show that in realistically sized genomes error catastrophe is a major hindrance to the speed at which evolution could occur, even when ignoring all the other unrealistic assumptions. With realistic mutation rates, the program shows how slow evolution would be, even given the remaining unrealistic constraints, such as perfect selection.Added to that, the issue of irreducible complexity makes it clear that the vast amount of biological information that we see in organisms today could not have arisen from random processes, even with natural selection to supposedly aid the process.Spetner points out16 that no one has found a single point mutation that adds biological information (specified complexity). This is not to say that such a mutation cannot or does not happen, just that such mutations cannot be the mechanism for generating the vast amount of biological information that we see.
HOMOLOGY AND EMBRYOLOGY Homology made simple by Dominic Statham Have you ever noticed the many similarities that exist between different animals? Many animals have two eyes, two ears, four limbs, a heart, a brain, five digits (fingers and toes), etc. The natural world is full of these kinds of patterns and evolutionists have a special term for them. They call them ‘homologies’ or ‘homologous organs’ or ‘homologous structures’. Homologies simply refer to similarities which, according to evolutionists, are due to their being inherited from a common ancestor.So, according to evolutionists, the eyes of the different animals on the bottom row of fig. 1 are ‘homologous organs’ because
they inherited them from a common ancestor that had eyes. Similarly, the legs of these animals are ‘homologous structures’ because they allegedly inherited them from a common ancestor that had legs. So, referring again to the diagram in fig. 1, frogs, seals, birds and people are said to possess eyes and legs because they inherited them from a common ancestor that looked something like the one at the top. If you open a typical biology textbook that teaches evolution you will probably find diagrams like the ones in figs. 2–3. They show the similarities between the forelimbs (front legs or arms) of various animals. Each has a humerus shown in green, a radius shown in blue, an ulna shown in brown and digits shown in yellow. Evolutionists, of course, argue that there is a very straightforward explanation for these similarities—they were inherited, they say, from a common evolutionary ancestor. The forelimbs, they claim, are an excellent example of homology. Perhaps more than anything else, this kind of diagram has convinced many people that evolution is true. However, as with all arguments for evolution, when we scratch beneath the surface, we find that the argument collapses. Let’s see how this one collapses when it’s subject to scrutiny. The secrets of embryos Humans and frogs both have digits—that is, fingers, thumbs and toes. Now if humans and frogs have digits because they inherited them from a common ancestor, we would expect their digits to grow in a similar way. We would expect the embryonic development of the digits in humans and frogs to be basically the same, the same as in the common ancestor from which they are allegedly descended. But digit development in humans and frogs is different. With reference to fig. 4, in humans we start off with a spade-like structure and the digits—the fingers and toes—develop through the material between them dissolving away. The material between the digits is removed. (That’s how your fingers developed when you were in your mother’s womb.) In frogs it’s different. The digits grow outwardly and independently from buds. The material is added.1 If evolution were the correct explanation for why humans and frogs both have digits, we would expect their embryonic development to be similar—we would expect humans and frogs not only to have inherited the digits but because the similarity is supposed to be due to shared genes, also the same process of digit development. Interestingly, limb development varies even between one amphibian and another, for example between frogs and salamanders.2 What is so significant about all this is that these are not isolated examples. The embryonic development of so-called homologous structures isoften different— and not just with respect to limbs. As far back as 1894, the American embryologist Edmund Wilson wrote, “It is a familiar fact that parts which … are undoubtedly homologous, often differ widely … in [their] mode of formation.”3
Moreover, according to the late Spanish embryologist Dr. Pere Alberch, it is ‘the rule rather than the exception’ that homologous structures develop differently.4
Homology—a big problem for evolutionists Sir Gavin de Beer was one of the foremost embryologists of the 20 th century. He was a Fellow of the Royal Society, and went on to become the Director of the Natural History Museum in London. In 1971 he wrote a paper which he titled, Homology: an Unsolved Problem.5 Now Gavin de Beer was an evolutionist, he believed in Darwin’s theory of evolution; but he couldn’t reconcile this with the facts of embryology. In his paper he gave examples of homologous structures that developed in very different ways, from different parts of the egg or embryo and under the control of different genes. It was a mystery to him because it flew in the face what he expected to find as an evolutionist; hence the title of his paper calling homology ‘an unsolved problem’. He never solved this problem—and nor has anyone else.Gunter Wagner is Professor of Ecology and Evolutionary Biology at Yale University. Speaking of this same problem, the problem of reconciling the facts of embryology with the theory of evolution, he wrote, “The disturbingly many and deep problems associated with any attempt to identify the biological basis of homology have been presented repeatedly.” 6(Emphasis added.)Now they tell the youngsters in the schools and the students in the universities that evolution is the great unifying principle in biology. They tell us that Darwin explained the diversity of life. The celebrated evolutionist Theodosius Dobzhansky assured us that “nothing in biology makes sense except in the light of evolution.” But this is simply not true. The reality is that attempts to reconcile the facts of biology with Darwin’s theory give rise to many and deep problems. A creationist interpretation of homology
So what are we to make of all the similarities? Why do so many animals have two eyes, two ears, a heart, lungs etc? Why are the forelimbs so similar in different animals? Why is the natural world so full of these kinds of patterns? Well, normally, when people see a pattern they assume there must have been a designer; and in the absence of a satisfactory evolutionary explanation, strong patterns in nature surely point to just that—a designer. Common anatomy unifies the natural world and points to there being just one designer. Homology and homoplasy Rather than providing support for evolution, patterns of similarity seen throughout the living world, in addition to providing evidence for a single designer (see main text), actually resist naturalistic explanations, as the widespread occurrence of homoplasyindicates. To explain; quite often, animals have similar organs or structures which, in the thinking of evolutionists, cannot be explained by common ancestry. A good example is the ‘camera-eye’ which has a lens and retina, a design found in both humans and octopuses (see fig. 5). Since humans and octopuses are not thought to have inherited their eyes from a common ancestor, these are not regarded as homologous. Instead, evolutionists would refer to them as an example of homoplasy. This is also known as ‘convergent evolution’ because it is understood that the evolutionary process has ‘converged’ upon the same design independently. There are numerous examples of alleged homoplasy.8 Bats and dolphins both have echolocation systems that work in a similar way to man-made sonars.9 Some fish generate electricity, which they use to stun prey or ward off attackers, an ability that has supposedly evolved independently six times. 10 Similarly, tuna and mako sharks both move their tail fin with strong red central muscles attached to the fin with tendons. Yet in evolutionary terms, they could not have gained this (unusual for fish) mechanism from a common ancestor.11 The likelihood of evolutionary processes producing this level of similarity, based on chance mutations filtered by selection in randomly varying environments, seems very remote. Eyes are believed by some researchers to have evolved independently some sixtydifferent times.12Placentals (e.g. humans) are mammals whose young develop internally, in their mother’s womb, nourished through a placenta. Marsupials (e.g. kangaroos) are mammals that carry and suckle their young externally in a pouch. According to the theory of evolution, placentals and marsupials evolved from a common ancestor that looked a bit like a modern shrew. These early placentals and marsupials allegedly then evolved into many different animals. What is so difficult for evolutionists to explain, however, is why, in so many cases, placentals evolved almost identical forms to marsupials (see fig. 6).Many plants produce food and grow using energy from the sun, through a complex process called ‘photosynthesis’. One form of this is named ‘C4 photosynthesis’ and is particularly complex. Because of the differences between the plants that use the C 4process, evolutionists again have to argue that this evolved independently more thanthirty times.13,14 It seems mind-boggling that a process of such complexity could have evolved once; but to claim that this happened so many times stretches credibility beyond all reason. It requires a lot of blind faith to be an evolutionist! Also, sometimes structures alleged to be homologies must be explained away as homoplasies when the evolutionary family tree is changed. For example, based on supposedly homologous features in their skulls and teeth, whales were dogmatically proclaimed to have evolved from mesonychids, an extinct type of large predatory ungulate (animal with hooves). But DNA similarities convinced evolutionists that they evolved from another group—artiodactyls (‘even-toed’ ungulates), similar to the hippopotamus. So these supposedly definitive homologies must be re-interpreted as homoplasies.
Evidence for evolution? Evolutionists say that similarities undeniably point to common ancestry. But this is clearly not true, as has been shown, because close similarity is frequently found in creatures where evolutionists concede that common ancestry cannot be the explanation. Despite this, evolutionists even define homology as ‘similarity due to common ancestry [i.e. evolution]’. At the same time, homoplasy is defined as ‘similarity due to [convergent] evolution’. Hence, in the thinking of evolutionists, similarity with common ancestry is evidence for evolution, and similarity without common ancestry is evidence for evolution. Whatever similarity they find, then, is evidence for evolution!‘Homoplasy’ is no more than terminology masquerading as an explanation. The concept of homoplasy is not derived from scientific evidence but from blind faith. This faith rests upon the arbitrary assumption that natural processes can explain everything—including rampant ‘convergence’, however improbable this might appear.
Refuting Evolution 2—Chapter 6 A sequel to Refuting Evolution that refutes the latest arguments to support evolution (as presented by PBS and Scientific American). by Jonathan Sarfati, Ph.D. with Michael Matthews Argument: Common design points to common ancestry Evolutionists say, ‘Studies have found amazing similarities in DNA and biological systems—solid evidence that life on earth has a common ancestor.’ First published in Refuting Evolution 2 Chapter 6 Common structures = common ancestry? In most arguments for evolution, the debater assumes that common physical features, such as five fingers on apes and humans, point to a common ancestor in the distant past. Darwin mocked the idea (proposed by Richard Owen on the PBS dramatization of his encounter with Darwin) that common structures (homologies) were due to a common designer rather than a common ancestor.But the common Designer explanation makes much more sense of the findings of modern geneticists, who have discovered just how different the genetic blueprint can be behind many apparent similarities in the anatomical structures that Darwin saw. Genes are inherited, not structures per se.So one would expect the similarities, if they were the result of evolutionary common ancestry, to be produced by a common genetic program (this may or may not be the case for common design). But in many cases, this is clearly not so. Consider the example of the five digits of both frogs and humans—the human embryo develops a ridge at the limb tip, then material between the digits dissolves; in frogs, the digits grow outward from buds (see diagram below). This argues strongly against the ‘common ancestry’ evolutionary explanation for the similarity. Development of human and frog digits Stylized diagram showing the difference in developmental patterns of frog and human digits.
Left: In humans, programmed cell death (apoptosis) divides the ridge into five regions that then develop into digits (fingers and toes). [From T.W. Sadler, editor, Langman’s Medical Embryology, 7th ed. (Baltimore, MD: Williams and Wilkins, 1995), p. 154–157.] Right: In frogs, the digits grow outward from buds as cells divide. [From M.J. Tyler, Australian Frogs: A Natural History (Sydney, Australia: Reed New Holland, 1999), p. 80.] The PBS program and other evolutionary propagandists claim that the DNA code is universal, and proof of a common ancestor. But this is false—there are exceptions, some known since the 1970s, not only in mitochondrial but also nuclear DNA sequencing. An example is Paramecium, where a few of the 64 codons code for different amino acids. More examples are being found constantly.1 The Discovery Institute has pointed out this clear factual error in the PBS program. 2 Also, some organisms code for one or two extra amino acids beyond the main 20 types. 3The reaction by the PBS spokeswoman, Eugenie Scott, showed how the evolutionary establishment is more concerned with promoting evolution than scientific accuracy. Instead of conceding that the PBS show was wrong, she attacked the messengers, citing statements calling their (correct!) claim ‘so bizarre as to be almost beyond belief.’ Then she even implicitly conceded the truth of the claim by citing this explanation: ‘Those exceptions, however, are known to have derived from organisms that had the standard code.’ To paraphrase: ‘It was wrong to point out that there really are exceptions, even though it’s true; and it was right for PBS to imply something that wasn’t true because we can explain why it’s not always true.’But assuming the truth of Darwinism as ‘evidence’ for their explanation is begging the question. There is no experimental evidence, since we lack the DNA code of these alleged ancestors. There is also the theoretical problem that if we change the code, then the wrong proteins would be made, and the organism would die—so once a code is settled on, we’re stuck with it. The Discovery Institute also demonstrated the illogic of Scott’s claim.4 Certainly most of the code is universal, but this is best explained by common design. Of all the millions of genetic codes possible, ours, or something almost like it, is optimal for protecting against errors.5 But the exceptions thwart evolutionary explanations. DNA comparisons—subject to interpretation Scientific American repeats the common argument that DNA comparisons help scientists to reconstruct the evolutionary development of organisms:Macroevolution studies how taxonomic groups above the level of species change. Its evidence draws frequently from the fossil record and DNA comparisons to reconstruct how various organisms may be related. [SA 80] DNA comparisons are just a subset of the homology argument, which makes just as much sense in a young age framework. A common Designer is another interpretation that makes sense of the same data. An architect commonly uses the same building material for different buildings, and a car maker commonly uses the same parts in different cars. So we shouldn’t be surprised if a Designer for life used the same biochemistry and structures in many different creatures. Conversely, if all living organisms were totally different, this might look like there were manydesigners instead of one.Since DNA codes for structures and biochemical molecules, we should expect the most similar creatures to have the most similar
DNA. Apes and humans are both mammals, with similar shapes, so both have similar DNA. We should expect humans to have more DNA similarities with another mammal like a pig than with a reptile like a rattlesnake. And this is so. Humans are very different from yeast but they have some biochemistry in common, so we should expect human DNA to differ more from yeast DNA than from ape DNA.So the general pattern of similarities need not be explained by common-ancestry (evolution). Furthermore, there are some puzzling anomalies for an evolutionary explanation—similarities between organisms that evolutionists don’t believe are closely related. For example, hemoglobin, the complex molecule that carries oxygen in blood and results in its red color, is found in vertebrates. But it is also found in some earthworms, starfish, crustaceans, mollusks, and even in some bacteria. An antigen receptor protein has the same unusual single chain structure in camels and nurse sharks, but this cannot be explained by a common ancestor of sharks and camels. 6 And there are many other examples of similarities that cannot be due to evolution. Debunking the ‘molecular clock’ Scientific American repeats the common canard that DNA gives us a ‘molecular clock’ that tells us the history of DNA’s evolution from the simplest life form to mankind:Nevertheless, evolutionists can cite further supportive evidence from molecular biology. All organisms share most of the same genes, but as evolution predicts, the structures of these genes and their products diverge among species, in keeping with their evolutionary relationships. Geneticists speak of the ‘molecular clock’ that records the passage of time. These molecular data also show how various organisms are transitional within evolution. [SA 83]Actually, the molecular clock has many problems for the evolutionist. Not only are there the anomalies and common Designer arguments I mentioned above, but they actually support a creation of distinct types within ordered groups, not continuous evolution, as non-creationist microbiologist Dr Michael Denton pointed out in Evolution: A Theory in Crisis. For example, when comparing the amino acid sequence of cytochrome C of a bacterium (a prokaryote) with such widely diverse eukaryotes as yeast, wheat, silkmoth, pigeon, and horse, all of these have practically the same percentage difference with the bacterium (64–69%). There is no intermediate cytochrome between prokaryotes and eukaryotes, and no hint that the ‘higher’ organism such as a horse has diverged more than the ‘lower’ organism such as the yeast.The same sort of pattern is observed when comparing cytochrome C of the invertebrate silkmoth with the vertebrates lamprey, carp, turtle, pigeon, and horse. All the vertebrates are equally divergent from the silkmoth (27–30%). Yet again, comparing globins of a lamprey (a ‘primitive’ cyclostome or jawless fish) with a carp, frog, chicken, kangaroo, and human, they are all about equidistant (73–81%). Cytochrome C’s compared between a carp and a bullfrog, turtle, chicken, rabbit, and horse yield a constant difference of 13–14%. There is no trace of any transitional series of cyclostome → fish → amphibian → reptile → mammal or bird.Another problem for evolutionists is how the molecular clock could have ticked so evenly in any given protein in so many different organisms (despite some anomalies discussed earlier which present even more problems). For this to work, there must be a constant mutation rate per unit time over most types of organism. But observations show that there is a constant mutation rate per generation, so it should be much faster for organisms with a fast generation time, such as bacteria, and much slower for elephants. In insects, generation times range from weeks in flies to many years in cicadas, and yet there is no evidence that flies are more diverged than cicadas. So evidence is against the theory that the observed patterns are due to mutations accumulating over time as life evolved. Does homology provide evidence of evolutionary naturalism? by Jerry Bergman Summary Homology involves the theory that macroevolutionary relationships can be proven by the similarity in the anatomy and physiology of different animals. Since Darwin, homology has been cited in textbooks as a major proof for evolution. A review of the literature on homology indicates that the theory does not provide evidence for evolutionary naturalism, and that the common examples of homology can be better explained by Creation. Furthermore, increased knowledge about the genetic and molecular basis of life has revealed many major exceptions and contradictions to the theory which, as a result, have largely negated homology as a proof of evolution. Extensive comparisons of skeletons, muscles, nerves, body organs, cell ultrastructure and biochemistry of different animal kinds have confirmed that a great deal of similarity exists in both their structure and function. By arranging or classifying large sets of anatomical structures according to the similarity of selected traits, evolutionary naturalists have attempted to demonstrate evidence for a long, gradual line of progressive animal changes terminating in the highest organism yet, humans. Evolutionists then argue that these comparisons prove the concept that all life evolved from a hypothetical ‘common ancestor’ protocell that they believe lived about 3.5 billion years ago.Called homology or the homology theory, since Darwin this view has been presented as a major evidence of macroevolution theory. An example of this reasoning is as follows:'If you look at a 1953 Corvette and compare it to the latest model, only the most general resemblances are evident, but if you compare a 1953 and a 1954 Corvette, side by side, then a 1954 and a 1955 model, and so on, the descent with modification is overwhelmingly obvious. This is what paleontologists do with fossils, and the evidence is so solid and comprehensive that it cannot be denied by reasonable people [emphasis in original].'1Homology is not merely a minor proof of evolution, but instead has been widely cited by evolutionists as one of themost compelling lines of evidence for their theory.2,3 Darwin concluded that homology was critically important evidence for common descent:'According to Darwin's theory of common descent, the structures that we call homologies represent characteristics inherited with some modification from a corresponding feature in a common ancestor. Darwin devoted an entire book, The Descent of Man and Selection in Relation to Sex, largely to the idea that humans share common descent with apes and other animals … . Darwin built his case mostly on anatomical comparisons revealing homology between humans and apes. To Darwin, the close resemblances between apes and humans could be explained only by common descent.' 4Darwin reasoned that the members of the same class of animals resemble each other in the general plan of their design and, in his words, this resemblance is critical because of the fact that 'the hand of a man, formed for grasping, that of a mole for digging, the leg of the horse, the paddle of the porpoise and the wing of the bat' are all 'constructed on the same pattern' and 'include similar bones in the same relative positions' is specifically what the theory of common descent would expect. 5 An early example of how homology was used to argue for macroevolution is a 1928 biology text which, in answer to the question 'Why do the individuals in a species have all of their parts homologous?', said:'The obvious answer is, that they all descended from the same ancestors … . Biologists carry this answer a step further and say that since homology within the species is the result of common ancestry therefore all homology is due to common ancestry and the closeness of relationship determines the number of homologous parts [emphasis in original].'6The argument from homology has been used in high school and college biology textbooks for generations. A survey by the author of 45 widely used recent college textbooks and 28 high school texts revealed that all of those that discussed evolution (except one) employed homology as a major proof for Darwinism. Most discussions were brief and almost identical in content and thrust. The following example was typical:'The seven bones in the human neck correspond
with the same seven, much larger, neckbones in the giraffe: they are homologues. The number of cervical vertebrae is a trait shared by creatures descended from a common ancestor. Related species share corresponding structures, though they may be modified in various ways.' 7Conklin even claims that the only natural explanation for homology is evolution, implying that no intelligent design explanation exists. In his words the fundamental resemblances between embryos, larvae and adults'are just as genuine homologies as those between adult structures, and the only natural explanation that has ever been found for such homologies is inheritance from common ancestors … . These fundamental resemblances, or homologies, as they are technically called, call for some explanation, and the only natural explanation that has ever been proposed is evolution.'8A much more recent quote illustrates how this line of reasoning is still being used today to argue that the evidence of homology for the common ancestry of all life is 'very strong'.'Why is it that bats and whales have so much in common anatomically with mice and men? Why do virtually all vertebrate forelimbs have the same basic "pentadactyl" (five fingered) design? (This is one of numerous examples of "homologous" structures exhibited by related species.)' 9The author concludes the answer is evolution. Barr lists homology as the first argument on his list of evidence for evolution. As the above quotes show, the same line of reasoning has been used to 'prove' evolution for more than a century. However, Dobzhansky admitted that 'homology does not prove evolution, in the sense that nobody has actually witnessed the gradual changes in the millions of consecutive generations which led from a common ancestor to a bird on the one hand and to man on the other'. But, he adds, homology strongly suggests evolution; 'the facts of homology make sense if they are supposed to be due to evolution of now-different organisms from a common stock. They do not make sense otherwise.'10 Origin of the homology theory The comparative anatomy argument called homology was probably first popularized by Huxley in 1863 to argue for human evolution. In hisMan's Place in Nature he gathered what Milner concludes is 'overwhelming evidence' for many close homologies 'muscle for muscle and bone for bone', proving the case for homology. 11The concept of homology originally meant only that a set of structures was fundamentally similar. It was first elaborated in 1843 by one of Darwin's most informed critics, Sir Richard Owen. 12,13 Before Darwin, homology observations were explained by a concept called idealarchetypes, meaning the designer used the superior design prototype throughout his creation. A branch of this worldview now is calledintelligent design theory.14 It was not until after Darwin that homology implied common ancestry. After Darwin's ideas spread, the structural similarity in many animals that had been obvious to anatomists for generations was reinterpreted as evidence for common descent.15 An evaluation of homology as evidence for evolution That some similarity exists when certain aspects of life forms are compared is obvious. The question is: 'Does the similarity that exists prove that one structure evolved into another and, ultimately, that the complex evolved from the simple?' The simplest and most obvious explanation for the fact that morphological similarities between bones, sensory organs, lungs, or gills exist among most higher animals is that the requirements of life are similar for similar living things, and some designs are preferred in constructing animals because these designs are superior to competing designs.All automobile, bicycle and pushcart tyres are round because this design is superior for the function of most tyres. A tyre homology does not prove common descent, but common design by engineers throughout history because of the superiority of the round structure for rolling. Likewise, most vertebrate kidneys are similar structurally because they have a similar physiological role in the body and consequently must be similar in both structure and function.Homology also does not prove that a set of animals is related by descent because both similarities and differences exist for any two animal types, and traits often are chosen by evolutionists only because they seem to provide evidence that two animals are related. The only criterion that was used by Darwinists to select examples of homology was: 'Does the example support what is assumed to be an evolutionary relationship?' Other examples are ignored or explained away. This fact is so well recognized, and so many examples exist that contradict the explanation of common descent, that evolutionists have attempted to separate most putative examples of homology into two types: analogyand homology. The division is based on a distinction between similarity due to common ancestry, or homology, and resemblance which is due solely to similarity of function, called analogy. An example is the forelimbs of humans, horses, whales and birds which are judged homologous because'they are all constructed on the same pattern, and include similar bones in the same relative positions because these are all derived from the same ancestral bones. The wings of birds and insects, on the other hand, are analogous: they serve the same purpose, but do not constitute modified versions of a structure present in a common ancestor. The wings of birds and bats are homologous in skeletal structure because of descent from the forelimb of a common reptilian ancestor; but they are analogous in terms of their modification for flight—feathers in birds, skin membranes in bats.' 16In other words, if a design similarity supports evolutionary assumptions, it is listed as an homology and is accepted as evidence for evolution. Conversely, if a design similarity does not support evolution, it is called analogy, and the conclusion is drawn that the similarity exists because a certain design is highly functional for a specific body part, and not because of a common ancestor. Many analogous structures are assumed to exist due to convergent evolution, which is defined as the separate evolution of similar structures because of similar environmental demands. 17 Convergent evolution also is used to explain similar structures that have formed from different embryo structures or precursors.Many examples of homology are actually better explained by analogy, and the resemblance that exists is often due to similarity of function and/or design constraints. The forelimbs of humans, whales and birds are similar because they serve similar functions and have similar design constraints. The conclusion that two homologous bones are similar because they are putatively 'derived from the same ancestral bones' (as Barr claims) is not based on direct evidence but instead on a priori conclusions demanded by macroevolution. Jones concluded that' … the evolutionist argument from homology lacks scientific content. This particular lack has very serious implications; it strikes at the root of all attempts by evolutionists to give homology an objective basis and distinguish homology (similarities due to descent) fromanalogy (similarities not due to descent). The only way they can recognize analogous variation, especially when due to convergent evolution is by criteria (e.g. genetic or embryological) which we now know do not hold for organs of "unquestionable" homology. The evolutionist concept of homology is now shown to be entirely subjective.'18Stephen J. Gould suggested that 'the central task of evolutionary biology is … the separation of homologous from analogous likeness', and then emphasized that 'homology is similarity due to descent from a common ancestor, period'.19 The problem with this definition is that without direct knowledge we cannot know ancestry. In answer to the question 'Can we identify fossil ancestors of species alive today?', University of Michigan Professor Mark Siddall contends that this is impossible and that the use of stratigraphic data when assembling phylogenies must be based on speculation.20'By the late 1970s this "Idol of the Academy", what Pearson has called "ancestor hunting" but which Eldredge aptly named "ancestor worship" had been thoroughly debunked.' 20Huxley understood as far back as 1870 that when dealing with fossils, which are the only evidence we have of past life, one cannot distinguish uncles and nephews from fathers and sons.21 Among the many reasons ancestors cannot be distinguished from sister taxa, as noted by Siddall and others, is that there can be no positive evidence of ancestry, only inferences. Lack of evidence can only allow it as a possibility or an ad hoc postulate.22Although many similarities exist in almost all animal structures, structural variations are the norm. Often the variations found in the animal world seem to exist solely to produce variety, and not for the purpose of
conferring a survival advantage.Some examples in humans are as follows:Attached earlobes: The allele for free earlobes is dominant to the recessive a allele for attached earlobes.Tongue rolling: The R allele enables one to roll their tongue into a U shape and is dominant to the r allele (these persons lack this ability).Hitchhiker's thumb: People who can bend the last joint of their thumb back to an angle of 60 degrees or more have the recessive alleleh and those who cannot have the dominant allele, H.Bent little finger: A person with the dominant allele B can lay their hands flat on a table and while relaxed are able to bend the last joint of the little finger toward the fourth finger. Those with the recessive allele b cannot do this.Interlacing fingers: People with the C allele can cross their left thumb over their right thumb when they interlace their fingers. The Callele is dominant over the c allele, which results in the person normally crossing their right thumb over their left.PTC tasting: Those with this the dominant allele T trait can detect a bitter taste in paper impregnated with phenylthiocarbamide (PTC) when they chew on it for a few seconds. Those persons with the recessive allele cannot taste this chemical.Widow's peak: The W allele (for widow's peak, a pointed hairline) is dominant to the allele which produces a straight hairline. 23To argue for macroevolution via comparisons according to 'complexity' judgments also is problematic because an enormous number of exceptions exist.The comparative anatomy argument fails completely when an attempt is made to trace all living forms of life (and even fossils) back to their postulated universal common ancestor(s). Few skeleton, muscle and brain counterparts exist in single-celled animals (or in many developmental stages afterward).No biological or logical requirement exists to vary the design of bones, muscles and nerves needlessly in every living form beyond what is necessary to adapt the animal to its environment. Although variety is universal in the natural world, variety that interferes with the life process or an animal's survival usually is avoided in animal design. Design constraints severely limit the possible variations in an animal's anatomy, and excess deviation from the ideal can interfere with the animal's ability to survive.The many similarities that exist among members of the animal kingdom is the result of the fact that a single designer created the basic kinds of living 'systems', then specially modified each type of life to enable it to survive in its unique environmental niche. Examples of major environments for which organisms must be designed include the air, ground and water. Structures that serve similar purposes under similar conditions and that are nourished by similar foods ought to possess similarity in both design and function. This is illustrated in a critique of Berra's Corvette analogy cited previously:' … Berra's primary purpose is to show that living organisms are the result of naturalistic evolution rather than intelligent design. Structural similarities among automobiles, however, even similarities between older and newer models (which Berra calls "descent with modification") are due to construction according to pre-existing patterns, i.e., to design. Ironically, therefore, Berra's analogy shows that even striking similarities are not sufficient to exclude design-based explanations. In order to demonstrate naturalistic evolution, it is necessary to show that the mechanism by which organisms are constructed (unlike the mechanism by which automobiles are constructed) does not involve design.'24 Convergent evolution A major problem with homology theory is that many structures appear similar superficially yet differ significantly in such areas as anatomy, physiology, etc. Since such examples are not explained easily by homology, evolutionists have hypothesized an explanation for this problem called convergent evolution, which attempts to explain the analogy found.One of the most common examples of convergent evolution is wing evolution. Wings are believed to have evolved a minimum of four times; in birds, bats (in the order chiroptera), insects and reptiles (such as the pterodactyl). Scientists have also concluded that bird wings did not evolve from fly wings for several reasons. The main one is that no evidence of insects evolving into birds (or any other animal) exists in the many insect impressions in stone, or the many examples of insects in amber, that have been discovered.Consequently, although the evolutionary progenitors of birds are highly debated among evolutionists, insects are not considered likely candidates. The most common theory of bird evolution suggests that they evolved from dinosaurs or other reptiles. Thus, the wings of birds and insects are labeled not as homologous, but analogous, because powerful evidence refutes the idea that birds evolved directly from insects. This is one of many examples that evolutionists claim does not falsify homology theory because it was caused by convergent evolution. However, no evidence exists to support the convergent evolution theory though.A classic example of convergent evolution is the Tasmanian Tiger (a marsupial native to Australia) and members of the dog family (which are all mammals). The two animals appear remarkably alike physically, but geographical separation and evidence from the fossil record militates against the idea that one evolved from the other or both evolved from a recent common ancestor. For this reason, it has been proposed that they evolved independently into two animals that are so close in physical appearance that a close look at the two animals is required to tell them apart! The suggestion that two animals which look remarkably alike (such as the dog and Tasmanian Tiger) evolved independently is not tenable and is a major problem for evolution.Convergent evolution has been hypothesized to explain the numerous examples of homology in which the available evidence suggested that the animals under consideration were not closely linked by descent. An example of such gratuitous hypothesizing is the following:'Some similarities between distant species may be caused by adaptation to similar environments, which is known as convergent evolution. Development of streamlined fins in fish (teleosts) and flippers in dolphins (mammals) are analogous: they function alike, but are very different in underlying structure. … Linnaeus's original classification of animals does not distinguish between analogous and homologous structures. Creatures were often put in the same groups by resemblances to an imagined "divine plan" or "design". Since Darwin … species are classified to reflect the relative closeness or distance of their common ancestry.' 25One problem with the convergent evolution hypothesis is that it requires 'reinvention of the wheel' scores or even hundreds of times. The eye is hypothesized to have evolved independently as many as 60 different times.26 Given the small probability of the evolution of a single eye or organism, the likelihood of it occurring numerous times is indefensible. Gould noted that even if evolution were repeated a thousand times, it probably would not produce the human mind again.27 Vestigial organs and homology Another branch of comparative anatomy studies structures in humans (and other so called 'higher' forms of life) that were believed by evolutionists to be the remains of structures that were required or useful in 'lower', less evolved and less complex ancestral forms, but that now no longer are necessary. In this case, the homologous organ in the more advanced animal is less developed, or even deemed useless. Such homologous structures or organs are referred to as vestigial, with most examples being assumed remnants that resulted from the loss of an earlier, better developed structure. Evolutionists used to proudly point to over a hundred such structures in humans, but the number has decreased consistently as anatomical knowledge has increased.Today, only a couple of examples at most are usually mentioned (and there is no doubt that even the few examples usually mentioned are useful and not vestigial). As Howitt 28 noted, the celebrated German anatomist, Wiedersheim, listed 180 vestigial organs in the human body, but with the increase of knowledge it has been found that every one of them has an important function, although the functions of some organs is presently viewed as minor, or as serving a back-up capacity.29,30Moreover, if some vestigial organs can be proven to exist, they provide support not for evolution, but for de-evolution|--|i.e. evolution-in-reverse. What the evolutionists must demonstrate is that the development of new and useful organs is occurring today. They also must prove that a process exists that can form new structures called nascent organs, instead of trying to document that once-useful organs now are useless. Evidence for the
development of new organs, or those in the process of evolving, would be evidence of evolution. As of now, no evidence of any nascent organ exists. Embryology and homology One major problem is that in many cases organs and structures which appear identical (or very similar) in different animals do not develop from the same structure or group of embryo cells. It is not uncommon to find fundamental structures (e.g. the alimentary canal) that form from different embryological tissues in different animals. For example, in sharks the alimentary canal is formed from the roof of the embryonic gut cavity; in frogs it is formed from the gut roof and floor; and in birds and reptiles it is formed from the lower layer of the embryonic disc or blastoderm. 31Even the classic example of vertebrate forelimbs referred to by Darwin (and cited in hundreds of textbooks as proof for evolution) has now turned out to be flawed as an example of homology. The reason is that the forelimbs often develop from different body segments in different species in a pattern that cannot be explained by evolution. The forelimbs in the newt develop from trunk segments 2 through 5; in the lizard they develop from trunk segments 6 to 9; in humans they develop from trunk segments 13 through 18.32 Denton concluded that this evidence shows the forelimbs usually are not developmentally homologous at all. As an example, he cited the development of the vertebrate kidney which provides a challenge to the assumption that homologous organs are produced from homologous embryonic tissues.'In fish and amphibia the kidney is derived directly from an embryonic organ known as the mesonephros, while in reptiles and mammals the mesonephros degenerates towards the end of embryonic life and plays no role in the formation of the adult kidney, which is formed instead from a discrete spherical mass of mesodermal tissue, the metanephros, which develops quite independently from the mesonephros.' 33The arguments used by evolutionists have taken on new meaning in view of the past half-century of research. For example Dobzhansky argued that'To be sure, some diehard anti-evolutionists still insist that homology means only that the designer gratuitously chose to make homologous organs in quite unrelated organisms. This opinion may be said to be implicitly blasphemous: it actually accuses the designer of arranging things so that they suggest evolution merely to mislead honest students of His works.'34This research supports ReMine's biotic message theory, the conclusion that the natural world was specifically designed to look like it did notevolve, but was created.35 ReMine uses a wide variety of examples to support his thesis which has been very favorably reviewed by the creationist community. ReMine notes that homology has been used as evidence against a designer for decades, but as this review shows, it strongly supports the biotic message theory. Biochemical homology The homology argument from biochemistry parallels the argument in anatomy. Evolutionists suggest that just as the study of comparative anatomy has found evidence of anatomical homologies, likewise research on' … the biochemistry of different organisms has revealed biochemical homologies. In fact, the biochemical similarity of living organisms is one of the most remarkable features of life … . Cytochrome enzymes are found in almost every living organism: plant, animal and protist. The enzymes of the citric acid cycle are also almost universally distributed. Chlorophyll a is found in all green plants and almost all photosynthetic protists. DNA and RNA are found in every living organism and, so far as we can determine, contain the same hereditary coding mechanism. The fact that underneath the incredible diversity of living things lies a great uniformity of biochemical function is difficult to interpret in any other way but an evolutionary one. Presumably these molecules were put to their current use very early in the history of life and almost all modern forms have inherited the ability to manufacture and use them.'36The fact that animals are 'so similar in their chemical make-up' has long been used to support Darwinism.37 But extensive biochemical research has revealed that the simplest reason for biochemical homology is that all life requires similar inorganic elements, compounds and biomolecules; consequently, all life is required to use similar metabolic pathways to process these compounds. Most organisms that use oxygen and rely on the metabolism of carbohydrates, fats and proteins must use a citric acid cycle which is remarkably similar in all organisms. Furthermore, the metabolism of most proteins into energy produces ammonia, which is processed for removal in similar ways in a wide variety of organisms. What evolutionists must explain is why billions of years of evolution have not produced major differences in the biochemistry of life.Many biochemical structures/systems in yeasts and other so-called 'primitive life' forms are almost identical to the biochemical families used in humans. With some minor variations, all life uses the same sugar and lipid family, the same 20 amino acids, about 14 vitamins and the same basic genetic code. 38Even the complex proteins used in all life are often identical or very similar. Correspondence even exists between very different forms of life such as prokaryotes and eukaryotes. Ribosomes from bacteria, even though translation signals and other differences exist, have enough similarity that they can be made to 'translate human messenger RNAs into human proteins—and vice versa'.39 The problem for evolutionists is that the biochemistry of all life, even that allegedly separated by hundreds of millions of years of geologic time and evolution, is too similar. Despite the many significant differences between the two basic cell forms (eukaryotes and prokaryotes), they are both' … remarkably similar on the biochemical level … . Procaryotes and eucaryotes are composed of similar chemical constituents. With a few exceptions, the genetic code is the same in both, as is the way in which the genetic information in DNA is expressed. The principles underlying metabolic processes and most of the more important metabolic pathways are identical. Thus, beneath the profound structural and functional differences between procaryotes and eucaryotes, there is an even more fundamental unity: a molecular unity that is basic to life processes.'40 Although many biochemical similarities exist in life, millions of biochemical differences exist that are inexplicable via evolution. Many of these differences do not provide a selective advantage as implied by the claim that Darwinistic mechanisms have fine tuned life for the past 3.6 billion years. Creationists suggest that such differences exist due to the need for ecological balance and because the designer chose to employ variety. Also, were one compound in an organism to be altered, scores of other compounds with which it interacts would often also need to be changed so that the entire biological system could function as a harmonious unit. Genetics and homology According to the evolutionary theory, homologous features are programmed by similar genes. Gene sequence similarity would indicate common ancestry since such similarities are unlikely to originate independently through random mutations. If the bones of the human arm evolved from the same precursors as the wing of a bat and the hoof of a horse as evolution teaches, then we should be able to trace these alleged homologies to the DNA that codes for them. Some geneticists thought this knowledge would allow them to find the chemical formula needed to produce an arm, leg, or other structure. But once biologists acquired a greater understanding of genetics, they found that what are labeled as homologous structures in different species often are produced by quite different genes.Homology predicted that features produced by similar genetic sequences are phylogenetically homologous. There are now so many exceptions to this prediction that the concept of genetic homology cannot now be said to be a rule, but the exception. The classic example is mutations in certain homeotic genes41 which can cause wholesale changes in morphology such as producing two pairs of wings instead of the normal single pair, or replacing a fly's antenna with a leg (or can even cause eyes to develop on the fly's leg). Genes that produce results similar to the homeotic genes for flies' wings have been found in most other animal kinds, including mammals and humans.42
In another example, the gene that controls mouse eye colour also happens to control the mouse's physical size; but the gene that controls the fruit fly's eye colour controls not the fruit fly's size, but female sex organ morphology. 43 Although mice and flies share a similar gene (called eyeless) which functions to control their eye development, the fly's multifaceted eye is profoundly different from a mouse's mammal eye. In both the fly Antennapedia and mouse eyeless, similar homeotic genes control development of structures which are not homologous by either the post-Darwinian phylogenetic or the classical morphological definition. 44The finding that similar genes regulate such radically different structures strongly argues against the concept of homology. So many genes used in higher organisms have multiple effects that Ernst Mayr once suggested that genes which control only a single characteristic are rare or nonexistent. The finding that a consistent one-gene/onecharacteristic correspondence does not exist has been a major set back to the Darwinian interpretation of homology. Because evolutionary biologists have failed to provide a biological basis for their homology research findings, Roth concluded 'that the title of de Beer's 1971 essay|--|Homology, an unsolved problem|--|remains an accurate description … . The relationships between processes at genetic, developmental, gross phenotypic and evolutionary levels remain a black box'.45 Research at the molecular level has failed to demonstrate the expected correspondence between gene product changes and the organismal changes predicted by evolution.24Evolution by DNA mutations 'is largely uncoupled from morphological evolution'.46 An example of this is the large morphological dissimilarity that exists between humans and chimpanzees despite a high similarity in their DNA.46 In short we now know:' … in general the homology of structures such as organs or modules cannot be ascribed to inheritance of homologous genes or sets of genes. Consequently, organ homology cannot be reduced to gene homology. Van Valen recognizes this too and therefore suggests, as an alternative, to reduce homology to a continuity of [developmental] information. Information is not the same as genotypic nucleic acid. But what it is exactly, and how it is continuous, is still an unsolved problem.'47 Conclusion As scientists learnt more about anatomy, physiology and especially genetics, the concept of homology increasingly came under attack. One problem however, was that examples which seemed to fit evolutionary assumptions were often cited, while the many examples that do not fit were ignored. And, in time, more and more examples were discovered that had to be ignored. Eventually, as one observer noted, homology led Darwinists to assemble very select examples that seemed to prove ancestor-descendant relationships that often were quite convincing. In addition, as Milton has observed,'It is homology that Darwinists rely on to bridge the gaps in the fossil record. … It is homology that underlies the diagrams drawn up by Darwinists from Haeckel to the present day showing how every living thing is related. Ultimately, however, it is homology that has provided the greatest stumbling block to Darwinian theory, for at the final and most crucial hurdle, homology has fallen.'48The recent information explosion in embryology, microbiology, genetics and especially molecular biology has revealed in minute detail how plants and animals are constructed at the molecular level. If the Darwinian interpretation of homology were correct, then we would expect that the same homologies found at the macroscopic level also exist at the microscopic, biochemical and genetic levels. What researchers in each of these fields often find, has greatly undermined the homology concept. So many exceptions now exist that molecular biologist Michael Denton concluded that the homology theory should be rejected. His main argument is that genetic research has not shown that homologous structures are produced by homologous genes and follow homologous patterns of embryological development. Instead, genetics has found that homologous structures are 'often specified by non-homologous genetic systems' and furthermore, the homology 'can seldom be extended back into embryology'. 49Why do most scientists accept macroevolution theory? A major reason is that it is now the accepted world view of scientists—an idea to which they are exposed from the earliest days of training, and by which they are surrounded daily. Most scientists are influenced by social pressure, and many believers fear recriminations from their fellow scientists if they do not conform to what currently is viewed as correct. To prove their orthodoxy, many scientists have become unscientific and have embraced the religion of 20th centurynaturalism.50 Belief in evolutionism requires a credulity induced partly by pressure to conform to a world of science that is saturated with naturalism. Fraud rediscovered by Russell Grigg Most people have heard of or been taught the idea that the human embryo goes through (or recapitulates) various evolutionary stages, such as having gills like a fish, a tail like a monkey, etc., during the first few months that it develops in the womb.The idea has not only been presented to generations of biology/medical students as fact, but has also been used for many years to persuasively justify abortion. Abortionists claimed that the unborn child being killed was still in the fish stage or the monkey stage, and had not yet become a human being.This idea (called embryonic recapitulation) was vigorously expounded by Ernst Haeckel from the late 1860s to promote Darwin’s theory of evolution in Germany, even though Haeckel did not have evidence to support his views.1 Data manufactured Lacking the evidence, Haeckel set out to manufacture the data. He fraudulently changed drawings made by other scientists of human and dog embryos, to increase the resemblance between them and to hide the dissimilarities. We reported on this particular fraud in a recent issue of Creation magazine.2Haeckel’s German peers (notably, in 1874, Wilhelm His Sr, professor of anatomy at the University of Leipzig) were aware of this fraud and extracted a modest confession from him, in which he blamed the draughtsman for blundering—without acknowledging that he himself was the draughtsman! 2Most informed evolutionists in the past 70 years have realised that the recapitulation theory is false. 3Nevertheless, the recapitulation idea is still advanced as evidence for the theory of evolution in many books and particularly encyclopedias and by evolutionary popularizers like the late Carl Sagan.4 But wait—there’s more Haeckel’s famous (infamous) set of 24 drawings purporting to show eight different embryos in three stages of development, as published by him inAnthropogenie, in Germany, 1874.When evolutionists say that the recapitulation theory is false, they usually do not mean to admit that comparing embryos gives no evidence of common ancestry. In fact, they still frequently highlight the assumed similarities between embryos in their early stages (called embryonic homology) as evidence for evolution. This assumption is based on the idea that such similarities are ‘common knowledge’. 5This alleged similarity of embryos has for years been resting, consciously or unconsciously, on a set of 24 of Haeckel’s drawings which he first published in 1866 in his Generalle Morphologie der Organismen, and then repeated in 1874 in his more popular Anthropogenie (see below). These purport to show embryos of fish, salamander, turtle, chicken, pig, cow, rabbit, and human in three stages of development.The various stages, particularly the earlier ones, show substantial similarity. Ever since these drawings
appeared, it has been assumed that they have given us something close to the truth about embryos of vertebrate species. So much so that they still appear in textbooks and popular works on evolution. 6,7In fact, no one has bothered to check—until now. It turns out that Haeckel’s fraud was much worse than anyone realised. It did not just affect the idea of recapitulation, it turns out that the similarities are much, much less than anyone thought. Fraud examined and exposed Top row: Haeckel’s drawings of several different embryos, showing incredible similarity in their early ‘tailbud’ stage. Bottom Row: Richardson’s photographs of how the embryos really look at the same stage. (From left: Salmo salar, Cryptobranchus allegheniensis, Emys orbicularis, Gallus gallus,Oryctolagus cuniculus, Homo sapiens.) Many modern evolutionists no longer claim that the human embryo repeats the adult stages of its alleged evolutionary ancestors, but point to Haeckel’s drawings (top row) to claim that it repeats the embryonic stages. However, even this alleged support for evolution is now revealed as being based on faked drawings.Michael Richardson, a lecturer and embryologist at St George’s Hospital Medical School, London, has exposed this further fraud, in an article in the journal Anatomy and Embryology,8 recently reviewed in Science9 and New Scientist.10Richardson says he always felt there was something wrong with Haeckel’s drawings, ‘because they didn’t square with his [Richardson’s] understanding of the rates at which fish, reptiles, birds, and mammals develop their distinctive features’.8 He could find no record of anyone having actually compared embryos of one species with those of another, so that ‘no one has cited any comparative data in support of the idea’. 8He therefore assembled an international team to do just that—examine and photograph ‘the external form of embryos from a wide range of vertebrate species, at a stage comparable to that depicted by Haeckel’. 8The team collected embryos of 39 different creatures, including marsupials from Australia, tree-frogs from Puerto Rico, snakes from France, and an alligator embryo from England. They found that the embryos of different species are very different. In fact, they are so different that the drawings made by Haeckel (of similarlooking human, rabbit, salamander, fish, chicken, etc. embryos) could not possibly have been done from real specimens.Nigel Hawkes interviewed Richardson for The Times (London).11 In an article describing Haeckel as ‘An embryonic liar’, he quotes Richardson:‘This is one of the worst cases of scientific fraud. It’s shocking to find that somebody one thought was a great scientist was deliberately misleading. It makes me angry … What he [Haeckel] did was to take a human embryo and copy it, pretending that the salamander and the pig and all the others looked the same at the same stage of development. They don’t … These are fakes.’ 11 More of Richardson’s photographs of embryos at the same ‘tailbud’ stage of development and to the same scale, showing the huge differences between various species. (From left: Petromyzon marinus, Acipenser ruthenus, Bufo bufo, Erinaceus europaeus, Felis catus, Manis javanica, Canis familiaris.)Haeckel not only changed the drawings by adding, omitting, and changing features but, according to Richardson and his team,‘he also fudged the scale to exaggerate similarities among species, even when there were 10-fold differences in size. Haeckel further blurred differences by neglecting to name the species in most cases, as if one representative was accurate for an entire group of animals’.9Ernst Haeckel’s drawings were declared fraudulent by Professor His in 1874 and were included in Haeckel’s quasi confession, but according to Richardson,‘Haeckel’s confession got lost after his drawings were subsequently used in a 1901 book calledDarwin and After Darwin and reproduced widely in English language biology texts.’9,12Will there now be a rush by libraries, publishers and sellers of evolutionist books to withdraw from circulation, rewrite and otherwise acknowledge the fact that the idea of embryonic similarities’ suggesting evolution is largely based on academic fraud? The embryo photos used in this article were kindly supplied by Dr Michael K. Richardson. They originally appeared in M.K. Richardson et al., ‘There is no highly conserved embryonic stage in the vertebrates: implications for current theories of evolution and development’,Anatomy and Embryology, 196(2):91–106, 1997, © Springer-Verlag GmbH & Co., Tiergartenstrasse, 69121 Heidelberg, Germany. Reproduced here with permission.
ARE THERE SIMILARITIES BETWEEN LIVING THINGS EVIDENCE FOR COMMON ANSESTRY OR COMMON DESIGN Saddle up the horse, it’s off to the bat cave by Daniel Anderson Published: 17 October 2006 (GMT+10) This is the pre-publication version which was subsequently revised to appear in Creation 30(2):40–41. Surprise, surprise! Evolutionists are now saying that bats and horses are more closely related than cows and horses. 1 In the prestigious Proceedings of The National Academy of Sciences, scientists studied genetic re-arrangements associated with retroposons, strands of DNA that copy themselves into RNA and then copy themselves back into DNA at different sites on a chromosome. In the evolutionary paradigm, closely related species share more of these rearrangements than more distant relatives.
Until this study, scientists considered bats and horses to be very distant cousins. They were shocked to discover that bats and horses shared a high degree of DNA similarity. "I think this will be a surprise for many scientists," says Norihiro Okada at the Tokyo Institute of Technology, Japan. "No one expected this." 2 Why such a surprise? Evolutionary scientists establish relationships between living organisms based on morphological and DNA similarity. Creatures that are anatomically similar are believed to be so because they possess a close evolutionary relationship—they are supposed to have inherited these characteristics from a fairly ‘close’ common ancestor. The same is true of creatures that are genetically very similar. So if two creatures are supposed to be evolutionarily close by one of these criteria, they should be by the other also— provided, that is, that the whole idea of common descent is valid. Applying this logic, researchers predicted that cows and horses would be much more closely related than bats and horses. Cows are anatomically, physiologically, functionally, and behaviorally rather similar to horses. On the other hand, even a child could identify the huge differences between bats and horses. Compared to horses and cows, a bat is rather different in its skeletal anatomy, mode of locomotion (flying), navigation (echolocation), soft tissue arrangements, diet, and lifestyle.Bats and horses should thus have been very different in their DNA, because of their obvious structural and functional differences. This shocking result revealed an egregious discrepancy between morphological and genetic data. More Problems The genetic data seems to also contradict the evolutionary interpretation of the fossil record. Horses supposedly evolved from a small quadruped beginning 35-55 million years ago, taking their modern form only in the last 1.5 million years. Cows supposedly began their evolutionary process about 23 million years ago. On the other hand, fully formed, modern looking bat fossils appear around 60 million years ago on the evolutionary timeline.Separated by such an immense supposed time gap, horse and bat DNA should have been much more different by now. Cows and horses, supposedly having evolved in overlapping time frames, should share much more similarity in their respective genomes. Implications When it comes to bats and horses, the facts just don’t add up for evolution. Common descent is based on a whole set of assumptions, extrapolations, and inferences. However, in this case, the hard scientific data reveal that common descent is completely invalid.2 As Okada said, in regards to the surprising discovery, “…We need to look at fossils from a new point of view…” He’s exactly right. Perhaps it is time to throw away the tired, old evolutionary glasses and replace them with a fresh pair of lenses. Are look-alikes related? by Don Batten My childhood best friend looked so much like me that our teachers, and even our friends, had a lot of trouble telling us apart. ‘Are you twins?’, we were often asked. However, there was no family connection as far back as anyone could trace. The similarity in our appearance was not due to being closely related—or, putting it another way—due to us having a recent common ancestor, like a common father, grandmother, or even great grandparent. It was just a ‘fluke’.The main (only?) argument for evolution is that similarities between living things are due to relatedness, or common ancestry. If two kinds of animals share a lot of common features, then they are ‘obviously’ closely related and so must have had a recent common ancestor—or so the evolutionary reasoning goes.1,2 Birds, for example, all lay eggs, have feathers and a specialized lung comprised of interconnected air sacs, so the evolutionist would say all birds had a common ancestor which had these features. Creationists would say that birds have these similarities because they were created with a common basic plan. People would assume that because my friend and I were so similar we must have shared a very recent common ancestor—like the same parents. They were wrong. In like manner, the evolutionists are often—not always— wrong in assuming similarity is due to common ancestry.Of course my friend and I are members of the same human kind and so we know that we had a common ancestor—who was a descendant of Japheth, in this case. However, the analogy is accurate—that the degree of similarity in appearance does not necessarily indicate the degree of genetic relatedness. As we shall see, evolutionists are forced to recognise this at times, but they (illogically) do not admit that such recognition undermines the main argument for evolution (if similarities occur that clearly are not due to common ancestry, how does the evolutionist know that any similarities are due to evolution?).If living things had a common designer, we would expect there to be many similarities—just like the early Porsche and VW ‘beetle’ have many similarities because they shared the same designer. If there were not these similarities in living things we might be inclined to
believe in many intelligent designers, not just one. I believe that things are created in such a way that the patterns we see defy a natural explanation—such as evolution—but support a supernatural explanation. In other words, the patterns of similarity cannot be consistently explained by any naturalistic (everything–made–itself) theory. Many creatures show similar features for similar structures and purposes.
Australian marsupial wombat (top) and a marmot.
Sugar gliders (top) look similar toThe extinct marsupial thylacine (top) flying squirrels. and the wolf. The more similar creatures are, according to the evolutionary argument, the more closely they should be related—that is, the more recent it is since they had the same ancestor. Take, as an example, the usual textbook illustration of the similarities between the limbs of animals with backbones (vertebrates) and people. Human beings have a five–finger/toe hand/foot pattern, and limbs with two bones attached to the hand/foot joined to a single other major limb bone. We share this pattern with bats and frogs and therefore, the evolutionist argues, we must share common ancestors with these
animals. That explains the similarities, we are told. However, if we look at the horse limb (right), we see that it is quite different to the human form. Frogs and people have remarkably similar limb structures, but horses, which are supposedly very much more closely related to humans, have a limb with little resemblance to the human limb. Just on the basis of limb structures, it might be reasonable to suppose that frogs and people are more closely related than people and horses. However, horses, as mammals, share many similarities to humans which frogs, as amphibians, don’t share—horses, like us, are warm–blooded, give birth to live young, suckle their young, have hair, etc. The evolutionist claims that horses and humans must be more closely related than frogs and humans. But what about the remarkable differences in the limbs of horses and humans? The evolutionist ‘explains’ the profound differences in the horse and human limbs as due to ‘adaptation’ in the horse. So, when the evolutionist confronts anomalies like the horse limb, a story is invented to ‘explain’ it. In this case the story is ‘adaptation’. The limb was supposedly ‘modified’ by natural selection to do a different job. However, this is a just–so story to explain away evidence which does not fit the common ancestry idea. Quolls and cats Marsupials are mammals which give birth to very immature babies which are suckled in a protective pouch. These include the kangaroos, koalas, wombats and possums of Australasia and the opossums of the Americas. Placental mammals nurture their young in the womb, which develops an elaborate nourishing structure called a placenta. The babies are born in quite a developed state compared to marsupials. Nearly all the mammals in Australia are marsupials. Why is this so? The evolutionist claims to have an answer: the marsupials evolved in Australia from a common ancestor which just happened to be here. 3Placental mammals—such as dogs, cats, horses, squirrels, mice, etc., evolved on other continents. That’s the story.However, there are many incredible similarities between marsupial and placental animals which defy this naturalistic story. Take the marsupial mouse, or dunnart, and placental mouse, for example. Some types are so similar it is difficult to tell them apart without close inspection to look for the pouch.The marsupial mole from the Northern Territory of Australia is incredibly similar to the golden mole of Africa. When the cuscus was first discovered in Papua New Guinea it was mistaken for a type of monkey. It has a flat monkey-like face, opposable digits on front and hind limbs, and a prehensile (grasping) tail.
Marsupial
Placental
Tasmanian ‘Tiger’ or Thylacine
Wolf
Feathertail Glider
Flying squirrel
Dunnart or Marsupial mouse
Mouse, Shrew
Cuscus
Monkey
Marsupial mole
Golden mole of Africa
Quoll
Cat
Bilby
Hare
Rat kangaroo
Rat
Wombat Marmot The number of similar marsupial and placental animals is astounding, if they just arose by the evolutionary Numbat Anteater processes of chance mutations and natural selection.The list could be extended by including extinct types such as the marsupial diprotodon, a hippopotamus-like creature. Table 1. Some marsupial and placental animals showing So there are many similarities which are not due to remarkable similarities. common ancestry, or evolution. How does the evolutionist account for these similarities? Here another story comes into play: many of the marsupials and placentals ended up looking like one another because they happened to be in similar ecological niches and so evolved similarly to fill those similar niches. This is another ‘just–so’ story. Such similarities are said to be due to ‘convergence’ or ‘parallel evolution’. ‘Convergence’ is really just a grab bag to put similarities which cannot be explained through common ancestry (evolution). This is supposed to account for similarities which do not fit the evolutionary scheme of descent based on other similarities.It stretches the bounds of credulity to believe that so many marsupials just happened, without any plan and purpose, to look so similar to their placental counterparts. It’s like trying to believe that two artists painted a series of almost identical paintings without reference to one another, or that the similarities between a VW and Porsche were not due to their having a common designer.Also, if being in a similar ecological niche automatically generates similarities, why is the kangaroo not more like cattle, horses or deer—the kangaroo’s ecological counterparts on other continents? The kangaroo throws a spanner into the logic of the ‘convergence’ story used to explain similarities which do not fit the evolutionary story.4Things were created in such a way as to confound naturalistic (everything made itself) explanations for the origin of organisms. Various ad hoc, or just–so, stories have been invented in an attempt to explain the many things which do not fit the evolutionary scheme, but they are just that—stories. A serious problem for homology by Robert E. Kofahl, Ph.D. Supposedly, inherited genes control inherited characters. Thus it would be reasonable to assume that homologous characters are controlled by homologous genes. These would be genes that control similar characters, but which have slowly evolved, changing with time, so that the inherited characters are also changed.Thus the front appendages of reptiles, mammals, birds, and humans are said to be homologous. Therefore, they must be controlled by homologous genes. The fact is, however, that it has been proved in many cases that homologous structures are not produced by homologous genes! In the vertebrates the embryo is constructed of a large number of segments which can be numbered, starting at the head end. Surely particular segments develop under the control of particular genes. We would reasonably assume the same for any particular structure, such as the front leg. Yet we see in the diagram that in six different vertebrates which allegedly inherited their front legs from a common ancestor, the front legs as well as the rear legs develop from entirely different groups of segments from species to species.Thus if the front legs (or rear legs) of these different creatures have been inherited from a common ancestor through evolution, we have the incredible idea that the job of producing the legs is, by evolution, passed slowly back and forth from group to group of different genes, which are themselves gradually changing to accomplish this fantastic juggling act.In his 1971 monograph, Homology, An Unsolved Problem (reference Oxford Biology Reader), Sir Gavin de Beer, one of the truly great embryologists of this century, posed the question for evolutionary theory which still is unanswered:‘But if it is true that through the genetic code, genes code for enzymes that synthesize proteins which are responsible (in a manner still unknown in embryology) for the differentiation of the various parts in their normal manner, what mechanism can it be that results in the production of homologous organs, the same "patterns", in spite of their not being controlled by the same genes? I asked this question in 1938, and it has not been answered.’ An illusion of common descent Peer Terborg One of the activities of evolutionary biologists is modeling ‘trees of life’. Before the advent of molecular biology such trees were predominantly based on morphological characteristics and ontogenetic traits. Nowadays, most modeling is based on molecular biology data. One of the surprises is that the well-known ‘Darwinian trees of descent’ are often not recapitulated by the genetic data. A Google search using the terms ‘comparative genomics’ and ‘unexpected’ resulted in over 60,000 hits, indicating that we can learn something unforeseen about the nature of mutations from comparative genomics. Since many mutations have been found in DNA ‘hot spots’, evolutionary trees are actually a byproduct, or artifact; a result of common design and the non-random nature of mutations. This novel view is supported by recent observations and provides an explanation for two phenomena associated with molecular phylogeny: homoplasy and nested hierarchy. Mutations that spontaneously and randomly appear in the germ line can be passed on from one generation to the next and can be followed in time. The current consensus is that mutations in a DNA sequence are introduced at random and occur only once—except in some ‘hot spots’. This view is summarized by Futuyma in an evolutionary textbook as follows:
“Mutation is random in two senses. First … we cannot predict which of a large number of gene copies will undergo the mutation … Second, and more importantly, mutation is random in the sense that the chance that a particular mutation will occur is not influenced by whether or not the organism is in an environment in which that mutation would be advantageous … “[That] Mutations occur at random … does not mean that all conceivable mutations are equally likely to occur, because, as we have noted, the developmental foundation for some imaginable transformations do not exist. It does not mean that all loci, or regions within a locus, are equally mutable, for geneticists have described differences in mutation rates, at both the phenotypic and molecular levels, among and within loci … “It does not mean that environmental factors cannot influence mutation rates: ultraviolet and other radiation, as well as various chemical mutagens and poor nutrition, do indeed increase rates of mutations.”1 If this view is correct, alignment of nucleotides, or ‘point mutations’, in the DNA of different species would be the best evidence for common descent. Random mutations in ancestral DNA sequences would also be present in all descendants according to the laws of inheritance. Hence, any alignment of ‘mutations’ can be considered molecular evidence for common descent. On the other hand, mutations that do not line up in phylogenetic analyses are de novo mutations introduced after the organism supposedly split into separate species. As such, they are evidence for the random character of mutations. Let’s critically analyze whether Futuyma’s view can stand in the light of current biology. To a certain extent Futuyma may be right. For instance, we may not be able to predict which gene will mutate. Or, whether advantageous mutations are deliberately induced as an adaptive response to the environment of the organism.2 There may be another aspect, however, that determines where a mutations is introduced—its DNA environment. As mentioned by Futuyma, some DNA sequences may be more likely to mutate than others because the site of mutation often depends on the molecular context. This fact is wellknown in genetics and has been covered extensively.3–6 Non-random mutations in Drosophila That mutation may not be an entirely random phenomenon first occurred to me when I read a paper by Schmid and Tautz that discussed the 1G5 gene of Drosophila melanogaster and D. simulans. 7 The gene, found in both species is a unique, single copy gene of unknown function, but is not a pseudogene. The 1G5 gene caught the authors’ interest because it was the fastest changing gene in the study. The sequence of the 1G5 gene is 1,081 base pairs (bp) long and contains only one small intron of 61 bp. Figure 1 shows all 75 polymorphic sites in an 864 bp segment (including the intron) of 13 populations of D. melanogaster and 4 populations of D. simulans. The authors concluded that almost none of the amino acid positions are under strong selective constraint because the fraction of polymorphic sites in the intron is comparable to the fraction of polymorphic sites in the coding region. In other words, the IG5 gene is evolving /changing in a neutral way in which selection is not involved. Drosophila melanogaster originally stems from the African continent but has been present in Europe and Asia since early history. Until 1875, Drosophila did not exist in Canada or in the rest of the North American continent. In 1900 it was also not present in Mexico or Australia. Japan was colonized only in the 1960s. The current Drosophila populations in Latin-America, Australia and Japan are all due to recent migrations, mainly from European and Asianpopulations. Based on the data, we can therefore make two interesting observations: 1. An Italian population invaded the Americas, first the USA (D. mel III) and then it migrated to Peru. In Peru it acquired the exact same mutation as the population in Japan (the A at position 835); 2. Drosophila populations from either Cyprus, Iraq or USSR invaded Canada and USA (USA II). The populations in Australia were not derived from the Italian (D. mel 7). Still the Australian population ended up with the exact same mutations the Italian population acquired in the USA (USA III). The Australian population (D. mel III) could have migrated from the USA (D. mel 11), and have acquired an A at position 637. A fraction of the mutations in the IG5 gene is found on exactly the same location but is not the result of common descent! Because none of the positions may be under selective constraint, the observed ‘shared mutations’ in the gene may be the result of a non-random mechanism—a mechanism that produces an illusion of common descent. An important question that needs to be addressed is whether such non-random mutations are the rule rather than the exception. If the fraction of such non-random mutations is much greater than assumed, an alignment of the mutations would suddenly not be compelling molecular evidence of Darwin’s common descent. Rather, the alignment may simply reflect the common biophysical properties of those organisms. Nonrandom mitochondrial mutations Mitochondria are the power plants of the cell. They convert sugars into biologically useful energy (ATP) and also generate heat. The more ATP generated, the less energy is left to produce heat. The efficiency of generating ATP and heat as a ‘byproduct’ appears to be a genetic trait. Genetic changes (‘mutations’) that result in an increase in the generation of heat automatically reduce the amount of ATP produced. People in the tropics will therefore tend to benefit from mitochondria that produce little heat and loads of ATP. In contrast, people in Arctic Regions benefit from mitochondria with a heat bias. A few years ago, an Australian team found that heat-generating mitochondria are indeed common in Arctic Regions.8 They explained it as the result of natural selection, but there is also good evidence these adaptive mutations may have occurred several times as non-random mutations. “An Italian study published in 2001, for example, showed that healthy centenarians in Italy have a high incidence of a certain mutation in the cytochrome B gene, which is part of the energyproduction machinery. … Remarkably, Wallace’s study has found that this lineage, and another found in Europe which also associated with longevity … have the same mutations. Yet the two mutations occurred independently of each other. Wallace’s study goes against the traditional view that the spread of most mitochondrial mutations occur by chance, says Alan Cooper, head of the Ancient Biomolecules Centre at the University of Oxford.”9
The non-random nature of mutations in mitochondrial DNA can be illustrated by a small deletion of nine nucleotides.10 The deletion is located between two genes in the mitochondrial control region, and is present at varying frequencies in Asia, Southeast Asia, Polynesia, and the New World, but also in sub-Saharan Africa. Comparing mitochondrial DNA sequences of sub-Saharan Africans with those of Asians revealed that both populations had independently acquired the deletion. The deletion also independently occurred in South-East Asia, Polynesia and the New World. Hence, the exact same mutations can be found in genomes independent of common descent. Natural selection and common descent are not required to explain the distribution of shared mutations. Rather, a common genetic mechanism explains such findings. Non-random mutations experimentally visualized Although non-random mutations are acknowledged as occurring in hot spots, it has been tacitly assumed that such mutations are most likely exceptions. This assumption, however, may be wrong. Experiments on mutation sites in the DNA of the common gut bacterium Escherichia coli have provided some remarkable results. “Of 293 independent mutations identified within the lacI−d sequence on the F plasmid, 63% are located at 19 medium-level hotspot sites. Of 120 base substitutions identified within the rpsL sequence on a multicopy plasmid, 63% are located at 9 hotspot sites. Recently, the rpsL mutation assay was adapted to analyze mutations in the same target sequence that had become integrated into the chromosome of E. coli (K. Yoshiyama, M. Kawano, A. Isogawa and H. Maki, unpublished results). In this case, 70% of 1555 base substitutions examined are confined to only two strong hotspot sites. The remaining 475 mutations are almost evenly distributed at 91 sites within the target sequence.”11 In bacteria, the nonrandom character of mutations can only be resolved after the analysis of hundreds of DNA sequences. If sufficient numbers of sequences are included, the majority of mutations are in hot spots. Base substitutions and single-base frame shifts, two major classes of spontaneous mutations, occur non-randomly throughout the genome. Within target DNA sequences there are hot spots for particular types of spontaneous mutations. Outside of these hot spots, spontaneous mutations occur more randomly and much less frequently. Hot-spot mutations can therefore be attributed to endogenous DNA lesions rather than to replication errors.11 Radiation-induced non-random mutations Direct evidence for environment-driven non-random mutations comes from studies carried out in areas with a high natural background of radioactivity. When unstable atoms drop or convert to a more stable energy state, they send out energy waves (beta and gamma radiation) and/ or emit a hydrogen particle (alpha radiation). The emitted radiation is better known as radioactivity. Radioactivity is highly mutagenic: it destroys the information in the DNA molecule. It has always been assumed that radiation is a random mutagen, i.e. the position at which mutations are introduced cannot be predicted. This is also the case for ultraviolet radiation and oxidative
stress. Surprisingly, however, radioactivity has now been shown not to be a random mutagen. Kerala, at the southern tip of India, is a densely populated peninsula with the world’s highest level of natural occurring radioactivity: the beaches contain radioactive elements such as thorium and monazite. Generations of fishermen have made a living here, as well as on nearby low-radiation islands. In 2002, mutations in the mitochondrial DNA were analyzed and compared to a control group. Twenty-two mutationswere identified in the DNA sequence of families living in the Kerala area, whereas the control population had only one mutation in the same sequence. The increased mutation rate in the Kerala area wasn’t unexpected, but the surprise was to find that the mutations were located at positions referred to by geneticists as ‘evolutionary hot spots’. The investigators reported that “Strikingly, the radioactive conditions accelerate mutations at nucleotide positions that have been evolutionary hot spots for at least 60,000 years.”12 Apparently, high energy radiation does not induce random mutation. In an environment with high levels of radiation, some positions are more likely to mutate than others. Over and over, radiation-induced mutations fall on the exact same hot spots. Therefore, positions where mutations occur in a DNA sequence may largely be (pre)determined. Homoplasy A comparison of human, chimpanzee and rhesus macaque genes revealed that many mutations are shared between the Rhesus macaque and humans but do not appear in chimpanzees.13 In other studies which compared human, chimpanzee and gorilla sequences this peculiar phenomenon was also observed, i.e. human genes often resemble those of gorillas, not chimpanzees.14 So whether humans are more ‘closely related’ to chimpanzees than to gorillas then appears to depend on which genes are compared. Only 55% of the human genes resulted in the expected Darwinian tree. The sharing of unexpected sequence arrangement is a common observation and is known as homoplasy. Scientists speak of homoplasy when DNA sequences are identical in organisms that are not closely related in an evolutionary tree. (Mutations in) DNA sequences often conflict with ‘known’ evolutionary trees. “Homoplasy has long been appreciated in theoretical phylogenetics, with much effort invested into understanding its causes and providing corrections for them. However, the observed patterns … give cause for concern that the extent of homoplasy is much greater than expected under widely accepted models of sequence evolution and that the attendant consequences for the limits to phylogenetic resolution are not sufficiently appreciated.”14 Apparently, homoplasy is fairly common (10–15% according to reference 14) and, in my opinion, simply reflects the non-random nature of mutations. Homoplasy is, in fact, nothing but part of the illusion of common descent caused by inter-species hot spots recognized and acknowledged by evolutionists. How do evolutionists discriminate between random and non-random mutations when they are modelling the tree of life? In other words, how do they differentiate between homoplasy and real common descent mutations? The answer is they don’t. It appears their trees are nothing but common design plus a handful of non-random mutations.Nested hierarchy Phylogenetic analyses often display nested hierarchy. This means that the genes of distinct organisms appear to us as groups within groups. For instance, the genes of humans usually group with primates. Primates group with mammals, which then group with vertebrates. The nested hierarchy is a reflection of DNA sequences that are more dissimilar in organisms that are more distantly related. This is what one might expect from common descent with modification; the longer the time since two organisms supposedly split from a common ancestor, the more differences should be observed. Nested hierarchy is therefore believed to present compelling evidence for evolution and meant to imply common descent. However, according to Francis S. Collins, the director of the Human Genome Project: “If these genomes were created by individual acts of special creation, why would this particular feature [nested hierarchy] appear?”15 Collins considers nested hierarchy a problem for special creation and it his main reason for accepting Darwin’s common descent. But the nested hierarchy observed among species that cannot reproduce may just be a result of the functional restrictions (between separate designs) and non-random mutations. Functional domains of proteins include sites for phosphorylation, glycosylation, ubiquitinilation, sumoylation and glutathionylation, as well as sites that interact with other proteins. The function of such domains is determined by specific sequences of amino acids that must be coded in the DNA. All functional domains and sites will contribute to the sequence identity of homologous genes in separate species. Phylogenetic analyses are therefore in effect a genetic mirage—the result of artificial constraints imposed by analysing functional domains together with nonrandom mutations—largely determined by the physico-chemical properties of the DNA sequence and its environment. The pseudogene argument revisited A pseudogene is a gene that has lost its function, usually due to the accumulation of debilitating mutations. A wellknown example is the GULO gene, which is inactive in humans. Hence, man cannot make vitamin C. In fact, all the families tested from one primate suborder, the Catarrhini, also lack the ability to make their own vitamin C, whereas those from the suborder Platyrrhini make this vitamin in the liver. Degenerative loss of vitamin C biosynthesis has evidently occurred quite frequently. A deletion mutation in humans is also present in chimpanzees, orangutans and macaques.16 This deletion is usually hailed as the ultimate evidence for the existence of a common ancestor for both humans and apes. Based on the occurrence of non-random mutations, could this shared deletion in primate genes simply be the result of an inter-species hot spot?Figure 3 shows the relevant part of exon X of the GULO gene in 11 organisms, including humans and primates. The deletion in nucleotide 97 is indicated by an asterisk. It is immediately obvious from the other sequences that position 97 is in fact a mutational hot spot. Reading position 97 from bottom to top, i.e. from rat to guinea pig, gives us the sequence A-C-G-A-C-A-G. Compare, for instance, the neighbouring nucleotides on positions 96 and 98. Both 96 and 98 read G-G-G-G-G-G-G and are therefore very secure, very stable positions. In contrast, the nucleotide on position 97 is highly unstable. Position 97 appears to be an inter-species hot spot, a highly unstable region that easily mutates. In man, chimpanzee, orangutan and macaque the deletion in this unstable position gives us an illusion of common descent.17 Discussion and outlook Two elementary and distinct classes of mutations occur in DNA sequences: 1) random mutations, and 2) non-random mutations. Here, random has been defined as genetic changes that are entirely the result of chance; where and when random mutations are introduced in a DNA sequence can neither be predicted nor foreseen. Random mutations are purely the physical outcome of the allpervading frictional damage that accompanies all molecular machinery.18 On the other hand, non-random mutations are the result of physico-chemical mechanisms; their position in a DNA strand reflects their non-random nature. There are two distinct types of non-random mutations: 1. ‘Veri’ (‘true’) non-random mutations, that occur in exactly the same location in all DNA sequence. These are non-random with respect to the position in the DNA sequence and it is very hard to distinguish them from shared mutations resulting from common descent; 2. ‘Quasi’ (‘almost’) non-random positional mutations. A quasi mutation is non-random in the sense that it occurs in a determined DNA sequence, although the nucleotide affected is random (either A, T, C or G). In genetic analyses, quasi non-random mutations help to discriminate between non-random mutations and common descent. We may not be able to predict when non-random mutations occur (except for radiation induced mutations),
but we can predict the position where they will appear. The incidence of veri and quasi non-random mutations is much higher than assumed—homoplasy is omnipresent—and there appears to be mutational cold spots, warm spots, hot spots and super hot spots. Because non-random mutations have only been observed/discovered in studies analysing a sufficiently large number of individuals, they were not know until recently. From large-scale genetic comparisons, that include hundreds of sequences of the same species, the position of non-random mutations can be estimated with a high level of accuracy. In addition, sequence analyses from many different species may help to localize interspecies hot spots. Upon close-up scrutiny, molecular biology has revealed that mutations are not just a random, chance-driven phenomenon. Although we do not yet know the ‘whys and hows’ of non-random mutations, what we do know is they create an illusion of common descent when they appear in organisms that cannot mate. Could the mammalian middle ear have evolved … twice? by David Catchpoole 21 November 2006 The amazingly complex middle ear of mammals has three bones—the incus, malleus and stapes, popularly known as the hammer, anvil and stirrup—while reptiles have only one. Because of its complexity, evolutionary theorists have long said it must have originated once only, in some ancestral creature from which all mammals today are descended. As an article in New Scientist put it: ‘The process was so complex that mammal experts assumed that it must have occurred only once, before monotremes split off from the other mammals more than 150 million years The middle ear of the cat (a ago.’1That’s not surprising. Consider the remarkable transformation that evolutionists mammal) has three tiny bones in maintain took place: three jawbones of the ancestor reptile somehow gradually it for precision transmission of migrated over generations (while the jaw kept being useful for chewing) to eventually sound that are supposed to have become the three bones that transmit sound in the mammalian ear.So it’s hard evolved from three bones in the enough to conceive of such an amazing series of events taking place once, let alone jaw of a reptile (same class as twice. But the discovery2 of a ‘115-million-year-old fossil of a tiny egg-laying mammal the chameleon). thought to be related to the platypus provides compelling evidence of multiple origins of acute hearing in humans and other mammals.’3 This raises the problem: ‘How can this supposedly rare and unexpected evolutionary change have occurred so commonly in early mammals?’3
In the various reports and commentary spawned by this fossil, no clear evolutionary mechanism is proposed, except to describe it as ‘a remarkable example of homoplastic evolution’ [another term for convergent evolution—the supposed independent evolution of similar structures].2,4In other words, as New Scientist reports, evolution ‘invented’ the mammalian middle ear twice: ‘The advantages of the middle ear are so great it was inevitable it should evolve twice in two groups with similar constraints.’ 1This is yet another example of the contortions evolutionists have to go through to try to make the fossils (which are not millions of years old but, in reality, largely a legacy of the Flood, only 4,500 years ago) fit with evolutionary theory. It requires blind faith to believe that things ‘so complex’ could have evolved once, let alone twice or more. And why would natural selection even bother? Reptiles hear quite well. (See Dr David Menton’s DVD presentation ‘The Hearing Ear and the Seeing Eye’, available from our online bookstore.)
Click image to enlarge.
Did eyes evolve by Darwinian mechanisms? by Jerry Bergman The evolution of the eye has always been a dilemma for evolutionists from Darwin’s time to the present. Although Darwin, Richard Dawkins and other evolutionists have tried to explain how an eye could evolve, their solutions are clearly unsatisfactory. Many kinds of eyes exist, but no progression of eye designs from simple to complex can be produced in the natural or fossil world. Furthermore, the simplest ‘eye’, the eyespot, is not an eye but pigmented cells used for phototaxis; yet even it requires an enormously complex mechanism in order to function as a vision system.
Figure 1. The compound eye of an insect. Note that the eye consists of hundreds or more separate eyes which, in some ways is more complex than the human eye. (After Mitchell et al.).48 The concept of irreducible complexity (IC) has become an important tool in intelligent design theory. One of the best examples of IC is the design of the animal eye. Eyes are critical because, for the ‘vast majority of animals’, vision is their ‘most important link to the world’.1 Darwin vividly recognized the problem of eye evolution and the serious impediment that it was for his theory. In his words,‘To suppose that the eye, with all its inimitable contrivance for adjusting the focus to different distances, for admitting different amounts of light, and for the correction of spherical and chromatic aberration, could have been formed by natural selection, seems, I freely confess, absurd in the highest possible degree.’ 2Nonetheless, Darwin felt the seemingly insurmountable problem of the evolution of what he called an organ of ‘extreme perfection and complication’ could be solved.2 He included a three-page proposal of intermediate stages through which eyes might have evolved via gradual steps.3 These stages included the following: photosensitive cell aggregates of pigment cells without a nerve an optic nerve surrounded by pigment cells and covered by translucent skin pigment cells forming a small depression and then a deeper depression the skin over the depression gradually taking a lens shape evolution of muscles that allow the lens to adjust. These stages in living animals are believed to constitute major evidence for the evolution of the eye. 4 Isaak claims that all of these steps are viable because all of them exist in animals living today: ‘The increments between these steps are slight and may be broken down into even smaller increments. Natural selection should, under many circumstances, favor the increments. Since eyes do not fossilize well, we do not know that the development of the eye followed exactly that path, but we certainly cannot claim that no path exists.’5 University of Chicago biology Professor Jerry Coyne wrote that human ‘ … eyes did not suddenly appear as full-fledged camera eyes, but evolved from simpler eyes, having fewer components, in ancestral species. Darwin brilliantly addressed this argument by surveying existing species to see if one could find functional but less complex eyes that not only were useful, but also could be strung together into a hypothetical sequence showing how a camera eye might evolve. If this could be done—and it can—then the argument for irreducible complexity vanishes,
for the eyes of existing species are obviously useful, and each step in the hypothetical sequence could thus evolve by natural selection.’6The dominant theory was outlined by Dennett, who concluded that all eye evolution requires is a‘ … rare accident giving one lucky animal a mutation that improves its vision over that of its siblings; if this improvement helps it to have more offspring than its rivals, this gives evolution an opportunity to raise the bar and ratchet up the design of the eye by one mindless step. And since these lucky improvements accumulate—this was Darwin’s insight—eyes can automatically get better and better and better, without any intelligent designer.’7Others are not so confident. Melnick concluded that the eye is a marvel and that ‘its immense complexity and diversity in nature, as well as its beauty and perfection in so many different creatures of the world, defies explanation even by macroevolution’s most ardent supporters.’ 8This paper explores these conflicting views. Evolution of the eye Advanced vision appears almost at the very beginning of the fossil record. The oldest eye in the fossil record, that of a trilobite, is a very complex faceted compound eye that ‘dates’ back to the Cambrian, conventionally dated about 540 million years ago.9,10 The fossil evidence shows that from the beginning of the fossil record eyes are very complex, highly developed structures. We also have ‘living fossils’, animals that have remained virtually unchanged since very early in history. University of Salford biologist, Laurence R. Croft, wrote that the ‘precise origin of the vertebrate eye is still a mystery. The fascinating thing about the evolution of the eye is its apparent sudden appearance.’ 11 Specifically, the fossils show that vision originated ‘in the early Cambrian’, which Darwinists put at ‘some 530 million years ago’. 12Furthermore, although the ‘Cambrian animals were not the same species as exist today … nearly all the modern phyla had rapidly come into existence, fully equipped with eyes as far as can be told from the fossils’ and during the Cambrian explosion ‘something remarkable seems to have happened … a rich fauna of macroscopic animals evolved, and many of them had large eyes.’ 12 Sir Steward Duke-Elder, the preeminent ophthalmologist at the time of his death in 1979, acknowledged the sudden appearance of the perfected vertebrate eye, noting: ‘The curious thing, however, about the evolution of the vertebrate eye is the apparent suddenness of its appearance and the elaboration of its structures in its earliest known stages. There is no long evolutionary story as we have seen among invertebrate eyes, whereby an intracellular organelle passes into a unicellular and then a multicellular eye, attaining by trial and error, along different routes an ever-increasing degree of complexity. Within the vertebrate phylum the eye shows no progress of increasing differentiation and perfection as is seen in the brain, the ear, the heart and most other organs. In its essentials the eye of a fish is as complex and fully developed as that of a bird or man [emphasis added].’13Biochemical studies have shown that the human lens contains‘ … proteins similar to those found in the cyclostomes (hagfishes and lampreys) that are the living descendants of the Agnatha, which originated the vertebrates about 450 million years ago. Thus these studies have confirmed the view that the vertebrate eye, and in particular the lens, has changed very little during the course of evolution.’14 Evidence for eye evolution from living animals Only about a third of all animal phyla contain species with proper eyes, another third contain species with light-sensitive organs only, and a third have no means of light detection, although many can detect heat.15 Nonetheless, of those animals with eyes, both vertebrates and most invertebrates, an enormous variety of eye designs, placement and sizes exists.10 The eyeball diameter ranges from less then a tenth of a millimetre in certain water fleas to 370 mm in the giant squid.16 Eye placement also varies, ranging from the common binocular vision employed by most mammals to the movable eye on each side of the head used by many lizards.The number of eyes in one animal can also vary from none to eight. In spiders alone the number ranges from zero to eight, always existing in pairs of two. Some eyes contain both a lens and a retina-like structure in a single cell.17 A complex telephoto lens was identified in the chameleon in 1995. The reason why so many designs exist is because eyes must serve very different life forms that live in very different environments. Animals live in the ground, inside of other animals, in the air, on land, in salt water and in fresh water. Furthermore, animals range in size from a water flea to a whale. Table 1. Mean numbers of myelinated fibres in the optic nerve of selected vertebrates. Note the enormous difference within each category. For example birds range from 408 to 988 thousand, mammals from 7 thousand to 1.21 million. (From Cousins50).Although many kinds of very different eyes are known, no direct evidence exists to support the evolution of the eye and its accessory structures. Furthermore, much evidence contradicts such evolutionary beliefs. For example, note in table 1 that the number of myelinated fibres in the optic nerve does not correlate with putative evolutionary development. A pigeon has almost as many fibres as a human. Many birds, such as the eagle and hawk, have excellent vision yet have half as many fibres as a domestic pig.Another example is visual pigments. The presumably highest, most evolved form of life, the higher primates, have only two cone photoreceptors, blue and green, but birds have a total of six pigments: four cone pigments plus pinopsin (a pineal photoreceptive molecule) and rhodopsin for black and
white vision.12,18 Put another way, chickens, humans and mice all have the rhodopsin pigment; mice in addition have blue and green; humans have blue, green, and red; and birds have these three pigments plus violet and pinopsin. For every colour that humans perceive, birds can see very distinct multiple colours, including ultraviolet light. Birds use infrared light (which we sense as heat) for night vision, allowing them to rapidly visualize their young in a dense, dark tree.The possibility of classifying eyes in living animals from simple to complex—simple types existing in simple animals and complex types in complex animals (which we will show cannot be done)—does not provide evidence for an evolutionary relationship. A primary problem is that this attempt is based only on eye characteristics as they presently exist. Historical eye evolution cannot be proven by listing a series of existing eyes from simple to complex and then arguing that the complex evolved from the simple because evolution requires that all existing eyes have an equally long evolutionary history.According to neoDarwinism, the simplest modern eye in living animals has had the same amount of time and evolutionary history as the most complex eye because life began about 3.5 billion years ago and all life today evolved from this point in history. Although Darwinists argue that many of these eyes are evolutionary dead ends, this would require an admission that these modern ‘simple’ eyes are only analogues or ‘similar’ to putative past ancestral eyes (to more complex modern types), which reduces their value as evidence.Darwinists need to determine the eye designs from which existing eyes have actually descended, one from the other, over time. Duke-Elder and Darwin (1872) before him were unable to do this, yet they offered their list of eyes of varying complexity as evidence of evolution. Cousins wrote:‘ … the crucial importance of this requirement to the theory of evolution was fully understood by Darwin, who stated that, in searching for the gradations through which an organ in any species has been perfected, we ought to look at its lineal progenitors. Indeed we ought; though he himself could not do so. It is deceptive to the reader to create a seriation beginning with eye spots as seen in unicellular organisms and call them, as does Duke-Elder (1958), the earliest stage of evolution.’ 19Croft concluded that the claim that we can line up eyes in an evolutionary sequence from very simple to very complex is false because research on the developmental history of the eye in widely differing species finds‘ … it remarkably similar. Indeed the basic features of the eye in different vertebrates are very much the same despite great variations in their mode of life and adaptation to habitat. Furthermore, unlike other organs such as the heart, there is no long evolutionary history with the eye. In essence the eye of a newt is as complex and fully developed as that of a man.’ 11Sinclair also concluded that vertebrates and most invertebrates, including insects and cephalopods (molluscs, including octopuses and squid), all have eyes with common visual elements, including ‘a similar photoreceptor design’, yet have a marked ‘dissimilarity of their appearance’.10The source of the design and evolution of the eye, Darwinists postulate, was a series of beneficial mutations that had to occur in appropriate unison in order to produce the set of structures required for eyes to function. The new mutation set, Darwinists argue, resulted in a superior structure compared to the old one, and this new and better eye improved the animals’ ability to compete against other forms of life. Some of the many problems with this conclusion were noted by Grassé in his discussion of Myrmelion (ant lion) anatomy:‘Have you ever seen a mutation simultaneously affecting two separate components of the body and producing structures that fit one another precisely? … have you ever beheld three, four or five simultaneous mutations with matching structures producing coordinating effects? … These are vital questions that demand an answer. There is no way of getting around them, or evading the issue. Every biologist who wants to know the truth must answer them, or be considered a sectarian and not a scientist. In science there is no “cause” to be defended, only truth to be discovered. How many chance occurrences would it take to build this extraordinary creature [Myrmelion formicarius]’?20An organ that did not aid the animal’s survival would use scarce energy, nutrients and body space and, if the organ were not used, would be at high risk for problems such as infection. An eye modification would not be selected until it was not only functional but produced a system demonstratively better than the existing organ. Only then could natural selection operate to choose from existing variations to perfect the organ beyond mere functional effectiveness.
Table 2. Land and Nilsson’s widely used classification system of eye designs. Other systems are also used today, illustrating the problems in arranging eye designs into hierarchies. Also note that the Land and Nilsson system also does not show a clear simple to complex design hierarchy. (From Land and Nilson12). Advanced eye designs Many kinds of eyes exist, and there are many schemes to classify them. The most basic classification system groups all eyes into four classes. The first is the camera type or ‘simple’ eye, such as exists in humans, which uses a focusing system to project a single, sharp image on the retina. The second type is the fixed focus compound type (figure 1) that uses multiple separate refractive units called ommatidia, such as used by trilobites and flies. The third type is a scanning eye that builds an image much like a television camera, such as is used in the small marine crustacean copilia, which in females takes up more than half of its body.21 The fourth type is the complex eye, found in cephalopods and certain advanced vertebrata, consisting of a cornea, iris, lens, retina and numerous accessory structures. 22This division obscures many major differences: some shrimp have a combined simple and compound eye, which is actually a third basic eye type, not a transitional form. This division system also greatly oversimplifies the variety that exists because ‘at least eleven distinct optical methods of producing images’ are now known. 23 The classification system used in this paper was developed by Land and Nilsson (2005) and is given in table 2 (see also figure 2). Problems with classification
Figure 2. Illustration of Land and Nilsson’s classification system of eye designs. Eye designs A–L are described in table 2. (From Land and Nilson12). Note that the most logical classification of eye types is into some type of evolutionary classification from simple to more complex, but this list does not lend itself very well to a hierarchy as postulated by Darwin. Actually, arranging just the 10 basic eye designs used in the Land and Nilsson system from simple to complex is impossible. For example, types A, B, C, D, E, F, H, and I appear similar in complexity, and types G and J appear more complex but are found in lower forms of life (in some winged insects and crustaceans). In Land’s classification the ‘simplest’ type (A) and the most complex type (J), are both found in crustaceans (crustaceans use designs in groups A, E, F, G and H, and molluscs those in group A and H). Nearly identical optical designs are found in very ‘distinctly unrelated animals’ such as fish and cephalopods. 24 The Land list groups the basic eye designs and optical systems only, ignoring the design of the retina cells, the many supportive cells, (such as the ganglion cells, amacrine cells, horizontal cells and bipolar cells), the other nervous system components, including the optic nerve, and the optical system-processing centre, such as the occipital lobe of the brain.Using these criteria would create even more problems in attempting to produce a hierarchy because the processing system is always much more complex than the light collection system, placing all known eye systems at the upper level of Darwin’s scheme. Of course, Darwin was not aware of the vision system’s enormous complexity or variety, nor was he aware of the complexity of the many accessory systems and processing structures such as the brain.The problems of producing a simple to complex hierarchy are illustrated by the fact that the ten types are also commonly arranged into four basic eye designs: the holochroal eye, the superposition eye, the schizochroal eye, and the human apposition compound eye. All of these basic eye designs require a system of focusing resolution, and a complex neurological processing system to enable the viewer to make sense of the large mass of constantly changing signals sent by the retina or other light sensitive cells via the optical nerve to the brain efficiently and rapidly.‘Despite decades of research, we still have only limited understanding of how vision actually works’, making it difficult to produce both consistent classification schemes and hierarchies in an attempt to postulate a reasonable evolutionary phylogeny.23 We do have a fairly good understanding of the eye structure itself, which allowed construction of the classification above. Contrary to evolutionary expectations, the eyes of phylogenetically distant life forms can be very ‘similar in a large number of details.’ 16Ironically, the greatest variety of eye design, not only in structure, but also in number and location, exists not among the vertebrates as Darwinism would expect, but among the socalled ‘primitive’ invertebrates.16 Invertebrates also have eyes that are, in some respects, superior to those of vertebrates. One example is the hemispherical eyes of most flies and other insects, which produce, unlike human and most vertebrate eyes, an image largely free of spherical distortion. 25 Human eyes have significant peripheral image distortion, but spherical eyes form a sharp image in all directions. However, humans do not have sharp peripheral vision because this is the function of the central retina called the macula. Our peripheral vision is for the detection of light and movement which trigger the fixation reflex to turn the eyes toward the stimulus.Another problem in the theory that eye designs represent an evolutionary sequence is that eyes from the three major phyla (vertebrates, arthropods and mollusca) arise from different tissues and are radically different.26 For this reason, evolutionists concluded that they have separate evolutionary histories, and the many
similarities that exist are due to presumed evolutionary convergence. 26 In essence, ‘we don’t know how it could possibly have evolved, so it must have evolved over and over.’ The eye differences would be due to the different needs and circumstances of each organism and its habitat, irrespective of any evolutionary connection. Yet another problem is the evidence for eye evolution forces the conclusion that most of these eye designs must have evolved ‘in a brief period during the Cambrian.’17 The simplest eye Darwinists often claim the primate eye is the most evolved, but many mislabelled ‘primitive’ eyes have advantages over ours. For example, the human eye can register up to 60 images per second; a lowly bee about 300 per second. For this reason, bees can see far better while rapidly moving. The motion picture standard (24 frames per second), to a bee, would be viewed as a series of still pictures. For humans the frames are blurred, giving the illusion of motion. This design innovation in so-called primitive animals is more complex than the corresponding structure in the human eye.The simplest eye type known is the ocellus, a multicellular eye comprising of photoreceptor cells, pigment cells and nerve cells to process the information—is step 4 in Darwin’s list.27 The most primitive eye that meets the definition of an eye is the tiny—about the size of the head of a pin—microscopic marine crustacean copepod copilia. Only the females possess what Wolken and Florida call ‘remarkable eyes which make up more than half of its transparent body.’ 28 Claimed to be a link between an eyespot and a more complex eye, it has two exterior lenses that raster like a scanning electron microscope to gather light that is processed and then sent to its brain. 29 It has retinal cells and an eye ‘analogous to a superposition-type ommatidium of compound eyes’.30 This, the most primitive true eye known, is at stage 6 of Darwin’s evolutionary hierarchy! Visual cell differences Evolution would predict that the more advanced an eye, the more detail it can pick up, a factor related to the number of visual cells. This is not what is often found. In a ‘simple’ visual system (brain and retinas) the smallest number of visual cells is found in the plethodontid salamander, T. narisovalis, which uses about 65,000 cells for the entire visual brain centre and 60,000 for the retina alone. This ‘extraordinarily low’ number of cells is used not because the animal is primitive but because it has a very small head, eye, and brain plus relatively large cells. 31 They add that the smallest extant salamander, T. pennatulus (which is much smaller than T. narisovalis), has about 94,000 visual cells and about the same number of retinal cells. For comparison, the brain visual centres of the frog S. limbatus contain about 400,000 cells. This illustrates the fact that evolution cannot be argued‘ … by asserting that the eye can be built up gradually from a single patch of light-sensitive skin through various stages, slowly reaching the complexity of the vertebrate camera eye. … the case for the evolution of the vertebrate eye or even a light-sensitive patch of skin … must be made in regard to the entire complexity of the living organism, at least insofar as that complexity supports vision (even in the least complex form). For this reason, the debate shouldn’t be about the evolution of the eye, but about the evolution of vision, and vision is always the vision of some particular kind of living animal, a living whole in which the integrated activity and experience of seeing, even in its simplest form, can take place.’32In addition to number of cell differences, photoreceptor cell differences also exist. The cells that provide the membrane surface for opsin molecules can be either ciliary or microvillar structures. The microvilli type dominates in invertebrates, and ciliary types in vertebrates. Even physiological responses vary widely. Light causes microvillous receptors of arthropods and molluscs to depolarize but causes the ciliary receptors of vertebrates to hyperpolarize. Invertebrates use inositol triphosphate for photo-transduction in the second messenger system, whereas vertebrate photoreceptors use cyclic Guanosine 5’-Monophosphate (GMP). Although opsin is the key molecule used to detect light in both vertebrates and invertebrates, regeneration mechanisms (reisomerization) of the chromophore/opsin system ‘are dramatically different among phyla’. 33 Other important differences include invertebrate eyes that are formed from the dermal surface of the ectoderm and vertebrate eyes that are formed from the neural ectoderm. 34Another problem for evolution is that at least 11 distinct optical methods are used to produce images. For one type to evolve into a more ‘advanced’ type ‘requires intermediate stages that are much worse or useless compared with the existing design. This would make a switch essentially lethal to animals that depend on sight.’ 35 For example, the advanced rods and cones in ‘primitive’ animals and the lack of evidence for their evolution has motivated some to conclude that the ‘basic tetrachomatic system evolved very early in vertebrate evolution.’36 Furthermore, no progression from simple to complex photoreceptors exists, but rather only ‘four spectrally distinct classes of cone pigment encoded by distinct opsin genes’ is found in the natural world.37 Evaluation of genes involved in eye development Conversely, similarities, such as the fact that some of the genes involved in eye development are very similar in most animals, argue for a single evolution of the eye. Yet, the difficulties of eye evolution are so great that eyes are hypothesized by some researchers to have independently evolved at least 40 and as many as 65 times. 38 As Fernald notes, at present, ‘we do not know whether eyes arose once or many times, and, in fact, many features of eye evolution are still puzzling.’ 23 A better explanation for the same gene being used by different animals (or plants) is for economy of design by a higher Intelligence.Vertebrate eyes could not have evolved in isolation because eye parts do not have a function as self-contained entities. Eyes are part of very complex, interconnected living organisms, and eyes are only one part of the vision system. 39 One gauge to help determine eye complexity is the number of genes involved in producing the eye—the more genes that are required, the more complex the eye may be. In the primitive Drosophila, so far 501 eye-related genes have been identified, or about 3.5% of its entire genome.24 Vertebrate eyes are estimated to involve 7,500 genes just to develop and regulate the retina—or about 30% of the entire human genome of 25,000 genes.24 Views on eye evolution have flip-flopped These problems are part of the reason why ‘views on eye evolution have flip-flopped, alternately favoring one or many origins.’40 The markedly distinct ontogenetic origin of eyes in very different species is one reason why eyes are postulated to have evolved 40 or more times independently.40 For example, the eyes in many molluscs, including some cephalopods such as squids and octopuses, are remarkably similar to vertebrate eyes. Both have a cornea, a lens, an iris and a retina. One of the major differences is, in one, the retina is inverted, compared to the other. 41Evolutionists attempt to solve this problem by assuming that the phylogenetic line that led to molluscs split very early in evolutionary history, long before the eye had evolved. Then they postulate parallel evolution—concluding that the two eyes evolved to be almost identical, yet were completely independent of each other. Of note is the fact that the most ‘primitive’ camera eye known (the nautilus pinhole eye) and the most advanced eye known are both found in cephalopods! Molluscs as a group contain a pigment eyespot design, a pigment cup (cupulate), a simple optic cup with a pinhole lens, an eye with a primitive lens (a murex marine snail) and a complex eye (the octopus), the latter which is the ‘most elaborate’ eye in the invertebrate kingdom.42 Embryonic origin of vertebrate eyes in contrast to cephalopod eyes Another major difference is found in the embryonic origin of many structures in vertebrate eyes in contrast to cephalopod eyes. For example, cephalopod eyes form from an epidermal placode by successive infoldings, whereas vertebrate eyes develop from the neural plate, and the overlying epidermis forms the lens. Yet another problem for eye evolution is that the eye of just one evolutionary related class, the vertebrates, ‘develops from a diverse collection of embryonic sources through a complex set of inductive events.’43
Conclusions Dennett wrote that the eye lens is ‘exquisitely well-designed to do its job, and the engineering rationale for the details is unmistakable, but no designer ever articulated it.’ 44 He concludes that its design is not real, but an illusion because evolution explains the eye without the need for a designer. This review has shown that evolution does not explain the existence of the vision system, but an intelligent designer does. The leading eye evolution researchers admit they only ‘have some understanding of how eyes might have evolved’.45 These explanations do not even scratch the surface of how a vision system could have arisen by evolution—let alone ‘when’.Much disagreement exists about the hypothetical evolution of eyes, and experts recognize that many critical problems exist. Among these problems are an explanation of the evolution of each part of the vision system, including the lens, the eyeball, the retina, the entire optical system, the occipital lobes of the brain, and the many accessory structures. Turner stressed that ‘the real miracle [of vision] lies not so much in the optical eye, but in the computational process that produces vision.’46 All of these different systems must function together as an integrated unit for vision to be achieved. As Arendt concludes, the evolution of the eye has been debated ever since Darwin and is still being debated among Darwinists.47For non-evolutionists there is no debate. Problems with the evolutionary interpretation of limb design by Dominic Statham Figure 1. The vertebrate forelimbs show a common design but develop in different ways. This is seen even between different orders of amphibian, e.g. frogs and salamanders. To evolutionists, the vertebrate forelimbs are a classic example of homology.1 Their similarities are regarded as undeniable evidence of descent with modification, and they appear in almost every educational textbook promoting evolution. Counter-arguments presented by creationists include the observation that digit development can be different in amniotes and amphibians2 (e.g. humans and frogs) and that the forelimbs grow from different embryonic segments (somites) in different species (e.g. newt, lizard and man).3,4 If descent with modification were the correct explanation for common forelimb design, we would expect the forelimbs to develop in similar ways and from the same parts of the embryo.A less well-known problem for evolutionists is the unique order of limb bone development seen in urodeles, something that has been clarified recently by Fröbisch and Shubin. 5 Generally, tetrapods (including anurans) show a distinct postaxial dominance in their pattern of limb skeletogenesis, meaning that the outer bones form before the inner bones. For example, the ulna leads the radius and the digits develop in the sequence IV-III-II-I. Salamanders, however, show a preaxial dominance, with the inner bones forming before the outer bones, for example, the radius leading the ulna, and digits I and II forming before III and IV. Also, whereas in most tetrapods the proximal mesopodial elements form before the distal ones (i.e. in a direction from tail to head), in salamanders this is reversed. Animation showing the different pattern of limb bone development in frogs and salamanders. As argued by ReMine,6 the natural world appears to have been designed so as to point to a general unity and thus a single designer, yet with exceptions that resist evolutionary explanations. All organisms use DNA but a few utilize a different DNA code, thus ruling out common ancestry.7 (To change from one code to another would require the absurdly improbable event of a simultaneous modification of both the DNA and its translation apparatus.) Similarly, vertebrate forelimbs show a common design, but develop in different ways, supporting the view that the different vertebrate kinds were independently created. If these two amphibian groups had really arisen from a common ancestor, the embryological pathways would not be expected to show such divergent characteristics. Morphology and molecules in conflict yet again1 by Reinhard Junker Figure 1. The roughly 8-cm-long fish-like lancelet Amphioxus. The notochord is a flexible supporting rod above the intestine, which is also formed during the embryonic development of vertebrate animals as the first supporting organ and which is replaced to a large extent in the course of ontogenesis by the vertebral column. The transparent lancelet lives in coastal sands (Image after Piotr Jaworski, www.wikipedia.org) A frequently used and apparently striking argument for the ‘fact’ of evolution is the supposed harmony between molecular similarity trees, and the ‘classical’ morphological family trees (based on physical shape and structure) which are commonly featured in the popular media. The technical literature, however, does not reflect such a harmony. In fact the very opposite can be seen, and the molecular data is bringing these established morphological
phylogenies/lineages into disarray.This fate seems recently to have overtaken the relationship between the tunicates (seasquirts), cephalochordates and vertebrate animals. All three groups together make up the phylum Chordata, characterized by the possession of a flexible supporting rod (the notochord). Salps and sea-squirts belong to the tunicates (saclike animals); a prominent representative of the cephalochordates is the fish-like lancelet or amphioxus (figure 1). Based on morphological similarities, the lancelet was for a long time unrivalled as the closest relative of vertebrate animals. But this is now being questioned by the extensive molecular studies of Delsuc et al.2 The researchers examined 146 nuclear genes from 14 deuterostomes (to which the chordates, hemichordates and echinoderms belong) and 24 other species as outgroups. Figure 2. Contradictory lines of descent. a) Classical textbook view, showing a gradual increase in complexity; b) Topology after the data of Delsuc et al. (After Gee3). The results placed the tunicates and not the cephalochordates (which include the lancelets) nearest to the chordates (figure 2). So this shifts the lancelets closer to the echinoderms than to the other groups. This also makes chordate monophyly uncertain, i.e. not all the chordates can be traced back to one single common ancestor. This would mean that such a marked key characteristic as the notochord developed independently at least twice. The authors indicate, however, that this result must be verified by additional data. If these findings are confirmed, one more key characteristic could no longer be used as an ‘indicator of ancestry’.Gee points out in a commentary that these results turn this textbook scheme of deuterostome evolution on its head.‘Rather than the steady acquisition of progressively more chordate-like (and, by implication, human like) features from an ancestor with nothing to recommend it, the story becomes one of persistent loss … The ancestor would have looked like a cross between an amphioxus and a larger, brainier, tunicate tadpole larva. Crazy? Possibly. But possibly not.’ 3In any case, it is clear that studies being driven by evolutionary assumptions are overturning current concepts of evolution. ‘From complex to simple’— this is not the way we learnt evolution. Tiktaalik roseae—a fishy ‘missing link’ by Jonathan Sarfati 15 April 2006 Fig. 1: Tiktaalik fossil. The secularized mainstream media (MSM) are gleefully promoting a recent find,Tiktaalik roseae (right), as the end of any creationist or intelligent design idea. Some paleontologists are claiming that this is ‘a link between fishes and land vertebrates that might in time become as much of an evolutionary icon as the protobirdArchaeopteryx.’1 So is Tiktaalik real evidence that fish evolved into tetrapods (four-limbed vertebrates, i.e. amphibians, reptiles, mammals and birds)? As will be shown, there are parallels withArchaeopteryx, the famous alleged reptile-bird intermediate, but not in the way the above quote claims!The alleged fish-to-tetrapod evolutionary transition is full of difficulties, explained in great detail in The fossil record of ‘early’ tetrapods: evidence of a major evolutionary transition? In this, it parallels the record of reptile-to-bird, Mammallike reptiles, land-mammal–to–whale and ape-to-human evolution; superficially plausible, but when analyzed in depth, it collapses, for many parallel reasons. For simpler summaries on the fossil record than the preceding linked articles, see The links are missing and Argument: The fossil record supports evolution. What was found? The above quote comes from two leading European experts in the alleged evolutionary transition from fish–tetrapod, Per Ahlberg and Jennifer Clack. It was about the find of well-known American leaders on the same alleged transition, Neil Shubin and Edward Daeschler, and which was the cover story for Nature.2,3 Clack, Shubin and Daeschler even previously featured on the PBS-Nova seven-part series, Evolution, Episode 2: Great Transformations about the origin of tetrapods.Shubin et al. found a 20-cm-long skull sticking out of a cliff. They found that this skull, superficially like a crocodile’s, was part of a fish that had a fin that was supposedly on the way to becoming a tetrapod limb. They ‘ dated’ it to 383 Ma (million years ago). Since it was in Ellesmere Island, Nunavut Territory (Canada), it was given a genus name from the indigenous Inuktitut word for burbot, or large, shallow freshwater fish. Is it transitional? Clack and others are naturally enthusiastic about Tiktaalik’s transitional status. But this is not surprising—to her, we are all fishes anyway! She states: ‘Although humans do not usually think of themselves as fishes, they nonetheless share several fundamental characters that unite them inextricably with their relatives among the fishes … Tetrapods did not evolve from sarcopterygians [lobe-finned fishes]; theyare sarcopterygians, just as one would not say that humans evolved from mammals; they are mammals.’4 This is reminiscent of University of Kansas paleontologist Larry Martin criticising overly enthusiastic ‘feathered dinosaur’ claims: ‘You have to put this into perspective. To the people who wrote the paper, the chicken would be a feathered dinosaur.’ 5 Clack also admitted: ‘There remains a large morphological gap between them and digits as seen in, for example, Acanthostega: if the digits evolved from these distal bones, the process must have involved considerable developmental repatterning. … ‘Of course, there are still major gaps in the fossil record. In particular we have almost no information about the step betweenTiktaalik and the earliest tetrapods, when the anatomy underwent the most drastic changes, or about what happened in the following Early Carboniferous period, after the end of the Devonian, when tetrapods became fully terrestrial.’1 Indeed, the evolution of land limbs and life on land in general requires many changes, and the fossil record has no evidence of such changes. Geologist Paul Garner writes: ‘[T]here are functional challenges to Darwinian interpretations. For instance, in fish the head, shoulder girdle, and circulatory systems constitute a single mechanical unit. The shoulder girdle is firmly connected to the vertebral column and is an anchor
for the muscles involved in lateral undulation of the body, mouth opening, heart contractions, and timing of the blood circulation through the gills.6However, in amphibians the head is not connected to the shoulder girdle, in order to allow effective terrestrial feeding and locomotion. Evolutionists must suppose that the head became incrementally detached from the shoulder girdle, in a step-wise fashion, with functional intermediates at every stage. However, a satisfactory account of how this might have happened has never been given.’ Indeed, Tiktaalik’s fin was not connected to the main skeleton, so could not have supported its weight on land. The discoverers claim that this could have helped to prop up the body as the fish moved along a water bottom, 3 but evolutionists had similar high hopes for the coelacanth fin. However, when a living coelacanth (Latimeria chalumnae) was discovered in 1938, the fins turned out not to be used for walking but for deft manœuvering when swimming. Thus all the claims about Tiktaalik are mere smokescreens, exaggerating mere tinkering around the edges while huge gaps remain unbridged by evolution. Similarly, all the hype about Archaeopteryx and alleged feathered dinosaurs is beside the point while feathers, the avian lung andflight are still an evolutionary enigma. See also Does a ‘Transitional Form’ Replace One Gap with Two Gaps? Transitional limb? Fig. 2: Cladogram of the pectoral fins on the tetrapod stem, from Ref. 3. Click to see larger image Quite aside from the huge problems explaining the origin of locomotion, there are other problems. The series of corresponding limbs (Fig. 2, right) does not appear to show the clear progression. Even from looking at it, it is not obvious that the Panderichthys limb belongs in between the adjacent ones in the series. It has fewer small bones. The authors themselves appear to recognize this: ‘In some features, Tiktaalik is similar to rhizodontids such as Sauripterus. These similarities, which are probably homoplastic, include the shape and number of radial articulations on the ulnare, the presence of extensive and branched endochondral radials, and the retention of unjointed lepidotrichia.’ ‘Homoplastic’ essentially means ‘convergent’ or ‘analogous’, i.e. independently evolved because of a common function (such as the wings of pterosaurs, bats, birds and insects, according to evolutionists), rather than evolved from a common ancestor (homologous, as evolutionists claim for features such as the different forelimbs here). But homology is alleged to be the evidence for evolution (despite many problems—see Common structures = common ancestry?) But appeal to homoplasy is really explaining away evidence that doesn’t fit the paradigm, and indeed such explaining away is ubiquitous. Two evolutionists admit: ‘Disagreements about the probable homologous or homoplastic nature of shared derived similarities between taxa lie at the core of most conflicting phylogenetic hypotheses.’7 In fact, when more characteristics than just one are analysed, homoplasies become even more necessary to explain away anomalies, as will be explained in the section Mosaic rather than transitional. Another major problem is that evolutionists appeal to the common pentadactyl 5-digit pattern as evidence for their common ancestry from a 5-digited creature. Yet the nearest creatures they have to a common ancestor did not have five digits! Acanthostega had eight, whileIchthyostega had seven. Fossil order Fig. 3: Alleged lineage including Tiktaalik, from ref. 1. Click to see larger image. Fig. 3 (right) does much to popularize evolution, but there are a number of problems. The caption admits, ‘These drawings are not to scale, but all animals are between 75 cm and 1.5 m in length.’ If size were taken into account, would there be such a clear progression? Compare a far more extreme example, the supposed land-mammal–to–whale sequence. This was also illustrated as equally sized, but Basilosaurus was 10 times longer than Ambulocetus. Another admission is, ‘The vertebral column of Panderichthys is poorly known and not shown.’ We should remember the Pakicetus fiasco: when a few bones were known, evolutionists drew it like a half-way land-water form. But when more bones were found, it was realized that it was a fastrunning land mammal. All the fossils of this entire series are assigned to middle-upper Devonian, or 385–365 Ma. Naturally, there are many problems with dating , but even under the evolutionists’ own scenario, there are problems. E.g. the entire fish-to-tetrapod transition is supposed to have occurred in 20 Ma, but other salamanders, according to Shubin himself, have remained unchanged for far longer : ‘Despite its Bathonian age, the new cryptobranchid [salamander] shows extraordinary morphological similarity to its living relatives. This similarity underscores the stasis [no change] within salamander anatomical evolution. Indeed, extant cryptobranchid salamanders can be regarded as living fossils whose structures have remained little changed for over 160 million years.’8 Fig 4: Lobe-finned fish and amphibians, according to evolutionary order. Click to see larger image. Even more importantly, the order is not right! Compare Fig. 4 (right): Panderichthys is dated earlier than its supposed predecessor, Eusthenopteron. And all are earlier than the undoubted fish, the coelacanth. This is yet another parallel with alleged bird evolution— undoubted beaked birds like Confuciusornis are 10 Ma older than their alleged feathered dinosaur ‘ancestors’. Evolutionists would argue that it is not a problem, for the same reason that sometimes a grandfather can outlive his grandson. This is correct, but one of the major ‘evidences’ of evolution is how the evolutionary order supposedly matches the fossil sequence. So the mismatch of claimed order of appearance with claimed phylogeny undermines the evolutionary explanation. Also, Acanthostega is allegedly a predecessor to Ichthyostega, but they were actually contemporaries.
Mosaic rather than transitional Many of the alleged transitional forms do not have structures in transition from one form to another. Rather, the alleged transitional nature is a combination of fully-formed structures that in themselves are not transitional. 9For example, Archaeopteryx has fully formed flight feathers, an avian lung and an avian braincase (which is why the ‘hoax’ claim is indefensible), but had allegedly reptile features like a tail and teeth. Alleged whale evolution also has a number of ‘modules’, as documented inWalking whales, nested hierarchies, and chimeras: do they exist? These creatures with a mixture of characteristics are called mosaics orchimeras.Also, who was the predecessor of whom in the case of Acanthostega and Ichthyostega? It depends on which characteristic one looks at: e.g.Ichthyostega's skull seems more fish-like than Acanthostega’s, but its shoulder and hips are more robust and land-animal–like.10The inconsistencies in progression are much like that of the Mammal-like reptiles: major trait reversals and discontinuities. Andrew Lamb, commenting on another alleged tetrapod claim by Per Ahlberg, Livioniana, points out:‘The same sort of reasoning and logic as was used in this article would apply to the fish-to-tetrapod series. In this proposed reptile-to-mammal series, features do not progress consistently. Some organisms towards the mammal end of the series are devoid of certain mammal-like features present in organisms closer to the reptile end of the series. The majority of the hundred-odd traits examined did not progress consistently.’Lamb’s paper demonstrates this, using Ahlberg’s own table, showing that:‘For example, Acanthostega, ninth organism in his series, boasts two tetrapod features that are absent in the tenth organism! ’ The same is true of the limb pattern as shown above. This is also consistent with a designer who used ‘modules’ of different characteristics. A better explanation When analyzed in detail, the evidence is consistent not with evolution, but with a particular form of intelligent design. But not just intelligent design in the broad sense, which allows for any sort of designer(s), even aliens (such as the Raëlian cult), and even can allow for evolution (Michael Behe, author of Darwin’s Black Box, accepts evolution, for example). Rather, it supports a particular subset of ID: the biotic message theory, as proposed by Walter ReMine in The Biotic Message. That is, the evidence from nature points to a single designer, but with a pattern which thwarts evolutionary explanations. In this case, the common modules point to one common designer, but evolution is powerless to explain this modular pattern, since natural selection can work only onorganisms as a whole. That is, it cannot select for particular head design as such, but only for creatures that have a head that confers superior fitness. But a designer who worked with different modules could create different creatures with different modules, that fit no consistent evolutionary pattern. But as we say, Design is not enough! Nature does not reveal the identity of the Intelligent Designer. Fortunately, the Designer already has. Mammal-like reptiles: major trait reversals and discontinuities by John Woodmorappe Summary Evolutionists repeatedly claim that their assembled chain of mammal-like reptiles shows a step-by-step morphological progression to mammals. Despite this, a close and simultaneous examination of hundreds of anatomical character traits shows no such thing, even if one takes basic evolutionary suppositions as a given. Very many, if not most, of the pelycosaur and therapsid traits used in recent evolutionistic studies to construct cladograms actually show a contradictory pattern of progression towards, followed by reversion away from, the presumed eventual mammalian condition. Furthermore, gaps are systematic throughout the pelycosaur-therapsid-mammalian ‘sequence’, and these gaps are actually larger than the existing segments of the ‘chain’. These sobering facts demonstrate that, however the supposed evolutionary ‘lineage’ of mammallike reptiles towards mammals is interpreted, it is divorced from reality. The so-called mammal-like reptiles are believed by evolutionists to be the ancestors of the mammals and to have become more mammal-like with the passage of time. Evolutionists consider anatomical traits to be mammal-like if they occur in modern mammals but not in other modern vertebrates.The highly-touted, alleged succession of mammal-like reptiles towards increasing ‘mammalness’ is not found at any one location on Earth. It can only be inferred through the correlation of fossiliferous beds from different continents. Judgments are made as to which stratum on one continent is older than another stratum on another continent. Moreover, intercontinental correlations are made even when the fossil genera do not correspond with each other. Instead, the correlations are based on the general similarity of specimens, as well as their assumed degree of evolutionary advancement.1 The circularity of such reasoning is obvious. Thus, despite the claims of some evolutionists, it is clear that such biostratigraphic correlations are not empirically self-evident:‘Stratigraphic correlations, like phylogenetic relationships, must be inferred from data and are not actually observations themselves.’2However, for purposes of an argument, it is acceptable to start with premises accepted by an opponent, even if I don’t accept them myself, and show that they imply a conclusion that undermines the opponent’s position—in logic, this is called reductio ad absurdum. Thus, in this work, I’ll presuppose that the evolutionist’s intercontinental correlations of therapsid fossils as true and valid. The same holds for evolutionary phylogenies and cladograms, as well as the anatomical deductions behind them. Despite granting all these concessions, it soon becomes obvious that many of the anatomicallybased evolutionistic claims, when analyzed, turn out to be questionable.3,4 A more fundamental issue, however, is that evolutionistic claims about transitional character states (however these states are defined) typically centre on a relatively small number of features. These features are pieced together and cited as examples of evolutionary change towards reptiles that are increasingly mammal-like. This claim is made despite the fact that evolutionists are usually not concerned with ancestordescendant relationships, but rather the degree of presumed Reconstruction of gorgonopsid therapsid (after evolutionary relatedness between mammal-like reptiles. Yet, using Stearn & Carroll).42 isolated bits of evidence, we could construct just about any progression we wanted. We could, for instance, arrange a sequence of spoons to show a progression in size, thickness, etc. And this would be all the more questionable if only partsof the spoons were considered (e.g. the spoons arranged to show a trend towards greater bowl size while the handles showed no trend at all).Clearly, a comprehensive approach is needed. All the anatomical features must be considered, not just a few. Accordingly, this work evaluates the claim that mammal-like reptiles, as arranged in succession by evolutionists (from pelycosaurs to mammals), show an essentially unbroken chain of progressively more mammal-like fossils. We examine large numbers of inferred morphological changes, simultaneously considering literally hundreds of characters that have been used by evolutionists in the construction of cladograms
(branching patterns showing alleged degrees of evolutionary relatedness of one form to another). Even though cladograms are not intended to identify ancestor-descendant relationships, each node (branching point) in the cladogram is taken by evolutionists to be, more or less, morphologically intermediate between the previous node and the successive one. How to evaluate numerous presumed evolutionary changes To keep track of hundreds of anatomical changes, and analyze these changes semi-quantitatively, requires a method of scoring the extent of each change, and tabulating the total number of changes. One way would be to sum the character polarities that evolutionists use to construct their own cladograms. 5 To briefly demonstrate the methodology used in the present study, I have arranged seven hypothetical organisms in a series (Figure 1), to indicate evolution from (A) to (G). This series can be viewed either in the traditional ancestor-descendant sense or in a cladistic sense. Cladistically, evolutionists would consider ‘organism’ (A) to represent the least derived (earliest evolved) state and (G) the most derived (most recently evolved), but without any necessary connotation of immediate ancestor-descendant relationships. Figure 1. Seven hypothetical organisms arranged in a series to indicate evolution from (A) to (G). The general stratigraphic succession of (A) through (G) is accepted as a given. In the traditional evolutionary sense, this series can be viewed as an ancestor-descendent relationship with (A) the ancestor of all other 'organisms'. Cladistically, (A) would be the least derived (earliest evolved) and (G) the most derived (most recently evolved). Of the five morphological traits shown, three are progressive (cap-morph, X-morph). Two are gradational (circle-morph, Xmorph) while the others have a polar nature, being either present or absent.Consider how progressive traits would be scored. Progressive traits proceed unidirectionally through the sequence that the evolutionists have constructed. Note that ‘organisms’ (A) through (D) don’t have the ‘cap-morph’ trait, but ‘organisms’ (E) through (G) do. This trait is a ‘presence-absence’ (zero-one) polarity trait, and can be scored as (0000111) in the sequence of seven ‘organisms’. In like manner, the ‘triangle-morph’ can be scored as (0000001), since it only appears in the most derived ‘organism’. The progressive ‘circle-morphs’, by contrast, are also gradational, increasing from zero to three circles per ‘organism’. This ‘evolutionary trend’ can be scored as (0011233).Look at what I call reversing traits: ones that change direction at least once in the accepted evolutionary sequence. For instance, note that the ‘bar-morph’ first appears in (C) and continues in (D), only to disappear in (E). It then makes an ‘evolutionary reappearance’ in (F) and persists in (G). This reversing trait can be scored as (0011011). As a final example, a reversing yet gradational trait is provided by the ‘X-morph’, which can be scored as (0102212).We can quantify the overall changes from (A) through (G) by summing the character polarities of all the traits. The sum is (0124568). However, this sum distorts the picture of the changes, because the reversing traits make the overall change appear much smoother (transition-filled) than it really is. If we only sum the progressive character polarities, a much less gradational chain is obtained (0011345). Thus, to circumvent the bias created by mingling numerous reversing traits with progressive traits, I omit the reversing traits entirely in Table 1. Where reversing traits are relatively few in number (Tables 2 and 3), I sum all the traits in one list, and only the progressive traits in another.To what extent could the hypothetical evolutionary progression from (A) through (G), as shown in Figure 1, support the evolutionary claim about ‘transitional forms’? Obviously, it depends not only on how the polarities are summed, as discussed previously, but also on which particular polarities are emphasized. The ‘circle-morph’ shows the most incrementally-filled progression of traits (0011233), and could be argued to support an evolutionary scenario. By contrast, the ‘cap-morph’ and ‘triangle-morph’ appear as sudden jumps without any gradual ‘evolutionary’ development. And the reversing characters, which go from ‘primitive’ to ‘derived’ and back to ‘primitive’ again, cannot be said to constitute an evolutionary trend by any stretch of the imagination. As we shall see, these same principles that apply to the hypothetical organisms in Figure 1 also apply to actual fossils of mammal-like reptiles, and the evolutionistic claims about their supposed series of ‘intermediate stages’ culminating in mammals.However, when analyzing character polarities in actual fossils, a few cautions are in order. To begin with, as discussed elsewhere, 6 genera of mammal-like reptiles are inflated by taxonomic oversplitting, a fact that is substantiated by more recent studies.7,8 Another concern lies in the way that changes in anatomical characters are scored. This can always be done, deliberately or subconsciously, in a way which favours the desired evolutionary outcome:‘By oversplitting apomorphies9 in its favor, one hypothesis can dominate over its rival without gaining any biological insight. One way to guard against this fallacy is to show how the apomorphies in support of a given hypothesis are biologically associated.’10Of course, the phrase ‘biologically associated’ smacks of evolutionistic just-so stories. However, in this study, I do not attempt to make any anatomical judgments, but rely on datasets provided by evolutionists. In this way, the negative conclusions regarding evolution become all the more compelling. Sources and types of data One way to limit the extent of potential biases in choice of apomorphies, 9 etc., is to use information from different authors, because each author has analyzed a largely-different set of anatomical characters. Accordingly, I employed three recentlypublished datasets for this comprehensive analysis as summarized in Tables 1, 2 and 3. To clarify the relationships between the members in each dataset, I have, as shown in all of the tables, assigned an identification number to each taxon.11 I have also used descriptive phrases for each entry in each table. 12 Although the use of these descriptors here is informal, they approximate those used by Kemp.13 Adjectives such as ‘primitive’, ‘medial’ and ‘advanced’ (or ‘derived’) are used solely to follow the evolutionists in orienting the particular taxon relative to the mammalian condition, and are not intended to have any other connotation.14 They are definitely not intended to endorse any notions of succession of mammal-like reptiles through time, relative evolutionary relatedness of mammal-like reptiles, lineages of mammal-like reptiles or ancestordescendant relationships.The first of the three datasets used in this study, by Sidor and Hopson, 15 is essentially a broad overview of the entire sequence, starting with pelycosaurs and culminating in mammals. Because, as noted earlier, large numbers of reversing characters tend to confound the overall scoring of trends in the acquisition of mammalian characters, I have excluded these 77 reversing characters. More on this later. The relevant part of the data is summarized in Table 1,16 and consists of 88 anatomical characters. 17 Not all of the taxons, however, have data available for all of the 88 useable characters. For this reason, all of the entries in Table 1 are each normalised by taking the sum of character polarities divided by the number of available characters, and then multiplying the quotient by 100.18 This is what I call the Mammalness Index in Tables 1–3. Overall skeletal characters ID Number
Description
Taxon
Mammalness Index Progressive Characters 88 of 165 useable characters from 181 total characters
1
primitive pelycosaurs
Ophiacondontidae
5
2
advanced pelycosaurs
Edaphosauridae
0
3
primitive sphenacodont
Haptodu
1
4
overall sphenacodont
Sphenacodontidae
3
5
primitive therapsids
Biarmosuchia
29
6
primitive therapsids
Anteosauridae
32
7
primitive therapsids
Estemmenosuchidae
32
8
varied therapsids
Anomodonti
33
9
primitive therapsids
Gorgonopsidae
43
10
advanced therapsids
Therocephalia
52
11
primitive cynodont
Dvinia
80
12
primitive cynodont
Procynosuchus
81
13
medial cynodont
Galesauridae
85
14
varied cynodont
Thrinaxodon
87
15
advanced cynodonts
Cynognathia
82
16
advanced cynodont
Probelesodon
101
17
advanced cynodont
Probainognathus
102
21
sister-group candidates
Trithelodontidae
109
26
mammals
Morganucodontidae
120
Table 1. Mammalness Index for mammal-like reptiles calculated from overall skeletal characters from Sidor and Hopson.15 The ID number approximates the relative position each taxon would have on one comprehensive cladogram (including all three Tables 1-3).11Descriptions approximate Kemp13 and reflect evolutionary notions of the mammalian condition. The descriptions are not intended to endorse these evolutionary notions. The second database used (Table 2) is much more restricted in its anatomical scope, being confined to the presumed evolutionary changes in the quadrate bone. In fact, much of the discussion about mammal-like reptiles as presumed transitional forms centres on the alleged evolution of the mandibular-auditory system. Luo and Crompton 19 have evaluated 14 characters relative to the quadrate bone in the reptilian jaw evolving into the eventual mammalian incus (one of the tiny bones in the ear). This data is summarized in Table 2. Because there are only 14 traits, exclusion of the reversing traits, as in Table 1, would have left only a few traits to consider. On the other hand, simply amalgamating the progressive and reversing characters for the sake of a larger database would have created bias in the data.20 As a compromise, both potential biases were set at cross-purposes towards each other by creating two separate columns in Table 2. These reflect the distinction I have made between all 14 traits (first column), and the five consistently progressive traits21 (second column). The small number of characters also necessitates a different approach, from that used in Table 1, in computing the Mammalness Index. Because there are only 14 traits, if one were to, as before, compute the relevant quotient and then multiply it by 100, it would cause serious distortion of the data.22 For this reason, the Mammalness Index in Table 2 is simply the sum of character polarities for each taxon. Quadrate skeletal characters Mammalness Index All Progressive Characters (5 of 14)
ID Number
Description
Taxon
Mammalness Index Characters (14)
8
varied therapsids
Anomodontia
2
0
9
primitive therapsids
Gorgonopsid
6
0
10
advanced therapsids
Therocephalia
3
0
12
primitive cynodont
Procynosuchus
1
0
14
varied cynodont
Thrinaxodon
5
3
17
advanced cynodont
Probainognathu
15
5
19
advanced cynodont
Massetognathus
13
9
20
sister-group candidates
Tritylodontidae
20
9
21
sister-group candidates
Trithelodontidae
21
12
26
mammals
Morganucodontida
25
13
Table 2. Mammalness index for mammal-like reptiles calculated from quadrate skeletal characters from Luo and Crompton.19 ID numbers and descriptions are explained in Table 1. The third database (Table 3), like the first database, is relatively comprehensive, compared with the second database. Table 1 can be pictured as a broad overview of the entire chain of mammal-like reptiles, while Table 3 resembles a detailed closeup of the latter part of the chain. The third database is intermediate in size between the first and second. 23 In Table 3, therefore, the progressive and reversing characters are treated the same as in Table 2, whereas the Mammalness Index is computed the same as in Table 1. The data in Table 3 also overcomes the limitations of the data in Table 1, which neglected ‘early mammals’ other than Morganucodontidae from consideration (as this would have largely limited the characters in Table 1 to those of the dentition24). In fact, Luo10 deliberately focused his analysis on cranial and dental characteristics. Luo’s analysis is more of a detailed view of the latter part of the ‘evolutionary’ chain, and as such, complements Table 1. Dental and cranial characters ID Number
Description
Taxon
Mammalness Index Characters (81 of 82)
Mammalness All Index Progressive Characters (53 of 81 of 82)
14
varied cynodont
Thrinaxodon
0
0
17
advanced cynodont
Probainognathus
18
7
18
advanced cynodont
Diademodontidae
19
7
19
advanced cynodont
Traversodontidae
35
7
20
sister-group candidates
Tritylodontidae
78
34
21
sister-group candidates
Trithelodontidae
58
54
22
mammal
Sinoconodon
100
104
23
mammal
Haldanodon
131
120
24
mammal
Triconodontidae
139
131
25
mammal
Dinnetherium
134
126
26
mammal
Morganucodon
132
128
27
mammal
Megazostrodon
117
122
Table 3. Mammalness index for mammal-like reptiles calculated from dental and cranial characters from Luo. 10 ID numbers and descriptions are explained in Table 1. Reversing traits are the rule among mammal-like reptiles As discussed earlier, I have made every concession to the evolutionist. I have not disputed the validity of intercontinental biostratigraphic correlation, the temporal succession of mammal-like reptiles, the objectivity of anatomical analyses, the fact that cladograms are not intended to identify ancestor-descendant relationships, etc. Despite all these concessions, the evidence, taken as a whole, fails to conform to all the evolutionary ‘ballyhoo’ surrounding the mammal-like reptiles. One of the most striking findings uncovered by this analysis is that the majority of anatomical traits (the ones actually used by evolutionists in the construction of their cladograms) do not show a unidirectional progression towards the mammalian condition! Of the 181 anatomical characters considered by Sidor and Hopson, 165 were deemed to be sufficiently complete, in terms of data, for further consideration in the present study 25 (Table 1). Of these 165, 88 were found to be progressive. In
stark contrast, no fewer than 77 of the 165 showed reversals of character. 26 This is not an isolated instance. As noted earlier, 9 of the 14 quadrate characters used by Luo and Crompton were likewise reversing (Table 2). Finally, in the analysis of 82 mostly dental and cranial characters, by Luo (Table 3), no fewer than 53 characters were found to be reversing. 27The abundance of reversing traits means that the mammal-like reptiles cannot, by any stretch of the imagination, be portrayed as some sort of quasi-lineage (even a crude one) culminating in mammals. (Nor, for that matter, can individual mammal-like reptilian genera be placed in a lineage. According to Kemp, 28 few extinct vertebrates are sufficiently unspecialized, in terms of morphology, to be the direct ancestors of other vertebrates).Furthermore, the proliferation of reversing traits makes it difficult for evolutionists to decide which mammal-like reptiles, and inferred early mammals, are, evolutionarily speaking, closest to each other. This confusion is reflected in the construction of widely-contradictory cladograms. 29 To illustrate this, I now use a system of brackets to illustrate two of the four mutually-contradictory sets of evolutionistic nested hierarchies relative to the taxons numbered in Table 2. They are: 8—[(9—10)—<12—|14—{17—19—20—(21—26)}|>] versus 9—/8—!10—[12—<14—|17—19—21—(20—26)|>]!/ The large number of reversing traits also takes to task the evolutionistic claim about stratomorphic intermediates. To begin with, stratomorphic intermediates have validity only if one can legitimately infer ancestor-descendant relationships. This is not true of mammal-like reptiles, as noted earlier. Can it be said, in the context of mammal-like reptiles, that a less mammallike genus will inevitably be situated stratigraphically below a more mammal-like one? Apart from the fact that this argument takes the biostratigraphic correlation of mammal-like reptiles at face value (as I have done for purposes of this study), any such notion is soundly contradicted by the numerous reversing traits uncovered by this analysis. It is sobering to realize that a given mammalian trait can appear, disappear, and then freely reappear anywherethroughout the entire evolutionaryconstructed sequence of mammal-like reptiles. As a result, if all of the mammalian traits are considered together, it becomes obvious that any ‘stratomorphic’ sequence of mammalian traits as a whole is crude at best. Mechanisms related to the Flood should have no difficulty generating a sequence of organisms that happens to show a crude stratomorphic progression of mammalian traits interspersed with numerous other traits showing no progression at all (that is, the reversing traits).Of course, evolutionists have a series of stock rationalizations to cope with reversing traits. They can, for instance, allow for some traits to actually reverse themselves during the course of supposed evolution. But this makes their whole argument internally inconsistent: we are asked to believe that the ‘progressively-appearing’ mammalian traits constitute powerful evidence for evolution, while the more numerousreversing mammalian traits do not mean anything. Heads I win, tails you lose. And, owing to the fact that cladograms are not presumed to identify ancestor-descendant relationships, the evolutionists can always pigeonhole any reversing trait as a ‘specialization’ in that particular mammal-like genus.25 This allows them to ignore contrary evidence and to perpetuate their illusion of a generalized ‘chain’ of mammal-like reptiles that becomes progressively more-mammalian. Analysis of discontinuities From Tables 1–3 we see that the traits usually considered unique to mammals are distributed variously throughout the mammal-like reptiles. While this distribution is not haphazard or random, it does not form lineages. We will now see that the remaining gaps between these organisms are not gradualistic.Remember that mammal-like reptiles are not just any group of extinct creatures. They are supposed to be the very showcase of step-by-step, transition-filled evolutionary change. On this basis alone, the mammal-like reptiles should be subject to the strictest standards for evaluating alleged gradational evolutionary changes. Thus, the significance of morphological discontinuities becomes magnified. Second, as noted earlier, whatever step-by-step changes to the mammalian condition do exist, these come only at the cost of having to discard large numbers of anatomical traits because they are reversing—i.e. appearing, disappearing and reappearing in the chain. If, despite such treatment, the discontinuities can be shown to be significant in those relatively few traits which are unmistakably progressive to the mammalian condition, the credibility of mammal-like reptiles as genuine evolutionary transitions becomes all the more doubtful.Third, and most important of all, the magnitude of any discontinuities must be addressed. Are they large or small? To answer this question, we must compare the size of each discontinuity with the range of anatomical information available from known fossils.30 Using the same methodology employed to score inferred morphological changes throughout the presumed evolution of mammal-like reptiles, one can place the discontinuities into a semi-quantitative perspective. Consider the most comprehensive sequence of mammal-like reptiles (Table 1). We can see the precipitous gap between the pre-therapsids (0–5) and therapsids (29–52). From the vantage point of the Mammalness Index of 120 for the listed inferred first mammals (the Morganucudontidae), the mammal-like traits in pelycosaurs and sphenacodonts are trivial in magnitude. This gap is all the more extreme because pelycosaurs and therapsids are each large, internally-diverse groups.This is only the beginning. It is eye opening to realize that the discontinuity between the therapsids (29-52) and cynodonts (80–109), at 28 points, is greater than the entire range of mammal-like traits within the evolution of the therapsids themselves, the latter of which amounts to 23 points! The gap within cynodonts (80–87 vs. 101– 109), while not as extreme, is nevertheless appreciable, and, at 14 points, is greater than both the ranges of the antecedents (7 points) and successors (8 points). Those with a strong background in vertebrate anatomy may want to consult the original sources and examine how the anatomical technicalities (here just summarized as numbered traits) fail to resemble anything like a gradational appearance of mammalian traits in the evolutionistic-constructed ‘chain’ of mammal-like reptiles.When the appropriate anatomical details of the middle part of the chain of mammal-like reptiles is analyzed, we find that the non-transitions grow in size. Consider all the characters relative to part of the inferred aural-mandibular evolution from mammal-like reptiles to mammals (Table 2). One is struck by the abrupt discontinuities between therapsids and early cynodonts (1–6), on one hand, and the advanced cynodonts (13, 15), on the other (we are, for a moment, excluding the trithelodonts and the tritylodonts). When we consider the latter two, both of which are the possible evolutionary sister groups of the earliest mammals, we observe yet another gap—between them (13, 15) and the inferred earliest mammals (20–25). In both instances, the gap is, once again, larger than the actual range of ‘mammalness’ that both precedes and follows the gap.The foregoing analysis of Table 2 actually understates the magnitude of the gaps because, as noted earlier, it does not consider the ‘smoothing-out’ effects caused by the inclusion of the reversing characters. Consider just the progressive characters in Table 2. Under such conditions, the discontinuities are stark. With the exception of the last member of the chain (the Morganucodontidae), every change in the sequence involves a series of jumps in increments of 2 or (usually) 3, and each such jump is relative to only 13 character points.Probably the most informative analysis of mammal-like reptiles as (alleged) transitional forms is the one which focuses, in detail, on the presumed changes from advanced cynodonts to the earliest mammals (Table 3). The sister-group cynodonts (Tritylodontidae and Trithelodontidae) rival each other for the status of the closest non-mammalian relatives to mammals. Yet, when all of the characters are considered, one is struck by the chasm between these sister-group advanced cynodonts (58 and 78) and the earliest presumed mammals (100–139). However, the ‘bottom falls out’ when only the progressive characters are considered in Table 3. Here, a giant evolutionary leap is required to make the presumed change from fairly advanced cynodonts (7) to the advanced sister-group cynodonts
(34 and 54). From there, another great gulf must be spanned in order to link the sistergroup cynodonts (at 34 and 54) with the earliest mammals (104–131).Thus, the gaps are as large, or larger, than the range of so-called mammalian traits actually present. This makes it difficult to maintain that even a crudely, ever-more-mammalian, quasilineage exists among the mammal-like reptiles. Furthermore, the reversing traits are more common than the gap-filled progressive traits. It is difficult to escape the conclusion that the evolutionistic-constructed pelycosaur-therapsid-mammal chain is little more than a motley group of extinct creatures crudely cobbled together into an Figure 2. Labial view of artificial evolutionary ‘progression’. Just because some ‘mammalian’ traits are present complex multi-cusped molar of in mammal-like reptiles, this does not entail evolution in the slightest. It simply means an extinct Mesozoic that some traits now considered mammalian (by virtue of the fact that they are found crocodilian from Malawi. These only in extinct mammals) once existed in some extinct non-mammals (Figure 2).31 extinct crocodilians are related Regardless of which choice the evolutionist makes for the closest non-mammalian to neither mammal-like reptiles relatives to primitive mammals, he/she must be content with either a rock or a hard nor mammals, and no place: evolutionist would contemplate ‘It is not known which cynodont family was ancestral to mammals, or whether all the these reptiles as ancestral to mammals originated from the same group (family) of cynodonts. In the vast literature mammals in any way. Yet their concerning mammalian origins, it is easier to find suggestions that one or the other dentition shows clear therapsid or cynodont family cannot be ancestral to the Mammalia, rather than to find resemblances to mammalian a positive answer.’32‘Both the tritheledontid-mammal hypothesis and the tritylodontidcheek teeth, and these mammal hypothesis are supported by large numbers of apomorphies in dentition, crocodilians also contain cranium and postcranial skeleton. Yet both are also contradicted by a substantial another mammalian trait—a amount of anatomical evidence.’33And, ironic to the fallacious argument about secondary palate (from mammalian traits appearing in correct ‘stratomorphic’ sequence,34 we have a situation Melhert).41 where one of the presumed sister groups (Tritylodontidae) is actually more mammalian than the first recognized mammals! Consider the following unenviable dilemma faced by evolutionists: ‘The main difficulty with the tritylodontid-mammal hypothesis is that too many apomorphic features of tritylodontids are more derived than the corresponding features in primitive mammals such asSinoconodon and Adelobasileus ... . By contrast, the main weakness of the trithelodontid-mammal hypothesis is that far too many trithelodontid characters are primitive ... [emphasis added].’35‘Primitive’ and ‘derived’, of course, are in comparison with the presumed earliest mammals, though neither the trithelodonts nor the tritylodonts are capable of being connected to the inferred earliest mammals in an ancestordescendant lineage. Table 3 shows that a near doubling of characters (in fact, tripling if Tritheledontidae is chosen as the sister-group) is necessary to bridge the chasm between the sister-group cynodonts and the inferred primitive mammals. For evolutionists who portray the sister-group cynodonts as ‘almost mammals’, this is a sobering result.Several creationist scholars have pointed out the lack of evidence for gradational change in the mandibular-auditory mechanism of the ‘advanced’ mammal-like reptiles towards that of the presumed early mammals. Interestingly, a few evolutionists have actually acknowledged this fact in print:‘Intermediate stages in the transference of postdentary elements to the cranium are poorly documented. Indeed, the only fossil evidence on this critical interval is the presence of persistent attachment sites for the anterior end of the postdentary unit in the primitive theriansAmphitherium and Peramus.’36Finally, owing to the fact that the ‘mammalian traits’ do not, by any stretch of the imagination, occur in a nested hierarchy in the mammal-like reptiles, evolutionists must blame this state of affairs on convergence. In this regard, the mammal-like reptiles are hardly alone among fossil vertebrates:‘The distribution of primitive and derived characters differs from lineage to lineage, showing that many features were evolved or lost convergently. As in the case of other major transitions in vertebrates, such as the origin of birds and mammals, the convergent origin of derived features makes it difficult to establish specific relationships, or to agree on objective criteria to differentiate tetrapods from their fish ancestors.’37 Conclusions Mammal-like reptiles may indeed qualify as the very best examples of transitional evolutionary change that evolutionary theory has to offer from the fossil record. This only shows the barrenness and intellectual poverty of macroevolution. When all of the characters used for the conventional constructions of cladograms are considered, the majority of mammal-like reptile characters do not consistently progress towards the mammalian condition. Instead, within the ‘evolutionary’ chain of mammal-like reptiles, there are many ‘reversals’ away from mammalian characteristics.The use of mammal-like reptiles as an argument for ‘transitional change’ (however one strictly defines it) rests upon special pleading (like everything else in evolutionary theory). So let us permit the evolutionist special pleading and pretend that the large numbers of reversing traits don’t exist, so that the argument can be based solely on the progressive characters. Even this does not let the evolutionist off the hook. To the contrary, the chain of mammal-like reptiles, when examined closely and with attention to many (instead of just a selected few) anatomical characters is full of major discontinuities. And very many of these discontinuities are as large, if not larger, than the ranges of characters which both precede and follow them. Therefore, the oft-repeated evolutionistic claim about mammal-like reptiles showing a series of intermediate stages to the mammalian condition is, at best, an exaggeration.Could not the evolutionists argue that, as more fossils are discovered, the gaps will close? Perhaps. At least they have been trying to do so since the days of Darwin, but with little success, despite a vastly larger known fossil record. Remember that, as shown elsewhere, 38 new fossil finds can just as easily accentuate the gaps as reduce or close them. Consider three new genera that have been described in the 1980s and 1990s: Sinoconodon, Adelobasileus and Haldanodon. As noted earlier, not enough is preserved of Adelobasileus to include it in Tables 1–3. When it comes to Sinoconodon, its existence does narrow the gap in Table 3 that would otherwise exist without it, but not by much in comparison with the gap that remains afterward. Haldanodon, on the other hand, cuts the other way. By virtue of the fact that its characters fall within the range for previously-known primitive mammals, its very discovery actually reinforces the gap between cynodonts and mammals.What if mammal-like reptiles never existed? Would evolutionary theory be crippled? Certainly not. Evolutionary theory is so plastic that anyseries of observations in the natural world could be cited in its favour! If anyone thinks that this is an overstatement, consider the following:‘Indeed, it was a fossil found in the Karoo in 1838—the skull of a mammal-like reptile with two large tusk-like teeth in its upper jaw—that first convinced the scientific establishment that mammals had evolved from reptiles, not directly from amphibians.’ 39‘T. H. Huxley (1880), for instance, proposed that amphibians gave rise to mammals. This conclusion was based on aortic arch patterns, heart morphology and features of the pelvis. Subsequent workers rejected Huxley’s ideas when theriodont pelvises, which were not known to Huxley, were found to be intermediate in structure between the pelvises of amphibians and mammals.’40 Clearly, the ruling evolutionary paradigm existed before the discovery of mammal-like reptiles, and would have flourished had these reptiles never been discovered. In that event, today’s evolutionists would be extolling some
extinct amphibian group as the transitions (or stratomorphic intermediates) leading up to mammals. Cladograms would be constructed to show the close branching pattern between that chosen group of amphibians and mammals.All else would fall in place according to the dictates of evolutionary dogma. The evolutionist triumphalists would be telling everyone that evolution is fact because of the many obvious similarities between the ‘ancestral’ amphibians and the ‘descendant’ mammals. Leading humanist scientists would inform us that anyone who questions the amphibian-mammalian transition cannot possibly be a scientist, no matter his degrees or publications. And, of course, the secularist fanatics would whip up considerable hysteria about the fact that the questioning of the amphibian–mammalian transition is a dangerous threat to the very survival of science and reason, and that, if not quickly reversed, it will soon return us to the Dark Ages. Walking whales, nested hierarchies, and chimeras: do they exist? by John Woodmorappe Summary Recent claims about ‘terrestrial’ whales are examined and refuted. The trends cited in whale evolution are rather superficial in nature, and little different from those that become apparent by lining up wheeled vehicles within a cladogram. A close examination of whale evolution in general, and whale-ear evolution in particular, demonstrates that most anatomical traits do not change in a consistent whale-like direction. Recently discovered pakicetids consist of cetacean ‘modules’ within otherwise non-cetacean bodies. These extinct creatures are examples of chimeric creatures. The cetaceans, mesonychids, and artiodactyls share a number of anatomical traits in a pattern that is inconsistent with any type of evolutionary nested hierarchy, and this argues strongly for the special creation of all these creatures. In Greek mythology, the Chimera was an animal whose body consisted of anatomical modules (part-goat, part-snake, and part lion) (Figure 1).1 Another familiar chimera is the mermaid.2 Evolutionists tell us that chimeric creatures do not exist because an extremely improbable set of circumstances 3 would have to take place in order to make their existence a reality. Therefore, organisms supposedly evolve as slightly modified versions of their ancestors, and thus culminate in a nested hierarchy of all living things. It is at this point that some evolutionists take a big leap. They speculate that an Intelligent Designer, repeatedly using the same bauplan (construction plan) while creating different forms of life, should create living things by assorting at least some of the modular units. This would result in truly chimeric animals, thereby preventing any sort of classification of living things according to a nested hierarchy. The nonexistence of chimeric creatures is supposed to favor organic evolution over Special Creation. Let us examine these premises. Figure 1. The Chimera according to Greek mythology: part goat, part lion, and part snake. Implications of chimeric creatures To begin with, the notion that the created living things should contain chimeric modules (assemblages of morphologies) 4 While we cannot know the motives behind the creation, we can easily see that extensive deployments of chimeric structures do not necessarily follow from intelligent design. This can be seen from all of the devices which man, the intelligent designer, has built, in which extensive usage of chimeric structures is uncommon.5 Finally, it takes little imagination to arrange manmade devices and machines into a nested hierarchy.6 What qualifies as a chimeric creature? The very existence of chimeric creatures depends upon its definition. Whereas chimeras involving entire half-body modules, such the humanmodule/fish-module of the mermaid, have not been discovered, less pronounced examples of mosaic creatures do exist, and do so in large numbers. Every time we hear the word ‘convergence’ in ‘evolspeak’, in reference to some anatomical attribute, we are actually hearing about a chimeric creature that has violated, to some degree, an evolutionary nested hierarchy.‘But’, evolutionists commonly say, ‘while individual traits, or small groups of traits can re-appear on an occasional and sporadic basis in different evolutionary lineages, it is inconceivable that a related series of numerous traits (i.e. a module) could reappear in a concerted manner, at least to an extent sufficient to cause the development of incorrect phylogenies.’Oh no? Consider the microorganisms, in which there is such a chimeric overlap of essential genomic components among and between the Bacteria, Eukarya, and Archaea, that an extensive ancient set of genetic exchanges is postulated. 7 Among marine invertebrates, the extinct cephalopods show such a bewildering assortment of chimeric conch morphologies that it is often difficult to distinguish presumed shared ancestry from convergence. 8 What’s more, these real-life chimeras also make it difficult to classify cephalopods according to higher taxonomic categories.When convergence of traits is extensive, we often hear evolutionists speak of ‘the mosaic nature of evolution’. As an example of this, the mammal-like reptiles are much more chimeric than ‘transitional’ creatures.9 Rather than a progression to ‘mammalness’, we observe an assortment of unmistakable reptilian traits and unmistakable mammalian traits.Let us now consider an example of chimeric creatures among land mammals. Hystricomorphy, a unique muskoskeletal pattern involving the jaw, enables the mouth to be opened in a large gape. Hystricomorphy is characteristic of the hystricomorph rodents, but has also now been found in the extinct saber-toothed Barbourofelis. Although it is believed that a highly-detailed phylogenetic analysis should spot the independent acquisition of the two complexes of traits, it is acknowledged that supposedly-unique character complexes could arise through convergence and ‘fool’ the evolutionist into believing that they had arisen from common ancestry.10
Figure 2. A generalized pedigree of supposed whale evolution. While not strictly indicative of inferred ancestordescendant relationships, each of the fossil organisms is supposed to be a ‘signpost’ indicative of the progressive appearance of ‘whaleness’. The nature of alleged transitional forms Two recently described pakicetids, Ichthyolestes pinfoldi and Pakicetus attocki11 (Figure 212) are supposedly transitional to true cetaceans.13Ironically, were this true, it would only support the common scientific-creationist contention about the rarity of ‘transitional forms’:‘Thewissen et al.’s discovery of these terrestrial cetaceans is one of the most important events in the past century of vertebrate palaeontology. Only a very few fossils, such as these, reveal a link between two groups of vertebrates that are hugely different in terms of evolution … . But the new fossils superbly document the link between modern whales and their land-based forebears, and should take their place among other famous “intermediates”, such as the most primitive bird, Archaeopteryx, and the early hominid Australopithecus(emphasis added).’14That (half-convincing) evolutionary transitional forms number a mere handful only repeats what creationist scientists (for example, Duane T. Gish15) have been saying for decades, and squarely refutes the anti-creationists who adamantly insist that transitional forms are common.Let us analyze what usually passes for ‘transitions’ in discussions surrounding the evolution of whales. To illustrate this, I have constructed a mock character-trait matrix (Table 1), and thence a cladogram (Figure 3) to show the gradual ‘evolution’ of a unicycle into an 18-wheeled truck.16 Note that the apparent progression seems, at first, to be somewhat convincing.17 However, a closer look reveals that the ‘step-by-step’ transition-filled progression is actually quite superficial,18 as it is full of discontinuities. (The pointing out of discontinuities is sometimes dismissed as an exercise in futility: of having two gaps whereas before there was one. As elaborated elsewhere, 19 however, it is themagnitude of the gap or gaps which is/are important and not the number(s) of alleged gap-filling organisms!) Even more serious is what is notpresented in the character matrix (Table 1) or cladogram (Figure 3)—namely specializations, 20 and the outright reversal of traits.21 The latter are very much part of the unmentioned story of ‘whale evolution’, as described below. Heavy Light truckAutomobile 3-wheel motorcycle2-wheel motorcycleBicycle Unicycle truck Horn 1 1 1 1 1 1 0 Manual steering 1 1 1 1 1 1 0 Multiple wheels 1 1 1 1 1 1 0 3 ln number wheels 9 7 4 3 2 2 0 Thick tyres 1 1 1 1 1 0 0 Motorization 1 1 1 1 1 0 0 Self stability 1 1 1 1 0 0 0 Backrest seating 1 1 1 1 0 0 0 Ln cargo capacity 5 3 1 0 0 0 0 Enclosed cabin 1 1 1 0 0 0 0 Steering wheel 1 1 1 0 0 0 0 Upward exhaust 1 1 0 0 0 0 0 Double wheels 1 1 0 0 0 0 0 Interior partition 1 1 0 0 0 0 0 Detachable units 1 0 0 0 0 0 0 Table 1. Mock character-trait matrix of wheeled vehicles. Most traits are polarized: 0-Absent and 1-Present. The number of wheels is indicated by three times the natural logarithm of the actual number of wheels, rounded off to the nearest whole number. The cargo space is denoted by the ratios of natural logarithms of the cargo volume relative to that of the automobile, based on a guesstimate. Do ‘fossil whales’ generate a chain of transitional forms? Earlier claims of ‘transitional fossil whales’ had been found wanting. 22 A recent National Geographic article23 calls the reader’s attention to a number of supposed trends24 in cetacean evolution. These are towards: 1) Greater aquatic specialization,25 2) Underwater hearing,26 3) Reductions in size of the hindlimbs,27 and 4) Migration of the nares (nostrils) towards the posterior of the skull’s dorsal (upper) surface.28 The alleged trend towards underwater hearing merits some attention, and is discussed in some detail below.The remaining three trends fail immediately because they are superficial in nature, and are not corroborated by detailed anatomical analyses, as elaborated below. Moroever, a close look at the relative positions of the nares in the skulls of just the five protocetid genera 29 while showing a slight trend towards more posterior placement with supposed time, also reveals the fact that this meager trend is completely overshadowed by the considerable differences in cranial geometry between the five genera. On this basis, any ‘trend’ towards increasingly posterior placement of the nares within protocetids, let alone within the entire Order Cetacea, is all but meaningless. It is literally like comparing apples and oranges, and making something out of the fact that one can arrange these fruits into a sequence showing progressively larger pores. The three-member ‘Nasal Drift’ sequence 28 in the National Geographic article is, in my opinion, disingenuous to the point of bordering on intellectual dishonesty—doubly so in view of the fact that most readers of that magazine are unsuspecting laypersons.
Figure 3. A mock cladogram of wheeled vehicles, showing ‘transitional’ changes leading to the ‘evolutionary’ emergence of 18-wheeled trucks. Using this as an analogy, but adhering to evolutionistic reasoning, the pakicetids are walking whales in the same way that unicycles are primitive trucks. The remaining trends are little better. The progressive reduction of hindlimbs is of dubious significance, if only because of the wide range of hindlimb sizes in the creatures involved. Moreover, modern whales sometimes sprout ‘hindlimbs’ of appreciable size (larger than those of ‘ancestors’, and thereby contrary to the trend in hindlimb reduction). Finally, even greatly reduced hindlimbs lack any necessary evolutionary connotation.30Let us now consider the forelimbs. Although different cladograms contradict each other, they are unanimous in grouping Pakicetus with Ambulocetus as sister groups.31 One can therefore appreciate the ironic fact that, in terms of forelimb anatomy, there is no actual trend but, to the contrary, a sharp discontinuity between the pakicetids and the ‘next successively-more cetacean-like creatures’, the ambulocetids (Figure 2):‘Ambulocetus probably swam using its hind limbs as the main propulsor, and its robust feet may be an adaptation for forcefully displacing water during swimming. Pakicetids, on the other hand, had the slender metapodials of running animals.’ 32The National Geographic conspicuously fails to mention this sharp discontinuity in its slick portrayal of the ‘Back to the Sea’ parade 25 of creatures. This only aggravates the borderline-deceptive practice of picturing both Pakicetus andAmbulocetus as having more aquatic-adapted appendages (fin-like legs, etc.) than could possibly be justified by fossil evidence. 33 To top it all off, the leading researcher in whale evolution, as quoted in National Geographic, engages in a crass misrepresentation of scientific creationists.34It is not only the limbs, but also the tail, which supposedly underwent extensive modifications in order to convert a terrestrial creature into an aquatic one. Entirely omitted in the National Geographic article is the fact that, owing partly to preservation problems, there is a lack of intermediates between tails and flukes:‘Despite recent discoveries of early cetaceans, such as Pakicetus, Ambulocetus, and Rodhocetus, there still remains a paucity of tangible physical evidence on the evolution of the flukes. Tail vertebrae in these fossils are lacking or incomplete, especially for the most terminal portions. To this add that (1) modern cetacean species exhibit the highly derived thunniform swimming mode and design, (2) no series of intermediate fluke designs exist, and (3) they are phylogenetically disjunct from their closest living relative (i.e., ungulates), which have specialized for terrestrial locomotion; thus little direct information is available to answer the evolutionary questions regarding the transition to flukes.’35We would never actually consider the bicycle as ancestral to the motor vehicles (Table 1, Figure 3) in spite of its ‘structurally intermediate’ character between the unicycle and the automobile. Why not free ourselves from the mental boxes of evolutionary thinking and give living things the same benefit? Note that, in contrast to the locomotion of the terrestrial pakicetids, that of the ambulocetids and rodhocetids is described as resembling the locomotion of modern sea lions, eared seals, and otters. 36 In fact, these creatures are actually endowed with lutrine (like an otter) and phocid (like a seal) relative limb proportions. 37 Why then not view these extinct creatures as little more than ecological counterparts of extant seals, otters, etc., and forget all of the evolutionary tales that have them transformed to whales? Are pakicetids transitional forms? To what extent are pakicetids intermediate in structure between the ‘generic’ artiodactyls on one hand and true cetaceans on the other? Gingerich38 has surveyed changes in four anatomical features (body mass, tooth length, bullar length, and femur length), over the supposed time interval of 37–50 million years ago, for fossil mammals which include six of the reputed cetacean genera39 shown here in Figure 2. With the exception of the inferred change in femur length (especially when body sizes are normalized), none of the remaining three features show even a self-consistent, unidirectional change with time! 40 What about the recently described pakicetid genera?11 The vast majority of the skeletal traits found in the complete skeletons are consistently unlike those of true cetaceans (ancient or modern). By no stretch of the imagination do we observe anything resembling a gradational trend of changes to true cetaceans:‘Aquatic postcranial adaptations are pronounced in late Eocene basilosaurids and dorudontids, the oldest obligate aquatic cetaceans for which the entire skeleton is known, and therefore can be used to evaluate pakicetid morphology. Aquatic adaptations of basilosaurids and dorudontids include … [nine features are listed]. Pakicetids display none of these features.’ 41As if all this were not enough, the few pakicetid traits once believed unambiguously indicative of an aquatic or semi-aquatic transitional lifestyle, are no longer necessarily considered thus.42 Consequently, the already borderline-deceptive practice33 of sketching Pakicetus as a semiaquatic-adapted creature, in a very recent issue of National Geographic magazine,43 is all the more inexcusable. And it is creationists who are supposed to be the purveyors of inaccurate and outdated information!The editors of National Geographic magazine would do well to communicate, very carefully to their lay audiences, the following sobering facts about the reconstruction of soft parts being unempirical (with very few exceptions), and in fact belief-driven: ‘Traditionally, Ambulocetus, an early cetacean, has been constructed with hair (bottom). As discussed by John Gatesy and Maureen O’Leary on pp. 562–570, hypotheses of phylogeny, however, determine how soft tissues, such as skin, are reconstructed in fossils.Recent cladistic studies suggest Ambulocetus was nearly hairless (top) [emphasis added].’44 Emerging ‘whaleness’: unsupported by anatomical details Up to now, the anatomical changes in the alleged land-animal-to-modern-whale progression have been followed only in response to the cursory and superficial ‘trends’ cited by evolutionists. As was the case with the mammal-like reptiles, 9 what is needed is a comprehensive survey of all of the relevant traits of this supposed transformation. Unfortunately, much data is lacking, making it all but impossible to meaningfully compute the relative numbers of progressive and nonprogressive anatomical traits,45 as had been done for mammal-like reptiles.9It cannot be stressed enough that, from an evolutionary point
of view, organisms situated at the point of trait reversal are chimeras consisting of ‘primitive’ and ‘derived’ features, and they will not fit any nested hierarchy.In spite of the problems with missing data in cetacean evolution, one can arrive at an extremely conservative46 estimate of the relative proportion of non-progressive traits. In order to minimize the possibility of artifacts caused by incomplete information, we can compare severalcladistic analyses by different authors, each of which use different anatomical traits, different outgroups for comparison, and different constituent taxa. Let us consider one analysis47 of basicranial, cranial, dental, postcranial, and live-tissue data (from living cetaceans). I trace the changes in character polarity which take place through all of the organisms listed in Figure 2, with modern whales represented byBaleonoptera and Tursiops. Out of the 123 anatomical characters evaluated by the cited authors, only 33 have data for at least 7 of the 8 taxa, and are considered further. Out of these 33, fully 24% reverse themselves at least once, and are therefore nonprogressive. To show that this is no fluke (pardon the pun), let us now focus on another cladistic analysis, which consists of 67 skeletal traits48 in a comparable range of fossil to modern cetaceans (Figure 2). Although 30% (183 of 603 data points) are missing, an astonishing 31% (21 out of the 67) traits are nonprogressive. He who has an ear, let him hear Let us evaluate, in some detail, the much-discussed evolution of the cetacean ear. It turns out that there is only one (one!) unambiguous bullar synapomorphy linking Pakicetus to the cetaceans, and simultaneously absent in all noncetacean animals.49 What about the numerous other auditory features supposedly involved in cetacean evolution? A detailed analysis of 64 aural and other basicranial traits,50 spanning the entire scope of cetacean evolution (and thus consisting of precetaceans, Archaeocetes, Odontocetes, and Mysticetes), has been performed. In this particular study, only 17% of the 1472 possible data points are missing. Almost half (44%) of the traits are nonprogressive! The situation gets even worse, from the ‘evolutionary progression’ point of view, if we focus our attention primarily on modern whales and their immediate (extinct) relatives. Using one archaeocete cetacean as the outgroup, and omitting one of the 28 traits which has more than half its data missing, one can examine the ‘intermediate stages’ involved. It is sobering to realize that two-thirds (17 of 27) of the traits reverse themselves.51As noted earlier about the National Geographic article, a handful of traits supposedly showing a trend in cetacean-ear evolution had been selectively highlighted. 26 Not mentioned are the large bodies of contrary evidence, consisting of numerous anatomical details that show no consistent trend towards ‘whaleness’. There is a whole suite of features, found in archaeocete whales, which are believed to have become (conveniently) ‘secondarily lost’ (or ‘reversed’) in the Odontocetes and Mysticetes. 52 Keeping in mind the extremely conservative nature of all of the above estimates, it is plain to see that any connotation of ‘cetacean lineage’ (e.g., Figure 2) is totally artificial. The supposedly progressive character of cetacean evolution (aural as well as non-aural) is completely unwarranted. Furthermore, rather than being the crown group of cetacean evolution (Figure 2), the extant mysticete and odontocete whales stand out as chimeras consisting of mostly derived but also many primitive features.Believe it or not, the hoary and long-discredited53 embryonic-recapitulation theory is dusted off and employed by some whale-evolution specialists 54 to infer the supposed fine stages of cetacean ear evolution. The fact that evolutionists feel the need to fall back on the recapitulation theory in order to infer alleged evolutionary changes is itself mute testimony to the fact that detailed structural intermediates illustrative of alleged cetacean aural evolution are lacking. Walking whales or walking chimeras? The pakicetids are an interesting set of chimeric creatures, consisting of an artiodactyl-like ankle and a somewhat truecetacean-like inner ear residing in a body that is otherwise hardly distinguishable from that of a typical extinct land-dwelling artiodactyl!:‘The newly found fossils include several skulls and postcranial bones from two early pakicetid species—which it seems, had the head of a primitive cetacean (as indicated by the ear region) and the body of an artiodactyl. All of the postcranial bones indicate that pakicetids were land mammals, and it is likely that they would have been thought of as some primitive terrestrial artiodactyls if they had been found without their skulls.’ 9The evolutionary ‘successor’ to Pakicetus is hardly better in this regard:‘Ambulocetus is recognized as a whale because of characters of its teeth and skull that it shares with other whales, and demonstrates that derived cetacean cranial characteristics were present in an organism with legs resembling those of modern terrestrial mammals.’ 55While certainly not as dramatic as the would-be discovery of a genuine mermaid, the chimeric structure of the pakicetids and ambulocetids could hardly be described in a more lucid manner. It is difficult to imagine how, by any stretch of the imagination, the pakicetids are supposed to qualify as gap-fillers between the terrestrial artiodactyls and aquatic true cetaceans. The fact that serious evolutionary scholars make such claims 14 only goes on to show the poverty of evidence for evolution, and the concomitant desperate lengths to which evolutionists will go to recruit some extinct creature as a transitional form.The recent finding of certain whale-like (actually seal-like) protocetids56 does nothing significant to close the huge chasm between pakicetids and true cetaceans. With the exception of possessing the artiodactyl-like ‘double-pulleyed’ astralagus (heel), these newly described protocetids are highly specialized, fully aquatic creatures, and not indicative of any compelling ancestral connections to the pakicetids or the ambulocetids.Let us now put ‘cetacean’ features into a broader context. It is hardly surprising that, as more fossils are discovered, our concept of the anatomical diversity of certain groups must expand: certain anatomical traits thought to be unique to particular mammalian orders turn up as chimeric assortments in other orders. Rather than demonstrating evolution, the chimeric cooccurrence of cetacean and non-cetacean features in extinct mammals only shows that certain features thought to be essentially cetacean (because they occur only in modern cetaceans and not in any other extant mammal) are not exclusively cetacean after all. It does not warrant the re-definition of cetaceans to absurd extremes, to encompass all of these chimeras, as is currently done by evolutionists.57 Figure 4. Mesonychians as the sister group of the Cetaceans. The chimeric mammalian orders, and failed nested hierarchy, are subject to either (or both) secondary-loss rationalizations (left), or convergent-evolution rationalizations (right). Cetacean relatives? The chimeric trichotomy Is it the Artiodactyls or is it the Mesonychians 58 that are the closest relatives to the Cetaceans? Until recently, the extinct Order Mesonychia was largely accepted by evolutionists as the sister group of Order Cetacea (Figure 4). A recent
analysis59 has demonstrated that the respective dental complexes of mesonychids and cetaceans stand out in uniting the two groups into a clade. This is supported by a variety of other mesonychid-cetacean synapomorphies. 60When the pakicetids were discovered along with a host of other finds, 61 the artiodactyls began to displace the mesonychids as the closest known relatives of cetaceans (Figure 5). The ‘double-pulleyed’ astralagus now appears to be an unambiguous component of both the pakicetid and protocetid skeletons. This synapomorphy (shared form) links artiodactyls and cetaceans as sister groups, to the exclusion of mesonychians, which do not possess this kind of specialized heel. 11 The three mammalian orders are clearly chimeras. Once again, the evolutionary nested hierarchies have been turned upside down, as chimeric creatures are incompatible with any sort of nested hierarchy, and only create headaches for evolutionists. The evidence places the evolutionist in a particularly unenviable position. Notions of ‘stratomorphic intermediates’ are of no help to him, as the stratigraphic order of fossils themselves does not show a clear-cut preference for one phylogeny over another.62 So which anatomical traits is he to reckon as phylogenetically informative, and which is he to reject and explain away? Having made his arbitrary decision, he is forced to make another one. Which rationalization is he to invoke—the one which supposes ‘backward evolution’ and character loss (Figure 4, left, and Figure 5, left), or the one which imagines that lookalike complex anatomical structures can independently arise in different lineages (Figure 4, right, and Figure 5, right)? How much more parsimonious to recognize an Intelligent Designer who used the same anatomical modulus in otherwisedifferent mammalian orders?Since rationalistic preconceptions won’t, of course, allow the evolutionist to consider the latter possibility, he is forced to stumble along in his imaginations and rationalizations. For some evolutionists, 63,64 the secondary ‘de-volution’ of the specialized artiodactyl heel is considered possible (Figure 4, left). Others 65 speculate that the ‘doublepulleyed’ heel is homoplasic. According to this thinking, the ‘double-pulleyed’ astralagus must have arisen twice independently (convergently) in artiodactyls and mesonychians (Figure 5, right).Conversely, if pakicetids are to be accepted as the closest known relatives of cetaceans, as the ruling paradigm dictates, all of the foregoing rationalizations must be placed in reverse. The evolutionist must now contemplate the ‘reverse evolution’ of artiodactyl teeth back towards a lessderived state (Figure 5, left). A recent study11 actually contemplates this evolutionary flip-flop.Alternatively, the cetacean-like teeth of mesonychians must be the product of convergent evolution (Figure 5, right). The latter rationalization, in fact, is the one that appears widely accepted by evolutionists.11,14,36,66 Such thinking constitutes a revolution of sorts in mammalian paleontology. Prior to the recent turn of events, teeth had been used for construction of mammalian phylogenies, more or less uncritically, for over a century. All this time, dental features had been generally considered too detailed to be capable of being duplicated independently via convergent evolution.66There is yet another set of rationalizations invoked for the conflicting phylogenies shown in Figures 4 and 5. It would have us believe that the most basal cetaceans, artiodactyls, and mesonychians have not been discovered, and these postulated fossils hold the key to our understanding of the correct evolutionary branching order.67 Apart from being ad hoc, this hypothesis is self-defeating because it invokes large gaps in the fossil records of the mammalian orders, and thereby implicitly repudiates the claim that fossil cetaceans qualify as a transition-filled sequence! It invokes nonexistent fossils to resolve problems in known ones. Figure 5. Artiodactyls as the sister group b of the Cetaceans. Although the players are reversed, the evolutionary game is the same: the chimeric mammalian orders, and failed nested hierarchy, are subject to either (or both) secondary-loss rationalizations (left), or convergent-evolution rationalizations (right). Conclusions In answer to the questions posed by the title of this report, the answers are: 1). No, walking whales do not exist. Just because pakicetids have somewhat cetacean-like middle ears and cetartiodactyla-type double-pulleyed heel bones, this does not yet make them whales—unless of course one is willing to entertain the most ludicrously-strained definition of a whale. Perhaps pakicetids are walking whales just as firetrucks are tomatoes on wheels (since both firetrucks and tomatoes are red, and both are filled with water). 2). Owing to widespread so-called evolutionary convergence, a nested hierarchy of living things exists only in part. The more detailed the anatomical analysis, the more the nested hierarchy breaks down. While full-bodied chimeric creatures, such as mermaids and mermen, do not exist, somewhat lesser examples of chimeric creatures, of which pakicetids and mesonychids are notable examples, definitely exist.Whenever evolutionists make assertions about the limits of convergence, they do so on an after-the-fact basis.68 As ever-more-detailed examples of convergence are found, evolutionists are forced to backpedal, thus ‘moving the goalpost’ of conceivable convergence. For a long time, evolutionists had tacitly supposed that detailed convergences of clusters of traits (modules), such as the independent acquisition of cetacean-like teeth in mesonychids and cetaceans (Figure 5, right), were a virtual impossibility. What is there to stop the evolutionists from saying, in case of the discovery of a mermaid-like chimeric creature, that even more pronounced convergence of modular units can occur than previously supposed? Evolutionary theory is so plastic that any observation could be fitted into it. The apparent absence of extremely-chimeric creatures cannot, by any standard of reasoning, be accepted as evidence for evolution. To the contrary, the existence of less-extreme chimeric creatures, notably ‘fossil whales’, argues strongly against a common evolutionary ancestry of living things. ARE EARLY EMBRYOS VERY SIMILAR?DO THEY RECAPITATULATE EVOLUTIONARY HISTORY? The ‘fish gills’ girl by David Catchpoole One of the most exciting things about addressing church congregations on the creation/evolution issue is meeting people afterwards who recount their
own interesting anecdotes on this topic. Recently in Perth, Western Australia, a middle-aged lady approached me and said, ‘Hi, I’m Carol. I’d like you to meet our living fossil. Here she is—our daughter, Leanne. A living fish fossil.’ Carol and Des Burgess, with daughter Leanne—and not a fossil, nor fish, in sight.Seeing my bewilderment, Carol and her husband Des explained that when Leanne was 12 years old, she developed an inflamed abscess in her neck. The surgeon in Perth, Australia, who drained the abscess explained that it was caused by bacteria infecting an area of cartilage in her neck, which he described as ‘leftover pieces of gill’—a legacy of our having evolved from fish ancestors.As the Burgess family emerged from the post-op consultation room, Leanne’s brother David turned to her and said jokingly, ‘See, I always knew you were lower on the evolutionary scale than me.’And when Leanne’s school heard of what happened, her teacher called Leanne ‘the fish girl’—a reference also to Leanne being a school champion swimmer at that time.But Des and Carol had raised their children to have a creation worldview. They had in fact begun subscribing toCreation magazine a couple of years earlier, so they knew that the surgeon’s claims about fish gills were wrong—hence David’s comment to his sister was very much a tongue-in-cheek jibe at the doctor’s ignorance. (Creationmagazine had earlier reported that the ‘fish gills’ story was widely believed and promulgated in medical circles, despite their own textbooks’ plain teaching that this belief is false 1,2 —see No fish for relatives below.) Ernst Haeckel Evangelist for evolution and apostle of deceit by Russell Grigg Known as ‘Darwin’s Bulldog on the Continent’ and ‘the Huxley of Germany’, Ernst Heinrich Philipp August Haeckel is notorious as the scientist who perpetrated fraud upon fraud to promote the theory of evolution.Born at Potsdam, Prussia (now Germany), on February 16, 1834, Haeckel studied medicine and science at Würtzburg and the University of Berlin, and was professor of zoology at Jena from 1865 until his retirement in 1909. The turning point in his thinking was his reading of Charles Darwin’s Origin of Species, which had been translated into German in 1860.In a letter to his mistress, written when he was 64 and had acquired the nickname of ‘Der Ketzer von Jena’ (the gadfly of Jena),1 he explained how he began as a creationist but after studying evolution became a free-thinker and pantheist. 2 Darwin believed that Haeckel’s enthusiastic propagation of the doctrine of organic evolution was the chief factor in the success of the doctrine in Germany.3 Ian Taylor writes, ‘He became Darwin’s chief European apostle proclaiming the Gospel of evolution with evangelistic fervor, not only to the university intelligentsia but to the common man by popular books and to the working classes by lectures in rented halls.’4In these he used enormous backdrops showing embryos, skeletons, etc., which has led to his presentation being described as a sort of ‘Darwinian passion play’! The Imaginary Monera Haeckel’s drawings of the eating habit and reproductive cycle of an alleged Moneron to which he gave the scientific name, Protomyxa aurantiaca, as published in his book The History of Creation. The extent of the detail is the measure of his fraud, as the Monera did not then and do not now exist! Haeckel’s enthusiasm for the theory of evolution led him to fraudulently manufacture ‘evidence’ to bolster his views. He was the first person to draw an evolutionary ‘family tree’ for mankind. To fill the gap in this between inorganic non-living matter and the first signs of life, he invented a series of minute protoplasmic organisms which he called Monera (plural of Moneron). These, he said, were ‘not composed of any organs at all, but consist entirely of shapeless, simple homogeneous matter … nothing more than a shapeless, mobile, little lump of mucus or slime, consisting of albuminous combination of carbon.’5,6 In 1868, a prestigious German scientific journal published 73 pages of his speculations, with more than 30 drawings of these imaginaryMonera, as well as scientific names such as Protamoeba primitivia, and the process of fission by which they allegedly reproduced,7 even though his detailed descriptions and elaborate drawings were totally fictional, as these ‘life particles’ were entirely non-existent.Later the same year, Thomas Huxley, Darwin’s champion in England, reported finding something that fitted Haeckel’s descriptions in mud samples that had been dredged from the bottom of the north Atlantic and preserved in alcohol. Huxley named them Bathybius haeckelii.8Unfortunately for Huxley, Haeckel, the Monera, and the theory of evolution, in 1875 a chemist aboard the expeditionary ship discovered that these alleged protoplasm specimens were nothing more than amorphous gypsum, precipitated out of sea-water by alcohol! 9 Haeckel refused to be moved by this confuting evidence, and for about 50 years the public continued to be duped by unrevised reprints of his popular The History of Creation (1876), complete with drawings of the Monera, until the final edition in 1923.10,11 The Non-Existent Speechless Apeman
Everything about Pithecanthropus alalus, or the ‘speechless apeman’ was the product of Haeckel’s imagination.To Haeckel, human reasoning was much more important than facts and evidence. He believed that the only major difference between man and the ape was that men could speak and apes could not. He therefore postulated a missing link which he called Pithecanthropus alalus (speechless apeman) and even had an artist, Gabriel Max, draw the imagined creature, although there was not a scrap of evidence to support a single detail in the drawings.A contemporary of Haeckel, Professor Rudolf Virchow (famous as the founder of cellular pathology and for many years president of the Berlin Anthropological Society), was scathing in his criticism—for Haeckel to have given a zoological name to a creature that no one had proved to exist was to him a great mockery of science.The Dutch scientist, Professor G.H.R.von Koenigswald, described the drawing thus,‘Under a tree a woman with long lank hair sits cross-legged suckling a child. Her nose is flat, her lips thick, her feet large, with the big toe set considerably lower than the rest. Beside her stands her husband, fat-bellied and low-browed, his back thickly covered with hair. He looks at the spectator good-naturedly and unintelligently, with the suspicious expression of an inveterate toper [habitual drinker]. It must have been a happy marriage; his wife could not contradict him, for neither of them could speak.’ 12 No such alleged ‘missing link’ has ever been found. The Infamous ‘Fish Stage’ in Human Embryos Haeckel’s doctored drawings of dog and human embryos as they appeared in his book The History of Creation25 Of all Haeckel’s dubious activities, that for which he is most famous, or perhaps most infamous, is his promulgation of the totally erroneous theory that the human embryo is initially identical with that of other mammals and then goes through a series of stages where it has gills like a fish, 13 a tail like a monkey, etc. Sometimes called ‘the law of recapitulation’ or Haeckel’s term ‘the biogenetic law’, this idea has been summarized in the mouthful, ‘ontogeny recapitulates phylogeny’, which means the development of the individual embryo repeats its alleged evolutionary history. The first thing to say about this dictum, is that ‘law’ it is not! The idea is now known to be completely false. It is therefore not surprising that Haeckel could not find sufficient anatomical evidence to make his theory convincing. Never one to let lack of evidence stand in his way, Haeckel manufactured the ‘evidence’ by fraudulently changing the drawings of embryos by two other scientists.In his book Natürliche Schöpfungs-geschichte (The Natural History of Creation),published in German in 1868 (and in English in 1876 with the title The History of Creation), Haeckel used the drawing of a 25-day-old dog embryo which had been published by T.L.W. Bischoff in 1845, and that of a 4-week-old human embryo published by A. Ecker in 1851–59.14 Wilhelm His, Sr (1831–1904), a famous comparative embryologist of the day and professor of anatomy at the University of Leipzig, uncovered the fraud.Prof. Wilhelm His showed in 1874 that Haeckel had added 3.5 mm to the head of Bischoff’s dog embryo, taken 2 mm off the head of Ecker’s human embryo, doubled the length of the human posterior, and substantially altered the details of the human eye. He sarcastically pointed out that Haeckel taught in Jena, home of the then finest optical equipment available, and so had no excuse for inaccuracy. He concluded that anyone who engaged in such blatant fraud had forfeited all respect and that Haeckel had eliminated himself from the ranks of scientific research workers of any stature.15,16 [See also Encyclopedic ‘truth’ … or wordly wisdom?] Haeckel’s Confession of Fraud The furor in German scientific circles was so great that Haeckel found it impossible to persist in his policy of silence. In a letter to Münchener Allegemeine Zeitung, ‘an international weekly for Science, Art and Technology’, published on January 9, 1909, Haeckel (translated) wrote:‘… a small portion of my embryo-pictures (possibly 6 or 8 in a hundred) are really (in Dr Brass’s [one of his critics] sense of the word) “falsified”—all those, namely, in which the disclosed material for inspection is so incomplete or insufficient that one is compelled in a restoration of a connected development series to fill up the gaps through hypotheses, and to reconstruct the missing members through comparative syntheses. What difficulties this task encounters, and how easily the draughts-man may blunder in it, the embryologist alone can judge.’ 17Discerning readers who compare Haeckel’s doctored dog and human embryo pictures with the originals (see photographs), will readily see that Haeckel’s ‘confession’ was itself a deliberate misrepresentation of the facts and essentially an attempt to justify and perpetuate his shameful forgeries.Despite this totally dishonest and grievously mischievous basis for the theory of embryonic recapitulation, and the fact that it has long since been discredited scientifically, the completely false idea that human beings retrace their evolutionary past in the womb has been taught as evidence for evolution in schools and universities in the past, and it is still included in many popular science books.18,19Even worse, the argument that ‘the foetus is
still in its fish stage so you are just cutting up a fish’ is used to this day by some abortionists to convince girls and young women that killing their offspring is OK. Concerning this, Dr Henry Morris writes. ‘We can justifiably charge this evolutionary nonsense of recapitulation with responsibility for the slaughter of millions of helpless, pre-natal children —or at least for giving it a pseudo-scientific rationale.’20 Haeckel and the Rise of Nazism Sadly, in spite of all of his unsavoury activities, Haeckel was overwhelmingly successful in Germany, not only in having evolution widely taught as the accepted story of origins, but also in imposing a unique form of social Darwinism and racism on the German national ethos. ‘He became one of Germany’s major ideologists for racism, nationalism, and imperialism.’21,22This involved the concept that the Germans were members of a biologically superior community (akin to Nietzsche’s ‘super-man’).Unfortunately for mankind, Haeckel’s evolutionism laid the foundation for the intense German militarism that eventually contributed to World War I. And then,‘Social Darwinism, racism, militarism, and imperialism finally reached their zenith in Nazi Germany under the unspeakable Adolph Hitler … Hitler himself became the supreme evolutionist, and Nazism the ultimate fruit of the evolutionary tree.’23
The original drawings of a dog embryo (4th week) and a human embryo (4th week) by Ecker.26 The extent to which Haeckel fraudulently altered these is apparent by comparison with the picture above. A fishy story by Carl Wieland ‘Tweed boy had fish gills in his neck’. The headline was not that of some cheap tabloid paper, the type which is as likely to feature a phony photograph of a goat-human hybrid as to report Elvis running a hamburger cafe in Tibet. It was a respected Australian regional daily, The Northern Star (New South Wales) of October 30, 1993 (‘Tweed’ in the headline refers to the town of Tweed Heads).The fuss was about a small fragment of cartilage (10-15 millimetres long) which had been removed from the neck of an 11-year-old boy. It was referred to as a ‘fish gill’, and as ‘fish gill cartilage’. The parents were reported as saying, ‘The doctor told us that if our son had been a fish he would be able to breath [sic] under water.[ 1] He said it was a gill — like in a fish’.The report seemed to directly quote a medical authority as saying that the tissue found in this boy’s neck was hard cartilage ‘exactly the same as found in the gills of fish’. Little wonder that the boy had experienced ‘some teasing at school’! Human cartilage Knowing that we humans have human (not fish) DNA and can therefore make only human (not fish) cartilage, I rang the pathologist referred to in the A scar on the boy’s neck shows where article, who confirmed that the histology (microscopic appearance) of this the alleged ‘fish gill’ cartilage was cartilage was not in any way distinguishable from removed. Occasionally, human cartilage ordinary human cartilage.The whole article seemed to be strongly promoting may be abnormally ‘seeded’ during the mistaken belief that the human embryo, as it develops, goes through the development of the embryo, and this is stages of its pre-human evolutionary ancestry. It actually stated that in the what grows in a person’s neck. The first few weeks of life the human fetus ‘develops six gills’.Few, if any, cartilage taken from the boy’s neck is respected embryologists today accept this belief that the human fetus about the size of one of Australia’s repeats its past evolutionary history. In a major textbook on human smallest coins. The pathologist who development (Jan Langman, Medical Embryology, fourth edition, Williams & examined the ‘fish gill’ cartilage Wilkins, Baltimore, 1981) we read that ‘in the human embryo real gills — confirmed that its microscopic branchia — are never formed’.2 appearance was indistinguishable from Superficial similarity human cartilage. There are pouch-like structures which form in the fish embryo and which look superficially similar to the pharyngeal pouches or grooves in the human embryo (these were formerly incorrectly called branchial (i.e. gill) grooves). However, whereas in fish this region develops gills, in humans it forms very important, and quite different, structures in the
head and neck region, structures which have nothing to do with gills in either form or function.These structures include several which contain cartilage (such as the voice-box, or larynx). So it is not at all surprising, in a fallen world, that there should occasionally be an aberration of normal embryonic development, such that a clump of laryngeal-type cartilage (for example) is incorrectly ‘seeded’ in the side of the neck during development in the womb, and begins growing.Actually, such ‘embryonic rests’ or ‘remnants’ (not remnants of our evolutionary ancestry, but remnants of our own tissue which ended up in the wrong place), when they involve softer tissues than cartilage, are well-known in the neck region. 3 So-called ‘cartilage rests’, as in this case, are much rarer, but have been described. 4 There is therefore no mystery, and no evolutionary significance, to finding this tiny scrap of ordinary human cartilage in a human neck.It is tragic how readily the secular media, which will give virtually no exposure to visits by distinguished creation scientists, will publish such misleading and erroneous reports which reinforce evolutionary beliefs.
The human umbilical vesicle (‘yolk sac’) and pronephros—Are they vestigial? Published: 2 May 2009(GMT+10) This week we feature an enquiry from university student André Z of New Zealand, whose biology lecturer teaches that the “yolk sac” (umbilical vesicle), the pronephros, and other human embryonic structures are vestigial, constituting evidence that humans evolved. André also asks about so-called “endogenous retroviruses” (ERVs). Below is André’s enquiry, followed by a response by Andrew Lamb andJonathan Sarfati. Hello, I study 2nd year biology (BSc/BA) at a university in NZ. I have searched your site and not found any (or much) relevant information from a creationist perspective on two common evolutionary arguments in particular. Embryo development—the human embryo has some structures which serve no purpose in adults and resemble the embryos of ‘simpler’ organisms, which do have a use for these structures. The pronephros ‘kidney’ is effectively the same as in simpler animals, but in humans it degenerates by the 6th week. The yolk sac is apparently vestigial, having very little purpose in humans—certainly my lecturer is fond of it as evidence for evolution. Related to the comment on the yolk sac is something my lecturer was rather keen on repeating; that an engineer would not design a system such as found in the embryonic blood circulations. The claim is that the ‘mixing’ of oxygenated/poorlyoxygenated blood in e.g. the embryo’s heart is rather inefficient—I assume the idea is that poorly oxygenated blood shouldn’t really be mixed back in with oxygenated blood after circulation. Endogenous retroviruses—I have read the two articles on your site on these, and I am no expert on the details, but the extreme similarity in the location of some ERVs in the genetic sequences of different creatures such as chimps and humans, and a pattern of differences in these ERVs (or their surrounding genetic sequences) which fits evolutionary phylogenies, seems to support a common ancestry of different mammalian species. Is there a story in our genes, when we examine specific examples of similarity (rather than broad similarity biochemically which is arguably required to an extent for nutrition purposes and such)?—i.e., I am not convinced of the strength of your arguments concerning molecular similarity and would appreciate any further comments or hints. Thank you, André Z Hi André Many vestigial arguments like those your lecturer pushes are based on the long-discredited theory of embryonic recapitulation, supported by the forged diagrams of German Darwinist Ernst Haeckel (1834–1919). More recent research shows that even the embryonic similarities that appear in many biology textbooks were actually based on Haeckel’s forgeries. There are just too many anomalies for the recapitulation idea to work: The “tail” in the human embryo does not mean that we descended from tailed animals. In fact, the human embryo also has a post-anal gut. Does this mean that we descended from an animal with such a thing?Some of the numerous examples of embryonic development which are contrary to the supposed evolutionary sequence are: the mammalian heart forms before the circulatory system, the teeth form before the tongue, and the whale embryo never has a four-legged phase.Therefore, since embryonic recapitulation is utterly defunct, any argument based on it should not trouble anyone.Another common evolutionary claim is that the pharyngeal arches of the human are vestigial gill slits, but these pharyngeal arches are neither gills nor slits! Refutations we have published of this claim can be found by entering “gill slits” in the search field near the top right of our website. [Update: according André, Gill slits were discussed by my lecturer and the Haeckel-esque simplistic story which has previously been attached to them was debunked by him; it is clear that the pharyngeal arches do not develop into slits in humans (though the possibility that they may sometimes ‘break through’ seemed to be left open).] Potentially helpful resources re human embryology include: Does the human fetus temporarily develop gills, a tail, and a yolk sac?, largely adapted from Gary Parker, Embryonic Development, pages 54–63 in: Creation: Facts of Life. Alex Williams, Abortion argument unravels, Creation 27(4):16–19, September 2005.
Jerry Bergman and George Howe, “Vestigial Organs” Are Fully Functional, Creation Research Society Books 1990. Andrew Lamb, Human tails and fairy tales, 1 September 2007. See especially the quotes from embryology textbooks in the References section at the end of this article. Embryonic development Another important point with embryology is that the needs of the developing embryo are as important as those of the adult. The “tail” ensures that there is an adequate blood supply to the developing leg buds in the embryo. The development of the kidneys is an example of this (see below). Just as many temporary structures such as scaffolding, ramps, rubbish chutes, portaloos, etc. are needed on a construction site, but are superfluous once the building is completed, so too it is reasonable to expect there to be temporary structures needed by a growing organism, that may no longer be needed by the fully grown adult.Still another point is that some structures develop only when induced by other structures. An embryology textbook explains:“Organs are formed by interactions between cells and tissues. Most often, one group of cells causes another set of cells or tissues to change their fate, a process called induction. In each such interaction, one cell type or tissue is the inducer that produces the signal, and one is the responderto that signal. … Examples … include … gut endoderm and surrounding mesenchyme to produce gut-derived organs, including the liver and pancreas, limb mesenchyme with overlying ectoderm to produce limb overgrowth and differentiation; and endoderm of the ureteric bud and mesenchyme from the metanephric blastema to produce nephrons in the kidney [more below]. Inductive interactions can also occur between two epithelial tissues, such as the induction of the lens by epithelium of the optic cup.” 1The book goes on to explain, “Cell-to-cell signaling is essential for induction, for conference of competency to respond, and for cross talk between responding cells.” Then it explains these complex biochemical processes.Induction explains another favourite evolutionary “proof”: teeth in embryonic baleen whales, supposedly proving that they evolved from toothed whales. But Louis Vialleton (1859–1929), who was Professor of Zoology, Anatomy and Comparative Physiology at Montpelier University, southern France, argued:“Even though the teeth in the whale do not pierce the gums and function as teeth, they do function and actually play a role in the formation of the jaws to which they furnish a point d’apui on which the bones mold themselves.” 2Douglas Dewar (1875– 1957), a prominent British creationist who strongly refuted evolutionary arguments around WW2, supported Vialleton’s argument in several ways:the embryonic teeth are very different in disposition, form and number from the toothed whaleswhy would toothless whales acquire extra teeth, then scrap them and replace them with the new structure of baleen plates;there is a parallel example in humans, where microcephalic individuals with very poor or non-existent teeth development suffer from receded jaws. These poorly developed jaws are due to “a deficiency or actual total failure of development of the dental germs, the effect being that the investing jaws likewise fail to execute their normal growth and evolution.” 3With these principles out of the way, we’ll now tackle the “yolk sac”, pronephros (plural pronephroi), embryonic heart, and “endogenous retoviruses” in turn. Embryonic kidney development The above embryology textbook points out that the pronephros serves an important role as an inducer, as explained above: “Formation of the pronephric kidney (i.e., pronephros) lays the foundation for the induction of the mesonephric kidney (i.e., mesonephros), and it in turn lays the foundation for the induction of the metanephric kidney (i.e., metanephros). Hence, formation of a pronephric kidney is really the start of a developmental cascade leading to the formation of the definitive kidney.”4Also, Dewar suggested that the pronephroi have a function in the very early embryo, and its “simple” structure and positioning are appropriate for this function:“As the embryo must have a kidney to rid himself of waste products at an early stage, one has to be developed while the complicated adult kidney is being formed. Accordingly what is known as the pronephros or head kidney is first formed. This consists of a row of two or three nephridia on each side of the body. These nephridia are tubes, one end of which opens into the body-cavity and the other end into a common duct leading to the exterior. Each nephridium comes into contact with a bunch of tiny blood-vessels known as a glomerulus. From the blood in these the waste products of the embryo are taken up by the nephridia and so passed out of the embryo. As the embryo increases in size new nephridia are formed behind the first ones. These are of more complicated structure and are described as a second kidney, the mesonephros or middle-kidney. As the mesonephridia increase in number the pronephros gradually undergoes atrophy. A kidney of the mesonephros type suffices to carry off the waste products of comparatively simple organisms; in consequence in fishes it persists throughout life as the functional kidney. In some cases the pronephros also persists. The mesonephros is inadequate for the needs of organisms higher [i.e. more complex] than fishes, in consequence a far more complicated kidney—the metanephros or hind-kidney—develops behind the mesonephros. When this final kidney is ready to function, the nephridia of the mesonephros become absorbed, but their duct persists, being used to carry the male genital products. …“The reason why the early embryonic kidney, instead of being converted into, is replaced by the adult kidney, thus appears to be, not that the embryo is compelled to recapitulate prepiscine and piscine stages, but that embryonic conditions require the kidney to be situated far forward—a position that would be inconvenient in the adult.”5As yet medical research has not confirmed Dewar’s inferences about the function of the pronephros, but research has shown the pronephros to have the crucial function of inducing development of the kidney, as related earlier in this article. But the next stage, the mesonephros,does have kidney function, which would vindicate Dewar’s argument that it is designed for what it does and where it does it:“Although there is evidence of urinary function in the mammalian mesonephric kidney, the physiology of the mesonephros has not been extensively investigated. Urine formation in the mesonephros begins with a filtrate of blood from the glomerulus into the glomerular capsule. The filtrate then flows into the tubular portion of the mesonephros, where the selective resorption of ions occurs. The return of resorbed materials to the blood is facilitated by the presence of a dense plexus of capillaries around the mesonephrous tubules.“The structure of the human mesonephros is very similar to that of adult fishes and aquatic amphibians, and it functions principally to filter and remove body wastes. Because these species and the amniote embryo exist in an aquatic environment, there is little need to conserve water. Therefore the mesonephros does not develop a medullary region or an elaborate system for concentrating urine as the adult kidney does.”6 Yolk sac Evolutionists sometimes argue that the yolk sac of mammals is vestigial, being small and devoid of yolk, in contrast to birds and reptiles. However, an embryology textbook points out that it is vital to the embryo because of other functions associated with it.7As creationist biologist Dr Gary Parker points out, “The so-called ‘yolk sac’ is the source of the human embryo’s first blood cells, and death would result without it!” (Creation: Facts of Life, page 56). Evencreation-hostile Wikipedia acknowledges its importance, saying “it functions as the developmental circulatory system of the human embryo, before internal circulation begins” (Yolk sac).In fact, most embryologists no longer call it “yolk sac” but “umbilical vesicle”. Here is a relevant excerpt from a contemporary textbook: Significance of the Umbilical Vesicle Although the umbilical vesicle is nonfunctional as far as yolk storage is concerned (hence the name change), its presence is essential for several reasons:It has a role in the transfer of nutrients to the embryo during the second and third weeks when the uteroplacental circulation is being established.Blood development first occurs in the well-vascularized extraembryonic
mesoderm covering the wall of the umbilical vesicle beginning in the third week (see Chapter 4) and continues to form there until hemopoietic activity begins in the liver during the sixth week.During the fourth week, the endoderm of the umbilical vesicle is incorporated into the embryo as the primordial gut (see Fig. 5-1). Its endoderm, derived from epiblast, gives rise to the epithelium of the trachea, bronchi, lungs, and digestive tract.Primordial germ cells appear in the endodermal lining of the wall of the umbilical vesicle in the third week and subsequently migrate to the developing gonads (see Chapter 12). They differentiate into spermatogonia in males and oogonia in females.8Here is a comment from another textbook: “The definitive yolk sac remains a major structure associated with the developing embryo through the 4 th week and performs important early functions. Extraembryonic mesoderm forming the outer layer of the yolk sac is a major site of hematopoiesis (blood formation; discussed in Ch. 13). Also, as described in Chapter 1, primordial germ cells can first be identified in humans in the wall of the yolk sac.”9 Embryonic heart The reason why the mammalian embryonic heart is at first a simple tube is, not that mammals evolved from fishes, but that, as the mammalian embryo must have a functioning heart at a very early stage, the simplest possible heart is formed.— Douglas Dewar The evolutionary lecturer claims design flaws, but I would challenge him to design a better system that develops from a single cell and keeps the creature alive. Once again, the “simple” heart is vital for the embryo at this stage of development. Dewar explains:“The so-called fish heart and gill-arches have to be formed because the head region of the embryo from a very early stage onwards, requires a copious blood supply. This necessitates the early formation of a heart or pumping organ and a simple system of blood vessels. These have to be formed before there is time to develop the four-chambered heart necessary to the higher animal. …“The heart develops as follows: Two tiny tubes are formed which run parallel. Those coalesce to form a single tube; the wall of the front part of this thickens and the thickened part becomes separated from the thinner hind part by valves. The heart is now an effective pumping machine composed of two communicating chambers … In fishes this type of arrangement persists throughout life, being suitable for a gill-breathing animal … Animals higher up the scale need a more complicated heart and in them the embryonic heart becomes three-or four-chambered … by the growth of a septum in one or both of the chambers.“Clearly then, the reason why the mammalian embryonic heart is at first a simple tube is, not that mammals evolved from fishes, but that, as the mammalian embryo must have a functioning heart at a very early stage, the simplest possible heart is formed. As development proceeds the form of the heart changes to meet the increasing demands made upon it.”10 Endogenous retroviruses The term “endogenous retroviruses” is inherently misleading—see the ‘Endogenous retroviruses‘ section within the article Junk DNA, asteroid impacts, and supernovas.You said you have read our two articles related to ERVs. We have previously published articles refuting the general “shared mistakes” claim by evolutionists: John Woodmorappe, Are pseudogenes shared mistakes between primate genomes? Journal of Creation 14(3):55–71, 2000. John Woodmorappe, Potentially decisive evidence against pseudogene shared mistakes Journal of Creation 18(3):63–69, 2004. ERVs act as promoters, starting transcription at alternative starting points, which enables different RNA transcripts to be formed from the same DNA sequence. We find the arguments in these two articles compelling. [André informed us he had also read the instructive overview Junk DNA: evolutionary discards or God’s tools? Which likewise discusses ERVs]Extreme similarity (homology) of component parts is to be expected if things have the same Designer—seeAre look-alikes related? Indeed, in most cultures that have existed around the world, such similarities would bring great honour to a designer, demonstrating his complete mastery over what he had made—seeNot to Be Used Again : Homologous Structures and the Presumption of Originality as a Critical Value.Our most recent article on ERVs, and specifically on this topic, is:Shaun Doyle, Large scale function of endogenous retroviruses Journal of Creation 22(3):16, 2008. This points out: Moreover, researchers have recently identified an important function for a large proportion of the human genome that has been labelled as ERVs. They act as promoters, starting transcription at alternative starting points, which enables different RNA transcripts to be formed from the same DNA sequence. … We’re not just talking about a small scale phenomenon. These ERVs aid transcription in over one fifth of the human genome!Since the so-called ERVs clearly have a vital function, this is consistent with a design explanation. Best wishes in your course. Andrew Lamb and Jonathan Sarfati CMI–Au
