Symposium: Causes and Etiology of Stunting
1
Introduction
Edward A. Frongillo, Jr. Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853–6301
This symposium considered why and how stunting of children occurs. As described in the comprehensive examination made by WHO of the use and interpretation of anthropometry (1995), stunting (i.e., short stature due to poor living environments) is one of the two most important indices of child well-being in use throughout the world. The assessment of stunti stu nting ng is int integr egral al to pub public lic hea health lth,, cli clinic nical al and res resear earch ch workers in many fields concerned with the well-being of children and with the biology of growth and development. In developing countries, ϳ40% of children Ͻ5 y of age are stunted [de Onis and Blo¨ ssner 1997, WHO Subcommittee on Nutrition (SCN) 1997]. This means that Ͼ200 million young child ch ildren ren are stun stunted ted.. The tim timing ing of stu stunti nting ng is rea reason sonabl ablyy understood in that most stunting occurs before the age of 3 y, and stunted children usually become stunted adults. The consequences of becoming and remaining stunted are increased risk of morbidity, mortality, delays in motor and mental development, and decreased work capacity (SCN 1997, Waterlow and Schu¨ rch 1994). The causes and etiology of stunting are much less understood sto od tha than n are its tim timing ing and con conseq sequen uences ces.. In par partic ticula ular, r, there is little understanding of why and how stunting occurs extensively in environments that are poor, but not desperately so, and in environments that seem to be improving. In a population, an individual child can become stunted or not. In addition, some populations are much more stunted than others (WHO 1995). This means that an understanding of why and how children become stunted is needed at both the individual and ecological levels. The objectives of this symposium were as follows: 1) review and synthesize our understanding about why and how young children become stunted, emphasizing new knowledge gained since 1993; 2) consider the implications of this understanding for efforts to improve child well-being; and 3) highlight new ideas about the causes and etiology of stunting that especially warrant further investigation in the next few years. An important foundation for this symposium was a workshop held in London in January 1993 to examine what was then known about the causes and mechanisms of linear growth retardation (Waterlow and Schu¨ rch 1994). From that workshop emerged the view that the causes and etiology of stunting include the following: 1) nutrition (energy, macronutrients,
micronutrients and toxic factors); 2) infection (injury to gastrointestin troint estinal al muco mucosa, sa, system systemic ic effec effects ts and imm immunosti unostimula mula-tion); and 3) mother-infant interaction (maternal nutrition and stores at birth, and behavioral interactions). The workshop group suggested that a priority for further research should be intervention studies that enable the differentiation among possible causal factors. The 1998 Experimental Biology symposium was timely because a number of important intervention studies have examined multiple causes of stunting during the five years that have passed since the 1993 workshop. The symposium was also timely because of some relatively recent D observations that affect how we think about the causes and ow n etiology of stunting. l o a Much of our thinking about why and how stunting occurs d e is depicted in the classic model of the nutrition and infection d r cycle (Tompkins and Watson 1989). As an explanation for of m how mal malnut nutrit rition ion and dis diseas easee res result ult in exc excess ess mor mortal tality ity of j n children, this so-called “vicious cycle” model has been sup- n. u planted plant ed by the synergism synergism mode modell (Scr (Scrimsh imshaw aw et al. 1968) that t r i t has now been demonstrated epidemiologically (Pelletier et al. oi n 1993 and 1995). Furthermore, it is not clear how much the o. r g nutrition and infection cycle helps us understand why and how b y stunting occurs. g At the individual level, an episodic model has been dem- u e s onstrated to explain daily patterns of linear growth (Lampl et t o al. 1992). Growth observed daily shows periods of stasis (i.e.,n no gro growth wth)) pun punctu ctuate ated d by dai daily ly sal saltat tation ionss of gro growth wth.. Th This is aM research suggests that stunting must result from a decreased y 7 , frequency of growth events, a decreased amplitude of growth 0 2 1 when an event occurs, or both. We do not know why and how 3 these might happen and which is more important. The postnatal time most susceptible to poor linear growth is after 3–6 mo and up to 24–36 mo (SCN 1997). Why poor conditions have less effect after this time is not understood. A common explanation is that poor conditions affect growth when velocity is greater, but this is not very satisfying, especially in light of LamplЈs observations about episodic growth. Stunting is a cumulative process that can begin in utero and continue to ϳ3 y after birth. Low birth weight is an important indicator of fetal/intrauterine nutrition and a strong predictor of subsequent growth and well-being. Recent data from de Onis et al. (1997) have shown that, in the least developed countries, ϳ23% of infants are born with low birth weight compared comp ared with ϳ7% in dev develo eloped ped cou countr ntries ies.. The pri primar maryy reason for these high rates of low birth weight is intrauterine growth gro wth ret retard ardati ation. on. We do not kno know w how mu much ch pre prena natal tal stunting contributes to the postnatal stunting we observe, and therefore how much attention relative to causes of stunting should be focused prenatally. Furthermore, because maternal
1 Presented at the symposium “Causes and Etiology of Stunting” as part of Experimental Biology 98, April 18–22, 1998, San Francisco, CA. The symposium was sponsored by the American Society for Nutritional Sciences and the Society for International Nutrition Research. Published as a supplement to The Journal of Nutrition.. Guest editor for the symposium publication was Edward A. Frongillo, Nutrition Jr., Cornell University, Ithaca, NY.
0022-3166/99 $3.00 © 1999 American Society for Nutritional Sciences. J. Nutr. 129: 529S–530S, 1999. 529S
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SUPPLEMENT
size, nutrition, and other factors are important determinants of prenatal size, why and how stunting occurs is potentially explainable at least in part by conditions that affected the previous generation. Recently, there has been substantial attention paid to the role of feeding mode on growth patterns of infants. For example, the WHO Working Group on Infant Growth (1994 and 1995) has shown that the pattern of growth for breast-fed and formula-fed infants differs substantially. Subsequent research has shown that the pattern of growth is not sensitive to the duration of breast-feeding (Cohen et al. 1994, Frongillo 1996). Why these patterns are different and what this might tell us about why and how stunting occurs is not understood. It has long been recognized that deficits in macronutrients cause stunting, but there has been increasing attention paid to the role of micronutrients. We must determine for which micronutrients do deficits limit growth and whether stunting is due primarily to deficits in single nutrients or in multiple nutrients simultaneously. The United Nations ChildrenЈs Fund, through its wellknown conceptual model and more recent Care Initiative (Engle et al. 1997a) has helped bring to our attention the role of maternal and child care in child nutrition. Understanding the ways in which care affects why and how stunting occurs is limited (Engle et al. 1997b). The UN’s Coordinating Subcommittee on Nutrition has just published its Third Report on the World Nutrition Situation. The prevalence of stunting and recent rates of progress differ substantially across regions (SCN 1997). We can explain about three quarters of the variability among countries in the prevalence of stunting by social, human development and economic factors (Frongillo et al. 1997). But we know less about why and how some countries improve and others do not (Gillespie et al. 1996). WHO has proposed that the goal for reducing stunting should be that the prevalence of stunting in any country should be Ͻ20% by the year 2020. Only about one quarter of developing countries meet that target now, and if past trends continue, only about one half would meet that target in the year 2020 (SCN 1997). It is important to identify what are the most important actions to be taken to make better progress, and what research be done to assist with these decisions. The papers presented in this symposium aimed to address many of these issues. Answering why and how stunting occurs requires fundamental understanding of how bones elongate to produce linear growth. This understanding has been lacking, but Wilsman, the first presenter at the symposium, provides some clues concerning the nature of this process (see: Farnum and Wilsman 1998, Wilsman et al. 1998). The paper by Rosado for this symposium presents evidence that stunting is associated with marginal deficiencies of several micronutrients simultaneously. Stephensen discusses current thinking about how infection may play a causal role in stunting. Black and Krishnakumar examine how factors such as child temperament, maternal depression, and responsiveness of maternal-
child interactions relate to growth failure. Ramakrishnan, Martorell, Schroeder and Flores present evidence on why and how stunting persists across generations. LITERATURE CITED Cohen, R.J., Brown, K.H., Canahuati, J., Landa Rivera, L.& Dewey,K. G. (1994) Effects of age of introduction of complementary foods on infant breast milk intake, total energy intake, and growth: a randomised intervention study in Honduras. Lancet 344: 288–293. de Onis, M. & Blo¨ssner, M. (1997) World Health Organization Global Database on Child Growth and Malnutrition. WHO/NUT/97.4. Programme of Nutrition, WHO, Geneva, Switzerland. de Onis, M., Blo¨ssner, M. & Villar, J. (1997) Levels and patterns of intrauterine growth retardation in developing countries. Eur. J. Clin. Nutr. 52 (suppl. 1): 5–15. Engle, P., Lhotska´, L. & Armstrong, H. (1997a) The Care Initiative: Assessment, Analysis and Action to Improve Care fo r Nutrition. United Nations Children Јs Fund, Nutrition Section, New York. Engle, P., Menon, P. & Haddad, L. (1997b) Care and Nutrition: Concepts and Measurement. International Food Policy Research Institute, Washington, DC. Farnum, C. & Wilsman, N. J. (1998) Growth plate cellular function. In: Skeletal Growth and Development: Clinical Issues and Basic Science Advances (Buckwalter, J., Ehrlich, M., Sandell, L. & Trippel, S., eds.), pp. 203–223. American A cademy of Orthopedic Surgeons. Frongillo, E. A., Jr. (1996) The Effects of Timing and Type of Complementary Foods on Post-Natal Growth. Report submitted to the Nutrition Unit, Division D o of Food and Nutrition, World Health Organization. Division of Nutritional w n Sciences, Cornell University, Ithaca, New York. l Frongillo, E. A., Jr, de Onis, M. & Hanson, K.M.P. (1997) Socioeconomic and o a d demographic factors are associated with worldwide patterns of stunting and e d wasting. J Nutr. 127: 2302–2309. f r Gillespie, S., Mason, J. & Martorell, R. (1996) How Nutrition Improves. ACC/ o SCN State-of-the-Art Series, Nutrition Policy Discussion Paper # 15. United m Nations Administrative Committee on Coordination/Sub-Committe on Nutri- j n .n tion, Geneva, Switzerland. u Jonsson, U. (1995) Towards an improved strategy for nutrition surveillance. t r i t Food Nutr. Bull. 16: 102–111. i o Lampl, M., Veldhuis, J. D. & Johnson, M. L. (1992) Saltation and statis: a model n . o of human growth. Science (Washington, DC) 258: 801–803. r g Pelletier, D. L., Frongillo, E. A., Jr. & Habicht, J. P. (1993) Epidemiologic b evidence for a potentiating effect of malnutrition on child mortality. Am. J. y g Public Health 83: 1130–1133. u Pelletier, D. L., Frongillo, E. A. Jr., Schroeder, D. G. & Habicht, J. P. (1995) The e s effects of malnutrition on child mortality in developing countries. Bull. WHO t o 73: 443–448. n Scrimshaw, N. S., Taylor, C. E. & Gordon, J. E. (1968) Interaction of Nutrition M and Infection. Monograph series 57. World Health Organization, Geneva, a y Switzerland. 7 SCN (1997) Stunting and young child development. In: Third Report on the ,2 World Nutrition Situation. United Nations Administrative Committee on Coor- 0 1 3 dination/Sub-Committe on Nutrition, Geneva, Switzerland. Tomkins, A. & Watson, F. (1989) Malnutrition and Infection: A Review. United Nations Administrative Committee on Coordination/Sub-Committe on Nutrition, Geneva, Switzerland. Waterlow, J. C. & Schu¨rch, B. (1994) Causes and Mechanisms of Linear Growth Retardation. Proceedings of an I/D/E/C/G Workshop held in London, January 15–18. Eur. J. Clin. Nutr. 48: S1–S216. Wilsman, N. J., Farnum, C. E., Leiferman, E. M. & Lampl, M. (1998) Consideration of growth plate biology in the context of growth by saltations and stasis. In: Saltation Stasis and Human Growth (Lampl, M., ed.). Smith-Gordon, London (in press). World Health Organization (1995) Physical Status: The Use and Interpretation of Anthropometry. Report of a WHO Expert Committee. Technical Report Series no. 854. WHO, Geneva, Switzerland. World Health Organization Working Group on Infant Growth (1994) An Evaluation of Infant Growth. Doc WHO/NUT/94.8. WHO, Geneva, Switzerland. World Health Organization Working Group on Infant Growth (1995) An evaluation of infant growth: the use and interpretation of anthropometry in infants. WHO Bull 73: 165–174.
