“Strong Medicine by Chris Hardy, D.O. and Marty Gallagher is an exhaustively researched resear ched,, clearly writt wr itten, en, and and practically useful useful g uide to improving impr oving your health. health. Improving health is fundamentally different than treating disease. This book represents the future of healthcare in our country. It requires the patient to assume responsibility, learn the basics, and then enhance their health through diet, exercise, sleep, and mindfulness. If you ar e looking lo oking fo r a quick fix, this this is not the book for you. If you understan understand d that there is no quick fix, then read this book and trust what you read. The information is accurate and relevant, simple to understand, and actionable.” —Pat rick Roth, Rot h, M.D., M.D., author of The End of Back Pain: Access Your Hidden Core to Heal Your Body , Chairman of Neurosurgery at Hackensack University Medical Cent Center er and the the director of its neurosur gical r esidency esidency tr tr aining pro gr am. “In the last 40-50 years we have experienced a huge rise in the chronic diseases affecting affluent societies across the world. We are generally fatter and less healthy than we were in the past. In this impressive new book Chris Hardy and Marty Gallagher take the roles of doctor and fitness coach to provide us with in-depth understanding about why this is happening and the steps we need to take to turn this around. This includes a comprehensive review of the latest scientific research—which is presented in an easy to understand format. The solution is presented as an integrated ‘Battle Plan’ which includes a detailed and well-explained training regime along with excellent nutritional advice, which will combine to provide a transformation to a fitter, stronger, stro nger, and healthier body. Most impor im por tantly tantly they show us the best way to to measure measur e the the progr pro gr ess we we are making towards this this goal. I would consider this as the most comprehensive and readable book I have seen on this larg e topic, and it provides pro vides a thor thorough ough discussion o f evidence evidence to support the nutritional and exercise advice. Some of the research is very new, and may be considered controversial. However, this is all presented for the reader to evaluate. What we have been doing as a society has not been working and this book—with its many exciting new ideas—may provide the plan to reduce the problems created by these chr chr onic diseases. di seases.”” —Dr. —Dr. Pet er Goo Go o t jes, Public Health Medicine Specialist, New Zealand “Strong Medicine is flat-out amazing. If you ever wanted to take your training and your nutritional theory to an elite level—better than 99.9% of certified personal trainers—this is the book for you. It’s all in here: genetics, gut bacteria, cutting-edge stress biology, molecular nutrition...even better, the ‘deep science’ is all explained so clearly (with charts, key points, photos and diagrams) that it’s almost impossible
to understand under stand and absor absor b it all fully. An automatic automatic classic in the field, which will not to surely surel y pro ve impossible impo ssible to sur pass. I bow down to to the Doc and to Marty!” Marty!” —Paul Wade, Wade, author, Convict Conditioning and Explosive Calisthenics Cali sthenics “Given the sad state of our society’s health and wellness literacy, Strong Medicine is just what the doctor should order. Chris and Marty come together to provide the reader with sound information addressing health and wellness from all angles. Whether it’s the impact of genetics, the use of biomarkers, proper physical training, the importance of sleep, and/or nutritional information, Strong Medicine has it covered. It is time that we restore and strengthen the fabric of our society by arming its citizens with the understanding of ‘why, instead of allowing them to meander around in ignorance from one fad to the next. Strong Medicine should be on the bookshelf of anyone serious about their health and wellness. Gratitude, Chris and Marty for such a fine reference.” —Dr. —Dr. Mike Davis, DPT “Strong Medicine is a rare gem that is a must-have for anyone who wants to take control of their health. Chris and Marty have organized an extremely thorough yet easy to understand encyclopedia on how to maximize your health, fitness and genetic potential. In a day day and age where we have never been mor mo r e confused about abo ut how to to eat, when when to eat, how to exercise and what is right vs wrong, as well as more unfit than ever before, this is the the new Bible for taking taking control contro l of o f your life. Why do do I say controlling controlli ng your life? Because Because this this book is about your your health, health, from fro m the inside out. No fads, no gimmicks, no “diets” to follow, just the truth about what you need to do to truly be healthy and fit. Without your health, you have nothing to enjoy in life. This book boo k is an essential essential r esource for f or any fitness fitness enthusiast enthusiast,, health health practitioner practitioner or coach.” —Zach Even-Esh, author, The Encyclopedia of Underground Strength and Conditioning “Strong Medicine is one of the most informative books recently published in the area of human health and fitness. The book not only explains bare-bone principles of human biology and wellness, it actually translates this knowledge into a practical strategy—hence ‘The Strong Medicine Lifestyle.’ Well written and backed by science, Strong Medicine present pr esentss impor tant tant yet yet controversial controversi al and perhaps arg uable
concepts in the area of stress response, nutrition and mental/physical conditioning. Highly recommended to anyone interested in ‘better survival in today’s world’.” —Ori Hofmekler Hofmekler,, author, The Warrior Diet “Strong Medicine is a declaration of unconventional and asymmetrical war against mortality. The authors’ weapon of choice is information, relayed masterfully in the form of an easy-to-understand and richly illustrated owner’s manual of sorts. This is an owner’s manual that is chock full of insights for every level, from fr om the seasoned physician to the absolute layman who who is i s new to to fitness. f itness. For the the gr izzled coach who who doesn’t have have medical medical training, Strong Medicine lays out crucial performance concepts like ‘hormetic dose’ in ways that are easy to understand regardless of your background. Dr. Hardy continues with insights into diet, nutrition myths, biochemistry demystified, intestinal fine-tuning, the chronic stress connection with disease, and then passes the baton to Marty Gallagher, who unleashes a plethora of exercise and training tips that are centered around five basic exercise categories. With well-shot photographs and clear diagrams to illustrate the important points of each posture, Gallagher lays out a beautiful plan of attack to combat weakness and mechanical decay, including easy-to-follow training programs. This is a book I plan to read & re-read a number of times as both a licensed medical medical pr ofessional and a strength & conditioning coach.” coach.” —Dr. —Dr. MARK MARK CHENG CHENG, L.Ac., Ph.D, contributing editor, Black Belt Magazine “I have had the pleasure of being with Marty Gallagher when he delivered the ‘Beta’ version of this book—and I flew home and realized that I needed to start from zero with my coaching of the basic movements. Combine Marty’s great insights with with the clearest explanation I have ever r ead that ‘Food ‘Foo d is Medicine’ and you you have a one-two punch that changes lives. An amazing book and well worth the time to read it and digest it (pun intended).” —Dan John, author, Never Let Go “Strong Medicine demonstrates the paradigm shift that we currently have in the world of physical development. We cannot put our fitness goals above our health goals. Health provides the foundation for fitness to start the process. Fitness in turn pays back health through maintenance and sustainability. The takeaway for this book: learn as much about your health as you do about your fitness and you’ll do ust fine.” —GRAY —GRAY COOK COOK,, author, Movement, co-creator, FM FMS S
STRONG MEDICINE MEDICINE How to Conquer Conq uer Chronic Chronic Disea Dis ease se and A chieve Your Your Full Ful l Geneti Geneticc Potent Potential ial Chris Hardy H ardy,, D.O D.O. MPH and Marty M arty Gallagher all agher
© Copyright 2015 , Chris Hardy Hardy and Marty Gall agher A D ragon Door Publi Publi cations, Inc. produc production tion Al l rights under Internatio Internatio nal nal and and Pan-Ame rican Copyrig Copyrig ht conventions. Published Published i n the the U nited States by: Dragon Door Publi Publi cations, Inc. 5 East County R d B, #3 • Littl e Canada Canada,, M N 5511 7 Tel: (651) 487-2180 • F ax: (651) (651) 487-3954 Credit card orders: 1-800-899-5111 • Email:
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No part of this book may be reproduc reproduced ed in any form or by any means without the the prior wri tten consent consent of the Publi Publi sher, excepting brief quotes used in revi ews.
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DISCLAI M ER : The authors authors and and pub publi sher of this material are not responsibl responsibl e i n any manner whatsoeve r for any injury that ma may y occur through rough fol lo wi ng the the i nstruc nstructions tions contained in this material . The activ iti es, physical and otherwise , described herei herei n for i nformational purp purposes oses only, may be too strenuous strenuous or dangerous for some people and and the the re ader(s) ader(s) should should consult consult a physi physi cian bef bef ore e ngaging in them. The content of this book is for i nformational and and educational educational purposes only and and should should not be considered medical advi advi ce, diagnosi s, or treatme nt. Re aders aders should not disregard, disregard, or del ay i n obtaini obtaini ng, medical advi advi ce f or any medical conditi on they may have, and should should see k the assistance assistance o f thei r health care care professi onals fo r any any such conditi ons because because of informatio n contained contained withi n this this publi cation.
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— CONTEN CO NTENTS TS — Courage age • Commitment Commitment FOREWORD: Honor • Cour by Craig Cr aig D. Thor Tho r ne, M.D. M.D.,, MPH, MPH, MBA MBA
PREFACE: Messages from the Authors INTRODUCTION
Phase I: Basic Training Basic Training Training I—C I—Cent entral ral Them T hemes es • Inflammation and and Oxidative Stress • The Gene-Enviro nment Connection • Hormesis • The Stress Response • Allostasis—“The Stress Stress Cup” Cup”
Basic Training Training II II—Nutrit —Nutrition ion and Metabolism Met abolism 101 • Introduction • Macronutrients • Metabolism Basics
Phase Pha se II: Knowi Knowing ng the Enemy Knowing Kn owing the t he Enemy Enemy I—The Gut: Gut : Guardian Guardian at t he Gate • Gut Healt Health: h: Fir First st Pri Principles nciples • Trig Trigger ger s of Int Intest estinal inal Inflammat Inflammation ion • Conclusion
Knowingg t he Enemy Knowin Enemy II—Obesity: II—Obesity: T he Enemy Enemy Within Wit hin • Int Intrr oduction: A Big Fat Pro blem • The Fat Cell Cell:: Dr. Jekyll beco mes Mr. Hyde • The Plague of “Diabesity “Diabesity”” • How We We Get Fat: the br brain, ain, hor mo mones, nes, and appetite
• Int Inter ervention: vention: The 8-step 8-step pr prog og r am for obesity o besity and diabetes
Knowingg t he Enemy Knowin Enemy III—C III—Chronic hronic Stress: St ress: T he Silent Silent Ki Kill ller er • Mind and Body: Body: Descar Descartes tes was was wrong • Stress and and Health • Mind Int Inter ervent ventio ions: ns: Brain Training
Knowingg t he Enemy Knowin Enemy IV—Circadi IV—Circadian an Disruption: T hief in the Ni Night ght • The Int Inter ernal nal Timekeeper • Sleep Architecture • Edison’s Folly? • Modern Solutions for a Moder Modern n Pro Problem blem
Phase Pha se 3: BATT BATTLE LE PLAN PLA N Battle Plan I—Strong Medicine Physical Training • Introduction • Strong Medicine Resistanc Resistancee Trai Training ning • Strong Medicine Medicine Basic Basic Cardio • Strong Medicine Adv Advanced anced Cardio
Battle Batt le Plan II—Stro II—Strong ng Medi edicin cinee Nutrition Nut rition • Food Sources and and Quality • Carbohydrate Tolerance • Feed your activity • A Week of Food Foo d
Battle Batt le Plan II III— I—Put Puttt in ingg It All Toget her • Lifestyle Change: Change: “The Neck Neck of Roy Buchanan’ Buchanan’ss Guitar” • Strong Medicine Lifestyle Change-Strategic Planning
Battle Plan IV—“Stuff You Can Measure” • In Introduct troductionion- biomarkers biomar kers and th thee “Holy “Holy Grail” Gr ail” • Cholestero l: What ar aree we measur measuring? ing? • Physical Measur easurement ement • Marker arkerss of Inflammat Inflammation ion
• Hear Heartt Rate Var ariabi iability lity
Epilogue About Ab out the Authors Acknowledgements Index
FOREWORD
HONOR • COURAGE • COMMITMENT Those are the bedrock principles of the United States Navy. These values have guided the strong men and women of the Navy to successfully meet all of their challenges since it began during the American Revolution, even with a few small ships, all the way to the large, powerful fleets and global reach of today. The health and fitness communities are filled with many committed enthusiasts who devote their time and efforts in educating and training the public towards better habits and wellness. But few have the personal, proven experience to present factbased evidence that blends nutrition, exercise, and psychological truths into strategies and techniques to truly “transform” us physically and mentally. The authors of Strong Medicine have this rare blend of foundational scientific theory and real-world empiricism. Chris Hardy, the ‘doctor’ co-author of Strong Medicine served in the Navy as a medical officer for nearly a decade, and still holds those values very closely in his personal daily mission mi ssion to share his expertise in nutrition, strength and conditioning. conditioning. In addition to his specialty training in preventive and integrative medicine, and his advanced public health achievements, he is also a certified strength and conditioning specialist. Marty Gallagher, the ‘coach’ co-author has been involved in high level sports and athlet athletics ics for fo r over 50 years now, capt capturing uring his fir st national national title and national national r ecords ecor ds as an Olympic weight lifter when he was only seventeen year old. In May, 2013 he set his most recent national records as a 64 year-old power lifter. Marty is not only a peerless athlete, coach, and writer, he is also the embodiment of “successful aging”, achieving and maintaining physical and mental abilities superior to many who are 40 years years younger. In Strong Medicine, Chris and Marty have combined their disciplines and their experiences and have applied a modern day military theme to provide a compelling
structure to help even those of us that lead regular lives to successfully change our lifestyle lifestyle habits habits for fo r the the long-term. lo ng-term. In our own daily lives, we experience so many threats to our physical and psychological well-being (think of them as modern day “predators”): the pressure to succeed in stressful work environments, commuting in traffic congestion, poor and over nutrition with processed foods, financial pressures in a consumer-driven envir environment onment,, and even even the the pressure pressur e to pursue meaningful recreation r ecreation and relief fr om anxiety. The list goes on and on. The concomitant increasing prevalence of chronic, deadly diseases such as obesity, diabetes, high blood pressure, heart disease, cancer and so many more “lifestyle” conditions puts an intense spotlight on interventions that can help turn this tide. While some of these are the result of structural and societal changes, many are the result of individual choices and poor habits that wreak havoc havoc on our o ur bodies and minds over time and ro b us of our full potential potential for long, healthy and productive lives. But we have much untapped ability to change many of the antecedents and conditions that lead to premature chronic disease and disability and help us achieve our full genetic potential. In this information age, there are countless guides to selfimprovement, and diet fads and fitness boots camps are abounding. Chris and Marty help us replace such “infor “infor mation mation o verload” verlo ad” with with user-fr user-fr iendly “know “know your enemy” enemy” information and evidence-based habits and actions so that we can commit to sustainable and manageable change. Think about this as you read Strong Medicine:
HONOR “I will bear true faith and allegiance…”. For the Navy, this means that officers need to make honest recommendations and be truthful in their dealings with each other, and with those outside the Navy. Officers should also encourage new ideas, take responsibility responsibility for f or their own actions, fulfill and exceed their responsibilities, responsibilities, and be mindful of their privilege to serve t heir fellow Americans. Americans. In Strong Medicine, the author authorss provide pr ovide an in-depth in-depth series of recommenda reco mmendations tions based on scientific scientific literature and other up-to-date information so that readers can honor themselves with the correct cor rect informat infor mation ion to make their their own o wn transformat transfor mation. ion.
COURAGE “I will support and defend…” means to have the courage to meet the demands o the mission when it is demanding or otherwise difficult. It also means ensuring that the resources entrusted to officers are used by them in a careful and efficient way.
Lifestyle change can be daunting. This book not only provides us with the knowledge needed to prevent disease and achieve better health but also a transformational roadmap, both physical and psychological, that can help us find the courage within to make the changes needed, and self-program new habits without being o verwhelmed. verwhelmed.
COMMITMENT “I will obey…” means to care for safety, professional, personal and spiritual wellbeing of self and others, and be committed to positive change and constant improvement. Commit to reading this book without rushing any section or trying to take short cuts, and don’t reject out of hand any parts of the holistic expert advice that it offers you.
t raining ng , then Now take take your time to read r ead this book as I did, beginning with basic traini knowing the enemy, and continue reading and using the knowledge and practical strategies presented all the way to the end (your new beginning) to do a crucial selfassessment to build your own battle plan. Consider all the rock-solid scientific principles presented as user-friendly quick medical notes, take home messages, coach’s corner notes, and even the gourmet organic recipes …. Then use all this latest intelligence together to honor your own life. You won’t regret it! Craig D. Thorne, M.D., MPH, MBA, Internal Medicine/Preventive Medicine Health Health Educator, Educator, Avid Runner and Lifelong Lifelo ng Learner Assista Assistant nt Clinical Clinical Pro fessor, Johns Hopkins Bloomberg Bloomber g Schoo Schooll o f Public Health Health Vice President and Medical Director, Employee Health and Wellness, Erickson Living Washington, D.C. November 2014
PREFACE
Let us be honest. Most Most of o f us buy diet and exercise exer cise books bo oks because we want to to have a better body. We are motivated to become involved with diet and exercise in an attempt to change the shape and configuration of our physique. We are dissatisfied with with how we look loo k and feel. We are hard-wired by Nature. She has programed us to try to look and feel attractive. We seek to attract mates and reproduce in order for our species to survive. We need to recognize this underlying inborn need. The quest for selfimprovement is inherent and not rooted in vanity. This primal drive to attract a mate and reproduce is the reason there is currently a multi-billion dollar industry dedicated to dieting and “lo sing weight.” weight.” Individuals spend large amounts of money every year looking for the elusive Holy Grail of dieting and exercise plans. The truth is that all diets work and all diets eventually fail. There is even documentation of people losing weight eating nothing but Twinkies. If calories are restricted, body weight will be lost in the shortterm, but every “diet” invented eventually fails without exception. Dieters gain their lost weight back—and then some. The diet industry wants the cycle of losing and gaining to continue; continue; it is goo d for business. business. The exercise scene is no better. Everyone wants to follow the latest “bootcamp style style beat-down” beat-down” exercise exercise pr ogram. og ram. These prog r ams often result in injury, burno burnout ut,, or both after a couple of months. Then, the once-enthusiastic trainee looks for the next fitness guru to whip them into shape again to achieve the beach body of their dreams. The real “inconvenient truth” is that the only way for sustainable physical transformation to occur is through lifestyle change—changing your eating and exercise exercise habits long-term. We will show you how to achieve your body composition goals without starvation diets or sacrificing taste. We will show you how to build a strong and lean body, and how to produce a physical foundation to both achieve your fitness fitness goals go als and slow the the physical physical degeneration of o f aging. aging . The methods for achieving these physical goals are all here in Strong Medicine, Medicine,
but there is a loftier purpose to this book.
Jim Morr ison said, “No “No o ne here gets out alive.” alive.” Indeed Indeed the the years years of o ur lives are a precious gift. The quality of our lives—how we live in the time we have—is paramount. Too many of us are robbed of the irreplaceable years of our lives, by dying prematurely from preventable chronic diseases. An equal number live their later years in severely debilitated states of body and mind. The epidemic of chronic disease is expanding at an alarming rate.
The military theme of this book may seem over the top to some. In our view it is entirely appropriate given what we are facing. Make no mistake, chronic preventable disease is killing many more people on earth every year than the total casualties of past world wars. Diseases such as diabetes, high blood pressure, heart disease, neurodegenerative disease (Alzheimer’s), cancer, and obesity are the true moder n enemies. A battle battle plan is needed. These diseases do not kill in the dramatic manner of bomb and bullet, but are still ust as deadly. These insidious killers wreak havoc on our bodies and minds. Many of us have friends and family succumbing to these killers. The slow metabolic destruction of diabetes or neurodegenerative diseases such as Alzheimer’s dementia ro b our loved ones of the very very essence of who who they are (or (o r wer wer e). We need to pull our collective heads from the sand and look up from our smartphones for just a minute. We need a call to action shocking us out o complacency. Sustainable lifestyle change based on firm underlying scientific principles is the only way to truly fight the epidemic of chronic disease while simultaneously achieving the aesthetic aesthetic physical physical changes chang es we desire.
To achieve sustainable lifestyle change you must understand underst and the foundations foundati ons on which the recommended changes are built . We will teach you the scientific and theoretical foundations for transformative lifestyle change. If we do not take the time to teach you why we recommend something, we are no different from the thousands of programs out there that just say “do this” without explanation. If you just j ust want to be told t old what to do without witho ut understandi unde rstanding ng why, you are doomed to continue being led around by the nose by the latest fitness guru, and wandering from diet to diet in ignorance, wondering why you continue to fail.
We will provide the tools and strategies you need to generate progress. Those who take the plunge and institute our tactics will feel better by the end of the first week, and will see tangible changes in body composition by the end of the second week. Friends and family will comment on the “incredible change” at the end of the first month. You can and will undergo an utter and complete physical and physiological transformation in three months—90 days—without any draconian training or o r concentr concentr ation ation camp nutri nutrition. tion. This book provides a framework that regular people leading regular lives can perform at home. Strong Medicine is a roadmap that leads the serious individual from unhealthy and uncertain into ever-improving levels of health, wellness and fitness. Because we are all individuals with individual needs, we have left out a certain amount of specificity with our recommendations. This is done for a reason. You will have to experiment and individualize our tactics to your needs; we are giving you a foundation. Strong Medicine offers you the opportunity to self-assess and create a customized template that can and will enable you to transform towards the healthy state-of-being that has eluded you for so long. You are holding the handbook of transformation, but you have to use it. Once you understand the concepts and grasp the consequences (of your lifestyle choices) the burden is on you. End the blame game; let us take take responsibilit r esponsibility y for our actions actions and choices.
We need one thing fr om those those that seek seek radical r adical transformat transfor mation—a ion—a burning desire to change. To change the body we must first change our mind. Every thwarted physical and health goal you ever had lies within your reach.
T here are are no shortcuts... short cuts...
DOCTOR’S RX American society is facing a bank-busting, people-crushing crisis in which “we the people” ar e unifo r mly unfit, unfi t, unhealthy unhealthy,, unhappy and sickly. We continue co ntinue to have skyrocketing, out-of-control growth in preventable chronic disease. As a flat statement of fact, this bleeding artery could bankrupt our economy. We need a reality check: • In 1965, the United United States States spent spent 5% of the gr oss domestic product pro duct on health health care car e expenses. For every $1 pr oduced by the USA, USA, only a nickel was spent on health care during duri ng this time. • In 2010 this gr ew to 17% o f GDP. GDP. • In 2030 we will spend spend 25% of GDP on health health care expenses; for fo r every dollar made, a quarter will be spent on medical care. • The United United States States spends mor e on health health care car e per citizen than any other country in the world, but we are ranked 37th for the effectiveness of our health care system. We spend more money on health care and have the most advanced diagnostic tools and technologies found anywhere in the world. But we are still failing miserably at treating the diseases that are costing us the most, both in human suffering and monetary monetary cost. co st.
The majority of health care dollars are spent on the treatment of preventable diseases: obesity, diabetes, and heart disease. Cancer is responsible for a significant amount of resources reso urces and suffering, suffering , yet many many cancers cancers are preventable preventable as well. Health care analysts give multiple reasons why we are spending ever more managing these diseases and predictably point to the growing aging population, costs of medications, costs of testing, and inefficiencies in providing medical care. An alarming number of healthcare professionals have simply given up on the idea of preventing these diseases. Managing diabetes, obesity, and heart disease is incredibly expensive, but for the most part, we should not have to manage these diseases long-term. They are reventable and for the most part, reversible .
It has not been for lack of trying. The Public Health community is filled with many talented and dedicated people who work daily attempting to improve public health through prevention. Billions of dollars are spent yearly on failed (often
doomed before they start) public health campaigns. This begs the question: why do we continu continuee to fail? It certainly is not for a lack of funding or effor t. Why do we continue to have ever-expanding growth rates in preventable chronic disease despite public health efforts?
Logic dictates that there are 4 possible answers to this question:
1. THE MESSAGES/RECOMMENDA MESSAGES/RECOMMENDAT TIONS FOR PREVENT PREVE NTION ION ARE WRONG Many of the messages are sound, but there are an unacceptable number of preventative recommendations based on outdated science that are flawed from their foundation.
2. COMMUNIC COMMUNICA ATION TI ON IS FLAWED FLAWED AND AN D INEFFECTI INEFFEC TIVE VE Public health authorities seldom explain “why” people should follow the recommendations in ways that can be easily understood, while still maintaining a sound scientific foundation. Public health officials usually underestimate the sophistication of the general public. The problem is not the public’s inability to grasp physiologic concepts, it is the public health and medical community’s inability to effectively communicate co mmunicate these concepts. Let us (public health) not blame blam e the public for our short-comings.
3. PEOPLE ARE CONFUSED CONFUSED BY CONFLICTI CONFLIC TING NG HEAL HEALTH TH RECOMMENDATIONS There is a tremendous amount of inconsistent information coming from “authoritative” sources, which is then further jumbled by popular media (internet, news media, etc.).
4. PEOPLE ARE UNWI UNWILLING LLING TO CHANGE CHAN GE Stopping preventable diseases usually requires lifestyle changes that many seem unwilling to make. In an oversimplification: many people are addicted to the substances, substances, foo ds, lifestyle and habits that created cr eated their their preventable disease. The core essence of this book is the identification, and effective communication of underlying causes of preventable health problems. We then present informed, ractical solutions that empower the reader. This empowerment and resulting self-
efficacy is essential, essential, as as many of us cannot rely o n our health health care providers pr oviders to teach teach us this type of information.
DOCERE? The U.S. healthcare system is currently at a crossroads. A 15-minute doctor’s office visit is becoming the norm, driven by the economic realities of a failing system. There is simply not enough time available for the physician to provide detailed preventive education in an individualized manner. The word “doctor” is from the original Latin docere, which means, “to teach.” Most of us who have experienced a recent visit with their doctor would probably agree that there is very little doctor-to-patient teaching happening in modern medicine. Most of the doctor’s time is spent managing medications to treat lab values instead of really treating the patient—much less providing any individualized education on prevention. If given the time, do most physicians currently have the education to impart this type of preventive teaching?
PRIMUM NON PRIMUM N ON NOCERE N OCERE (FIRST DO NO NO HARM) The public trusts the opinions and recommendations given by their health care providers. Unfortunately, most physicians simply do not have the expertise to give science-based recommendations regarding nutrition and exercise; but do so anyway. It is ironic that the medical education of our physicians devotes almost no time to learning exercise science and nutrition. Instead, most of their time is spent learning the use of pharmaceuticals. Chronic diseases are not cured by drugs, they are only managed. Lifestyle changes such as proper nutrition and exercise can and do cure many chronic diseases. Why are our physicians not better educated to put these interventions into practice? Too many doctors are put on pedestals by the public and viewed as all-knowing oracles possessing papal-like infallibility. Obviously this is nonsense, especially when it comes to exercise and nutrition. Many of my colleagues are just parroting what they have heard about nutrition and exercise and pass this on to their patients. They do not truly understand the subjects from the ground up like they do pharmaceuticals. Also, many doctors have long since forgotten the basics of biochemistry, anatomy and physiology learned in medical school. If we are going to practice prevention and health promotion, we as a profession have an obligation to really learn our craft from the ground up, using basic science as a starting point. We need
to use a “first principles” foundational approach to critically examine current orthodox recommendations. Physicians that use basic science as a foundation for critical thinking about wellness practice can be invaluable in this respect.
IT’S YOUR FAULT TOO... On the flip side, there is also a serious lack of elementary scientific literacy in our society. I do not buy the excuse that a basic working knowledge of the human body is beyond the grasp of most people. I know plenty of people who know EVERY detail about baseball and football statistics—without being a pro athlete. Countless men have an extensive knowledge of the mechanical workings of an automobile engines—yet learning a little about how your body works is somehow past our mental capacities? I think think not. We all NEED a basic working knowledge of the body to inform our lifestyle choices and preventive strategies; how else can we be true partners in our own health care?
PREAMBLE PREAMB LE TO TO PREV PREVEN ENTION TION
We are all individuals with individual needs and goals, but we all belong to the human species. So, the underlying principles of biochemistry and physiology still apply to all of us. We will show you how to use these ‘guiding principles’ placed within a central framework that still allows for individuality. This framework also allows for the incorporation of exciting new scientific advances. As long as we build on a solid foundation of underlying principles, subtle changes are easy to make. If we need to remodel our approach as new information comes to light, no worr ies—we ies—we have built built our house ho use on a strong foundation. foundation. This is not a “lose weight weight quick book,” though though your physical physical transfor mation mation will be profound through consistent application of the principles and tactics presented
within. We are after sustainable and long-term health, not quick fixes. The goal is to empower the reader and enable anyone to achieve their health and fitness goals while while joining jo ining the larger fight against chro chronic nic disease. disease.
Chris Hardy Har dy — Pacific Nor thwest, thwest, 2014 2014
THE COACH’S COA CH’S PERSPE PERSPECTIVE: CTIVE: IMPROVING THE FLESH MACHINE During the Dark Ages, trade guilds emerged as craftsman bonded together to share trade secrets. Rather than hording information, these men recognized that they all had a common quest and by combining their collective knowledge, they could dramatically “up” their level of collective expertise. A rising tide lifts all boats. When a guild is formed and functioning, the tradecraft always improves. Our guild is a group of likeminded individuals drawn together by a common quest: how best to heal, detoxify, mold and sculpt the human body while amplifying every athletic and health attribute. My little sliver of expertise is human performance and how to improve it. My job entails working with the world’s best strength athletes athletes and finest spec ops soldier so ldiers. s. My My rol r olee is to make the best in the the world wor ld better. better. The irreducible core of our guild is a doctor and a coach who are of one mind. We want to share techniques, strategies, tactics and philosophies that actually work. The doctor and coach have seventy years of combined experience, each operating in distinctly different worlds—but are drawn together by the gravitational pull of physical improvement. Not imagined or subjective improvement, but dramatic and objective improvement. The path of progress in each of our parallel universes (medicine and high level athletics) eventually intersected. The doctor and the coach met, compared notes and were struck by how the knowledge gleaned from each other’s world upped their own game—the coach became a better better coach and the doctor became a better better doctor. doctor . This book boo k is a transfor mational mational handbook based on proven pro ven tact tactics ics and rock-solid ro ck-solid science. “Strong Medicine” is the result of our alliance working in full-flight. We have a creative synergy that allows us to describe and prescribe techniques and tactics that are immediately useable by motivated readers. We are big on motivation. Give me a motivated, fired-up, morbidly obese individual over a nonchalant elite athlete any day of the week. For the truly motivated individual lucky enough to stumble across our methodology, transformation is not a matter of “if,” it is “when.” Members of our guild all seek physiological improvement—across the board. Name a physiological benchmark or category and we will start thinking about ways
to improve that capacity or benchmark. That is what we do for a living. In our world of uber-elite military and world-class athletics, results are the only thing that matter and the the only o nly thing that earns r epeat business. We have a ton o f r epeat business. business. We have extensive experience in engineering physical transformations; we churn out renovated humans like Chrysler churns out Dodge Vipers. Our results are based on the skillful blending of exercise, diet, psychology, and decades of empirical experience. Our insider techniques and non-traditional, counterintuitive tactics are unknown outside of a small circle of uber-elite military spec ops warriors, worldclass strength athletes, outside-the-box coaches, renegade scientists, and innovative medical medical pro fessionals. Members of our guild-alliance all are concerned with the same eternal core problem: how do we improve the form and function of the human body? Any and all aspects of fitness, all of remedial medicine, every diet and exercise tool, each and every fitness device, health profession, athletic tactic, strategy or approach—all were created to improve the human condition in some way. The core question is, “How exactly do we improve the human condition?” How do we improve the form and function of—as William Burroughs labeled the human body —“The Flesh Fl esh Machine.” Our guild is at the exact intersection of cutting-edge science and real-world medicine melded with high-level athletics, results-producing coaching, and elite military preparedness training. We combine tactics from both worlds and process these volatile methods to make them user-friendly for regular people. Our challenge was to achieve this ‘userfriendliness’ without compromising the vital, effective essence of each protocol. We have met this challenge by creating a multitier system that allows anyone at any fitness level to participate. We offer a game plan for the few with the gumption to put these ideas into practice. It is an indisputable fact that the methods and methodologies we are presenting work—these exact strategies are being used right now by the best in the world. The Tao of fitness exists and we can show you yo u “The Way Way..” We We can show sho w you how ho w to custom design your very own transformational template—but you need to learn some science and biology ultra-basics to be successful. We will teach you “The Process.”
In our world you do not get to skip ahead to the training, eating, and fun stuff without first getting the scientific, medical, and biological facts straight. We are teaching you how to fish—we are tired of giving you fish .
Marty ar ty Gallagher Gallag her — Pennsylvania, USA, USA, 2014 2014
INTRODUCTION
We are at war, and we are losing. We are losing badly. This is not a war against countries or ideologies. This war is not fought with bullets and bombs, but with pharmaceuticals. The frontlines of the battleground are our hospitals, clinics, and local doctors’ offices. This is a worldwide war against chronic disease and there are few places on Earth left untouched. The enemy is upon us in full force and the frontlines are collapsing. Despite Despite being equipped with with the the most mo st technolo technologi gically cally advanced weapons, our best soldiers—the medical professionals—seem unable to push back and destroy the enemy. enemy. At At best, best, they are only slowing slo wing the advance of this faceless adversar y. We We ar e throwing more and more resources into the war effort and are still failing miserably. The situation seems hopeless, as the war-effort is bankrupting us. We need your help as the last and best hope for pushing back the relentless advance of chronic disease. To become an effective fighter in this war, you will need training. We have to teach you how the enemy works from the inside out. You must under under stand the the enemy befor e you can effectively eff ectively fight fig ht and decisively win. This war will be fought fo ught one small s mall battle battle at a time, by one o ne individual at a time. You You are ar e the last line of o f defense and can become the key to to ultimate victor y. You will be rewarded for your courage and effort with the optimum health of your mind and body. You will emerge from your training with the physical appearance, fitness, and vitality that mirrors your full genetic potential. Join us in this fight. You are needed.
PHASE HA SE I: BASIC TRAINING Strong Medicine Basic Training is not easy, but can be accomplished by anyone with the requisite motivation. The foundations of your training are the central themes that underlie health and disease, and a primer on nutritional science and human metabolism.
It is important to have a basic understanding of this section to prepare you for the battle battle ahead. You You will be intro i ntroduced duced to concept co nceptss which may not no t be familiar. famil iar. There is quite a bit of information in Strong Medicine Basic Training, so spend some time here. Do not worry if you don’t get it all the first time through, because we will reinforce this training throughout the book. We do not expect the new to become a warr warr ior overnight. over night. Strong Medicine trainee to While you ar e learning the the fundament fundamentals als in basic training, we will also give you an early taste of the Strong Medicine Defensive Tactics. These tactics can immediately be put into action against the enemy—even without the full knowledge of the adversary. The Strong Medicine recruit who graduates from basic training will be ready for advanced training to understand the enemy and advanced tactics to stop chronic disease and optimize health.
PHASE HA SE II: II: KNOWING KNOW ING THE ENEMY Your Strong Medicine trainers know the enemy. We have gathered the military intelligence and analyzed their weaknesses. We know the chinks in their armor. We will systemat systematically ically impart this knowledge knowledge to you, as you ar e no longer l onger a recruit, r ecruit, but but still still have a lo t to to learn befor e you can lead your own for ces into into battle. battle.
You will get in-depth defensive tactics, tactics, and will under stand the the reasons r easons behind o ur tactics. Our tactics are graded as gold, silver, and bronze. The gold tactics are particularly devastating to the enemy and should be mastered early on. The silver and bronze tactics are very effective as well, and will ensure chronic disease stays down once it i t is put down. During this phase of your training we will periodically bring out Coach Gallagher to give you a reality check. He is a master Strong Medicine trainer and coach. He is rough around the edges but will give you the brutal truth without political cor r ectness— ectness—somethin something g we need need to to hear fr om time to time. Once you have gained the requisite knowledge about the enemy, you are ready to put your training into practice. You will be able to turn the Strong Medicine Defensive Tactics into a devastating offensive strategy against chronic disease.
PHASE PHA SE III: III: BATTL BATTLE E PLAN PLA N We will formulate the Strong Medicine battle plan in Phase III. This plan will be drawn from the knowledge and tactics you learned in Phases I and II. We will show you how to individualize a plan that is optimum for you. Phase III will also give you a stripped down but highly effective physical training program using original techniques and expert tactics to transform a flaccid body into a chiseled and powerful war machine worthy of a Strong Medicine Warrior. You will also get a short section on measurable analytics for monitoring the inner workings wor kings of your “flesh machine” machine” and and keeping keeping you o n the the right r ight tr tr ack. We have included the “military intelligence” we gathered on the enemy and the foundations for our tactics in the scientific references at the end of each chapter for your further reading and research if desired. These references are the sources and scientific scientific found fo undation ation on which we we have built built your training pr ogram. og ram. The science is always kept as basic as possible in Strong Medicine without losing the meaning, but trainees who want more should look for the Digging Deeper and the book. Technical Note boxes throug hout the Those of o f you willing to enlist and and join joi n us in the war war on chro nic disease, disease, let us get to it. Be a participant in this fight, not a casualty. Strong Medicine Basic Training awaits...
PART I
BASIC TRAINING
BASIC TRAINING I:
CENTRAL THEMES IN DISEASE AND HEALTH
This section teaches the rules of war before you hit the battlefield. Some of the concepts may be brand new to you, but it is important to spend some time here before moving on. If you do not quite get this section the first time through, do not worry, we will return to these five themes throughout your training. These themes are the underlying foundations of our defensive tactics against chronic disease, and for m our o ur templat templatee for achieving achieving your yo ur genetic genetic potential potential for fo r health health and fitness. fitness.
1. 2. 3. 4. 5.
Inflam Inflamm mation at ion and Oxidat Oxidative ive Stress St ress T he Gene-Environm Gene-Environment ent Connection Hormesis T he Stress Response Allost Allostasis asis and t he “Stress Cup” Cup”
We will start with inflammation and oxidative stress. These two processes are the underlying causes of most (if not all) preventable chronic diseases. It is crucial to understand how they work. Get to work recruit!
CENTRAL THEMES PART I:
INFLAMMA INFLA MMATION TION AND A ND OXIDATIVE OXIDATIVE STRESS
THE 4 CARDINAL SIGNS OF INFLAMMATION:
1. 2. 3. 4.
Redness (Rubor) Heat (Calor) Swelling Swelling (Tumo (Tumo r) Pain (Dolor)
Two interrelated physiologic processes— inflammation inflammation and oxidative stress — are recurrent themes in this book. These two processes are at the same time crucial to our survival as an or ganism and underlying underlying causes of disease.
INFLAMMATION The inflammatory response is directed by cells in our immune system and is
infectious diseases. absolutely essentia essent iall to heal fr om injury and to combat infectious During an acute injury or infection, redness and heat are produced from increased blood flow to the area. Swelling is the result of fluid and protein “leaking” from the blood vessels into the tissue. Pain results from the stimulation of nerve endings by certain chemical “messengers” called cytokines released by immune cells. This process can last for several days while the “battle” to clear the invading infection takes place, or the cells damaged from an injury are cleared. After the “battle,” things slowly return to normal. This is the basic process of acute inflammation.
T he primary primary generato g eneratorr of o f inflam inflammation (and result result ing ing oxidative stress) st ress) in our bodies is the immune system. A basic survey of the immune system is in order. The immune system is incredibly complex, and we will simplify immunological concepts without without dro wning in the details. details.
IMMUNOLOGY 101
T he Guardian Guardian The cells of the Innate Immune System are like the guards at the castle gate. They deal with anyone who “looks or acts suspicious.” In practical terms, this could be an initial encounter with bacteria/viruses or “foreign” protein fragments. The innate immune response is not targeted at specific antigens (tar (t argets) gets), but is a general protective response to anything “foreign.” Innate immune cells like dendritic cells or macrophages can “take” foreign invaders “prisoner”, destroy them, and display pieces of the prisoners like heads impaled on pikes mounted on the castle wall. Some of these guardians also r elease inflammatory chemicals called cytokines.
T he Adaptive Assassin Assassin Cells of the Adaptive Immune System are like assassins. They are known as Tcells and B-cells . Once they encounter pieces of a prisoner caught by the dendritic cells or macrophages of the innate immune system, they “adapt” themselves to become perfect assassins assassins for this this specific type type of prisoner. priso ner. The assassins target the specific patterns of proteins (antigens) unique to this “prisoner” for destruction. Then they clone themselves to make an army of assassins with one goal—destruction of this specific type of prisoner. These deathdealing clones spread throughout the body and wait to encounter another invader with a protein pattern identical to the original prisoner.
T he Assassin Clone Army Army These assassins are persistent, and wait in the shadows for their target to appear again. Once they encounter their prey, they release a barrage of destructive power in the form of antibodies and inflammatory cytokines.
The T-regulatory cell hippie preaching tolerance: “ Just stop the t he violence man! ” It is important to note that the immune system is not completely devoted to destruction. There is a type of T-cell in the adaptive immune system that helps control the assassins and produces an anti-inflammatory response. This type of Tcell is called a T-regulatory cell (Treg). Treg cells are like hippie antiwar protesters. We need a balance between protesters and assassins to prevent the immune system from attacking our own body tissues. Autoimmunity is the process of the immune system attacking attacking the body. body. The immune system generates and controls the acute inflammatory response needed needed for the the beneficial functions functions o f proper pr oper wound wound healing, fight fig hting ing infection, infection, and recovery from exercise. Chronic inflammation is also generated by the immune system in a process that is similar to acute inflammation, but instead of stopping after after several days, it continu continues es for much longer.
KEY POINT: Chronic inflammation is the result of continuous stimulation of the immune system. The constant release of inflammatory “cytokine” chemical messengers wreak havoc on the body and your health.
MEDICAL MEDICAL TRIVIA: T RIVIA: It is estimated that that 70-80% 70-80% of our immune system lives in o ur intestinal intestinal tract (our “gut”). “gut”).
OXIDATIVE OXIDATIVE STRESS STR ESS Working in tandem with inflammation is oxidative stress. Most of us have seen rust on old cars. Rust is the oxidative process at work on metal alloys containing iron. In the presence of moisture, oxygen in the environment reacts with iron to produce rust. Oxidation reactions also occur in our bodies. They are essential processes pro cesses in our physiolog y—unless y—unless they they get out of control. contro l. The oxygen free radical (also called reactive oxygen species, ROS ROS) is a type of molecule that causes oxidation and oxidative stress. ROS can form from various external and internal stressors such as pollution, infection, radiation, and cigarette smoking. ROS molecules are also products of normal metabolism in our cells . Many processed foods contain ingredients prone to oxidation, and can increase oxidative oxidative stress far beyond normal levels. Chemically speaking, stable molecules have electrons that travel in pairs, but a free radical is a molecule that has a lone unpaired electron. This unpaired electron makes the molecule extremely unstable and chemically reactive. This type of molecule really “wants” to pair another electron with the lone electron and will take an electron from a nearby molecule. “Stealing” an electron from a neighboring molecule will damage structures like cell membranes and even DNA. Long-term DNA DNA damage by fr ee radicals r adicals can cause mutatio mutations ns leading to cancer.
The Antioxidant Defense System (ADS). This is your body’s way of dealing with free radical radicalss (oxi (o xidative dative stress). st ress). They T hey are the “bouncers in the bar.”
T he “Free Radical” drunk guy thi t hinks nks he is is a superhero by the end of t he night night,, looking for some action.
QUICK FACT: You can think think of the free r adical as a drunk guy in a bar looking lo oking fo r a fight. The body has mechanisms to deal with free radicals called the
antioxidant defense systems (ADS). These systems are like bouncers in the bar who take the drunk outside before he hurts anyone. The balance in the body between the free radicals and the antioxidant systems determines oxidative stress. A couple of drunk guys can make the club experience somewhat entertaining for the other patrons, but the bouncers (ADS) will take care of them in shor shor t order.
T he ADS ADS “bouncer” taking taking out o ut t he trash... a couple couple of free radical radicalss are no problem. If the free radicals overwhelm the antioxidant defense systems (the bouncers), there is a state of high oxidative stress. The state of high oxidative stress is the result of free radicals starting chain reactions. The chain reactions form large amounts of new free radicals— like like a drunk who starts a bar fight that the bouncers cannot control. A free radical chain reaction can damage the membrane of a cell and lead to destruction of the cell. On a larger scale, it can damage your health.
High oxidative stress overwhelms the ADS “bouncer”
THE DELICATE BALANCE OF OXIDATIVE STRESS
The antioxidant system attempts to counteract free radicals generated internally by physiolo physiolo gic processes pro cesses and exte exterr nally from fr om the the environment enviro nment (food, (foo d, wate water, r, toxins, etc.). This balance is a constant push-pull process. Tipping the balance toward free radical generation increases oxidative stress and the antioxidant system quickly responds. Spending Spending too much time in either either dir ection ection is not a good go od thing long -term. -term.
The body actually needs some oxidative stress to maintain health, but not too much. Too much oxidative stress creates disease .
KEY POINT: It is very important to understand that some inflammation and oxidative stress is normal, beneficial “dose” normal, necessary, and even beneficial. This beneficial of inflammation inflammation and oxidat o xidative ive stress works thro ugh a process pr ocess called adaptation to stress str ess known as allostasis. hormesis, part of the positive adaptation allostasis. Low “doses” of oxidative stress may even extend our life span. Some beneficial effects of inflammation and oxidative stress: 1. Our immune system makes use of inflammation and oxidative stress in a controlled manner to kill invading micro-organisms. 2. Exercise and some compounds in fruit and vegetables contribute to beneficial inflammation and oxidative stress. Normal physiologic processes like metabolism of glucose and fats create free radicals (ROS). Your antioxidant systems can usually deal with these free radicals (except in the case of diabetes). A properly working immune system generates inflammation and oxidative stress to fight microbial invaders. Increased oxidative stress from the outside environment can also stimulate the immune system to produce inflammation. Inflammation and oxidative stress always travel together. “Importing” free radicals by eating rancid fats from processed foods adds extra oxidative stress that your system may not be able to control. Conversely, eating organic vegetables and fruit can stimulate the body’s internal antioxidant systems (ADS), making them stronger, more resilient, and more resistant to inflammation and out-of-control fr ee radicals.
KEY POINT: Where there is oxidative stress there is inflammation. Where there is inflammation there is oxidative stress. The two processes are inseparable.
DURATION MAKES ALL THE DIFFERENCE... Short-term increases incr eases in inflammation inflammation and oxidative oxidative stress are ar e necessary, necessary, nor mal, and even beneficial.
Short term, low lo w levels levels of o f oxidat o xidative ive stress are beneficial. beneficial. Intermittent short-term inflammation and oxidative stress are essential for proper functioning and defense of your body. However, if these processes continue for long periods of time, disease develops. Long-term inflammation and oxidative
stress st ress are t he underlyin underlyingg causes for fo r chronic preventable preventable diseases. The “link” in the chain from the underlying sources (the enemy) to chronic oxidative oxidative stress and inflammation inflammation r esulting esulting in chro nic preventable disease.
You will see the central theme of chronic inflammation and oxidative stress as underlying causes of disease throughout the book. In later chapters, we will focus on the sources of chronic inflammation and oxidative stress. These sources are the underlying causes “linked” to chronic inflammation and oxidative stress and the resulting chronic chro nic diseases. These sources are the enemy that we are fighting.
KEY POINT: Heart disease, diabetes, cancer, high blood pressure, neurodegenerative diseases (Alzheimer’s), asthma, and accelerated aging all have chronic inflammation and oxidative stress as underlying causes.
STRONG STRONG MEDICINE MED ICINE Strong Medicine is all about breaking the link between the enemy sources of chronic inflammation and oxidative stress, thus preventing chronic disease. We We will identify the enemy in Phase II of your training.
Most chronic inflammation and oxidative stress which cause preventable diseases are the result of our body trying to adapt to the outside “environment.” This environment includes...
• • • •
T he food foo d we eat. T he quality quality of our sleep. sleep. Our physical activi act ivitt y. T he stress st ress in in our lives. lives.
Our environment reacts directly with the genetic code contained in our DNA, and affects the way way our body functions in i n health and disease. As modern moder n humans, we can control many aspect aspectss of o f our o ur environment, environment, therefo therefore re we have have the the potential potential to cont co ntro ro l how our genes are expressed in a way to optimize health and achieve our fitness goals. The next section will describe just how this works.
CENTRAL THEMES PART II:
THE GENE-ENVIRONMENT GENE-ENVIRONMENT CONNECTION
GENETICS AND A ND EPIGENETIC EPIGENETICS S Our genes form a foundation that determines who we are as individual humans. The DNA contained in our genes makes each of us unique. While we have more similarities than differences, seemingly small genetic variations make us unique individuals. When DNA was discovered as the molecule of heredity in 1952, it was thought that genetic preprogramming was set in stone, and we all had individual predestined genetic g enetic fates. The idea i dea that DNA DNA is set-in-stone dominated do minated the latter latter half of the 20th century. One of the central ideas in evolutionary theory is that genetic variations happen at a relatively slow pace. The slow evolving changes in the DNA code are called mutations. As the 21st century began, another idea took hold in genetic research—a concept known as epigenetics, literally literal ly defined as “upon the gene.” Our genes are coll —instr uction n manuals manual s or o r “recipes “r ecipes”” fo r making co llect ections ions of DNA —instructio specific proteins in our bodies. The proteins made from the DNA instructions have a huge variety of functions.
• Prote Pro teins ins make up the the physical physical structure structure of our body body,, including including organs, or gans, blood vessels, skin, etc. • Pro teins function as the machinery machiner y that makes the necessary chemicals chemicals and hormones our bodies need. • Pro teins make up our immune system, which defends against invaders. The small sections of your DNA that contain specific instructions to make a specific protein are called genes. You can think of a gene as a single recipe in a cookbook that tells you how to make a specific meal. The human genome is the total collection of genes in our o ur DNA. DNA. The genome g enome is the complete cookbook cookboo k containing containing over 20,000 “recipes” (genes) to make specific proteins.
KEY POINT: The human geno me is the complete DNA DNA “cookboo “coo kbook” k” that contains over 20,000 genes. Each gene is a specific “recipe” to make a protein. In traditional evolutionary theory, changes to genes by mutations could be thought of as changing the recipe. This would be like taking a cake recipe that or iginally called for 4 eggs, and changing changing the the requirement requir ement to 5 eggs. Wheneve Wheneverr you read the cake recipe in the future you would see the instruction to use 5 eggs. Mutations physically change the recipe. The cake produced by the new recipe would be different than the previous cake, just as any protein produced after a mutation would be different than the original protein. The epigenetic system has quite a different way of acting on genes. In response to environmental signals (signals that originate from outside the body), the epigenetic system will “turn off” or “turn on” different genes. Epigenetics does not change the individual recipes ; the cake will continue to be made with 4 eggs. Epigenetic signals determine how many cakes are made, or if they will be made at all.
TURNING “OFF OFF”” Within the complete genome cookbook, epigenetic signals can make the pages containing certain recipes “stick together” so that they cannot be r ead. If you cannot read r ead the recipe you cannot canno t make the the specific meal. With DNA, DNA, if you cannot canno t read the gene g ene you cannot canno t make the the protein. pr otein.
TURNING “ON ON”” Epigenetic Epigenetic signals can also “boo kmark” a specific recipe r ecipe so it is made mor e ofte o ften. n. Genes “bookmarked” by epigenetic epigenetic changes will make large lar ge amounts amounts of their specific pro teins. teins. Similar to a favor ite recipe for pot roast or BBQ, the bookmarked recipes in the DNA cookbook are made often. If you could co uld only coo k meals that that were were in i n your cookbook, coo kbook, you would not be able to make meals on the recipe pages which are “stuck together.” You would make meals with the “bookmarked” recipes more frequently. This is a simplified explanation for how epigenetics works. Different genes (“recipes”) will be tur tur ned off o r turned turned on o n to meet the the internal or external external demands placed on the body. body. Some recipes will have the pages stuck together, and some will be bookmarked, depending on your “environment.”
YOUR YOUR “ENVIRONMENT” “EN VIRONMENT” The American American Herit Herit age ag e Dictionary Dictio nary defines “environment” as: “all of the biotic and abiotic factors that act on an organism, organism, population, population, or ecological community community and influence its survival and development.” We
refine refine the t he definition: definition: environment environment is our food fo od and water int int ake, air quality, physical surroundings, physical activity and lifestyle . Our transformative process focuses on food selections, activity, sleep and stress—the stress—the factor factor s in our o ur environment we we can control. Epigenetic changes impact i mpact how our genes interact i nteract with with what we eat, eat, our activity level, and and how we live our lives every ever y day. day. Epigenetic changes can make profound differences in our physical wellbeing. Handled incorrectly, our bodies will fail us prematurely. Handled properly, we can hold back the sands of time. Beneficial Beneficial envir onmental changes in i n diet and exercise will reverse preventable diseases such as type-2 diabetes. Epigenetics suggests that modern moder n maladies should be thought of as mismatches between a person’s genetics and their environment. By correcting mismatches, we can transform from afflict ion to health. health.
EPIGENETICS EPIGENE TICS CASE CASE ST STUDY UDY This hypothetical case study of identical twins illustrates how epigenetics works: John and Steve are born identical twins . Their “cookbooks” (genomes) are exactly the same down to every last recipe. In their late teens, John decides he wants to be a bodybuilder and Steve wants to start training to compete in ultra-endurance running. Before each man immerses himself in his newfound athletic passion, both stand 5’ 10”, weig weigh h 170 pounds, and have have a body composi com position tion of o f 10% body fat. John’s bodybuilding training consists of long hours in the gym lifting heavy weights to self-inflict intense muscle trauma. To speed recovery, he eats large
amounts amounts of protein pro tein.. John is sending “environment “enviro nmental” al” signals to his “cookbook” “cookboo k” for muscle growth. The “recipes” (genes) for muscle growth are bookmarked by epigenetic epigenetic signaling. Because of his chosen epigenetic path, John’s recipes for sustained energy output (the kind needed for distance running) have had their pages “stuck together” and are largely turned off. These unintended consequences happen so John can adapt to the specific environmental stresses (lifting weights while eating large amounts of protein) he is placing on his body. His muscles grow significantly, but he is in no shape shape to run r un a single mile. Steve begins his training at the same time as John. Steve stays away from the weight room and wears out several pairs of running shoes. He is training for a 50mile ultra endurance race. He trains his body to maintain high energy levels for extended periods of time. The “environmental signals” this type of endurance training is sending his “cookboo k” is for muscle endurance, endurance, not not muscle growth gr owth.. Over the months, while John is packing on muscle mass, Steve is leaning out, shedding unneeded muscle. Steve’s high volume endurance training enables his muscles to continue to power his running for hours on end, but he is certainly not going to win any bench press competitions.
KEY POINT Epigenetic changes ar e not set in stone once they are made. m ade. As your environment changes, your epigenetics will change. After a year of training, the identical twins are no longer identical. John is a muscled-up 200 pounds and gets winded running around the block. Steve is down to a rail-thin 140 pounds and has lost a significant amount of muscle mass and strength. John and Steve still have identical genetics , but epigenetic changes caused by different environmental stresses have made their bodies different—they are no longer identical identical after after a year o f sport spor t specific specific training. training. Epigenetic changes ar e not “set” once they are made. Recipes Recipes that wer weree once stuck
together can be bookmarked and vice-versa, depending on the signals from the environment.
WOMB TO THE GRA GRAVE VE Your epigenetic changes started when you were developing in your mother’s womb. What your mother ate, drank, and the stress she experienced while pregnant had a direct impact on your environment in utero. Epigenetic changes began in response to this environment and persisted after your birth. There is actually good science now which shows that some epigenetic changes can be passed from parent to child, much like traditional genes. A mother’s metabolic health and stress during her pregnancy can be passed down to the fetus in utero. The fetus’s “environment” consists solely of the mother’s body. If this environment is stressful, the epigenetics of the fetus will change to adapt to the stresses. Stresses in the mother such as gestational diabetes, psychological stress, and malnutrition WILL cause epigenetic changes in the fetus. These changes can exist in the infant after after birth. bir th. Recent epigenetic research on mothers who have experienced extreme stress prior to and during pregnancy has shown that their children are likely to develop anxiety and are less able to cope with stress later in life. Epigenetic changes are thought thought to to be responsible r esponsible for passing stress r esponses from mo ther ther to child.
RESEARCH UPDATE Recent r esearch esear ch has indeed shown that gestatio gestational nal diabetes in the mother during pr egnancy places places the the child at higher risk ri sk for developing developing o besity besity and diabetes diabetes later in i n life. It It is also clear that this happens happens through thro ugh epigenetic changes in utero. It is important to remember that epigenetic changes take place so that we can adapt to our current environment. This is why creating the best environment possible (the mother’s health) during pregnancy is crucial to the future health of the child. This lifespan view of the impact of the environment on our genes through epigenetic change has become a very important field of scientific study in recent
years. In the “nature versus nurture” environment argument, genetics trumps envir environment onment or environment tr tr umps genetics. genetics. The balance balance tips tips in favor of “nurture” “nurture” based on the findings of cutting-edge epigenetics research. “Nurture” starts in the womb. Just as the genome describes your complete DNA cookbook, the epigenome describes the current state of all of the recipes in the cookbook as “bookmarked” or “stuck tog tog ether.” ether.” As your environment changes during your life, changes in your epigenome take place to compensate. Mutations to DNA still happen and are important, but epigenetics provides real-time adaptations to environmental stresses that mutationbased DNA changes cannot match.
THE HEALTHY COOKBOOK Your environment includes nutrition, exercise, sleep and stress. These shifting shifting environmental environmental characteristics characteristics “boo kmark” and “stick together together ” the the generecipes g enerecipes of your genome-coo kbook—every kbook—every day, day, month, and and year. The ability to read (or not read) the individual recipes and how much each is made into a “meal” determines disease or health. This is highly individual individual and the the reason no diet or exercise plan is perfect or works for fo r everyone. We can optimize your epigenome by providing it with the proper pro per environmen enviro nmental tal signals signals for health. health. Epigenetics has emerged as a major way that we adapt to our environmental
stressors. These stressors can change our epigenome for better or worse. Exercise and food are beneficial in the right amounts, but unhealthy in the wrong dose. Figuring out these these beneficial beneficial doses leads us to the concept concept of hormesis. hor mesis.
CENTRA CEN TRAL L THEMES THEME S PA PA RT III:
HORMESIS
Stress is perceived as a negative thing. Yet exercise is self-induced stress and can be very beneficial. A central concept, common to all organisms, is a need for environmental stresses. In order to survive, thrive, and ultimately live our lives to their fullest potential, environmental challenges must be overcome. Nietzsche’s axiom, “That which does not kill me makes me stronger” is profoundly accurate in the world of DNA, genes and epigenetic science. Organisms —human or other wise—either wise—ei ther adapt to challeng chall enges es by becoming beco ming strong str ong er or they die. Challenges in the right amounts are not only beneficial, but necessary. Think of the profound differences in overall health and appearance when comparing the physique of an out-of-shape individual to that of a life-long athlete who exercises regularly reg ularly and eats eats a sound diet full of natural natural fo ods. A life devoid of physical challenges and inactivity sets a person up for an early death from metabolic diseases, obesity, muscle loss, fractures of weak brittle bones, etc. Unfit people degrade rapidly as they age. In our unchallenged, unfit era, this has unfortunately become the norm. Physical challenges of the requisite intensity slow the aging process to a crawl. Favorable and appropriate environmental challenges make our bodies stronger and more resilient through a process called hormesis. The hormesis concept originated in the study of toxicology. Although hormesis is still considered somewhat controversial controver sial in the academic academic circles o f toxicology, toxicolo gy, we we view hor hor mesis as a unifying
concept applicab applicable le to all enviro nmental nmental stressor s.
“THE POISON POISON IS IN THE DOSE”
Paracelsus: “The dose makes the poision”. Paracelsus, the 16th century Swiss physician and father of toxicology said, “Poison is in everything, and no thing is without poison. The dosage makes it either a poison or a remedy.” In other words, the amount or dose of a substance is what makes it harmful or o r helpful. helpful. Hormesis is an extension of Paracelsus’ statement. It implies that there are necessary doses of environmental challenges. The right “doses” provide beneficial adaption, while “overdoses” of the same challenges are harmful in the long-term. The doses that provide beneficial adaptation are said to be “hormetic” doses. Hormesis readily applies to nutrition, exercise, and lifestyle. While stressful “challenges” in the right “dose” are necessary to health, overdosing will have the opposite effect. When it comes to dosage, while “some” is good, “more” is not necessarily better. Overdose is as negative and deadly as an under-dose. Antioxidant supplements are heavily advertised and hyped, but research studies have shown that when antioxidants are isolated and supplemented, beneficial effects are not seen in humans. Some studies have shown that high-dose antioxidant supplements (vitamin E for example) can actually make some diseases worse and shorten life spans. As we discussed above, we need some oxidative stress to promote an adaptive response. This increases our internal antioxidant systems, and makes us more resilient to future stress. High-dose antioxidant supplementation neutralizes the
small amount of reactive oxygen species (i.e. free radicals) responsible for beneficial levels of oxidative stress. Neutralizing this beneficial oxidative stress
also neutralizes the favorable adaptive response necessary for health and longevity. If this seems counterintuitive, think of it this way—exercise is good for the body in the right doses, but too much can cause you harm. Eliminating exercise altogether, because too much can harm you, is using the same failed logic behind the idea of trying to eliminate all oxidative stress because we know that too much oxidative stress is harmful. Just as we need the right dose of exercise to make us stronger and more resilient, we need some oxidative stress to thrive through the adaptive response.
POLYPHENOLS Polyphenols Polyphenols are ar e a gr oup of natural natural compounds co mpounds found in fruits, vegetab vegetables, les, and plant products such as olive oil. Polyphenols have been promoted for antioxidant properties, free-radical defense, and as helping in the battle against oxidative o xidative str str ess and inflammation. inflammatio n. Recent r esearch esear ch has shown that that their their favorable favor able action action may not be directly r elated elated to polyphenols acting acting as antioxidants. Instead, Instead, polyphenols stimulate our antioxidant defense and cell protection mechanisms in an indirect way. These compounds promote a small amount of oxidative stress and create an environmental challenge which will will stimulate a beneficial adaptive response. respo nse.
EXERCIS EX ERCISE, E, NUTRITION NUTRITION AND AN D HORMESIS H ORMESIS Coaches and athletes know how to get faster and stronger by subjecting the body to physical demands. They are unknowingly invoking hormesis. To become faster and stronger the adaptive response must be triggered. There is a proper “dose” to trigger the adaptive response. Too little leads to no beneficial changes, and too
much often leads to overtraining. Sickly, injured endurance exercise addicts are examples examples of o f o vertrained individuals. individuals. Smart coaches and athletes also know the importance of recovery in making performance gains. Adequate recovery allows for maximum adaptation to the “exercise “exercise dose” and pro motes recovery reco very befor e the next next tr tr aining session. Consisten Consistentt exercise over dose and inadequat inadequatee r ecovery is “poison” to the the body. body.
The right ri ght “dose” “dose” is impor tant tant for both. High quality food and nutrition also fits into our hormesis framework. Macronutrient ratios of protein, starch, fiber and fat can be altered on a daily basis to fuel activity levels and serve physiologic needs. We need to account for individual genetic differences and tailor food quality, quantity and selections based upon different “dose” requirements, goals and preconditions such as obesity and diabetes. Both over-nutrition and under-nutrition, outside of your individual “ideal window” can have have very r eal health consequences. It will be easier to grasp the concept of hormesis visually in the diagrams that follow...
The above diagram illustrates the concept of hormesis. The x-axis (left to right) measures the “dose” of environmental challenge with an increasing dose as we move to the right. The environmental challenges can be anything previously discussed, with food and exercise being the obvious examples. The y-axis (top to bottom) represents the effect seen on the body that corresponds to a given “dose,” either either adverse or o r hormet hor metic ic (beneficial). (beneficial).
Point A: The yellow and red sloping curve on the left could represent inactivity (for exercise dose), or malnutrition (when looking at food dose). The low doses of activity or food cause “adverse” effects on the body. For food, Point A represents malnutrition. For exercise, Point A r epresents epres ents sedentary/lo sedentary/lo w activity activity..
Point B: As we move to the right with increasing doses of environmental challenges, we see the curve turn green and rise into the area of beneficial “hormetic” effects. This green area represents the beneficial “doses” of environmental challenges for food and exercise in this case.
Point C: Continuing to the right, the higher doses start making the curve drop into the yellow and red again, the territory of adverse effects and eventual death with high enough doses. For food, Point C represents over-nutrition and the resulting adverse adaptation of obesity. As far as exercise, Point C could represent r epresent overtraining. An alternate way of visually grasping hormesis is the arrow below. It shows the
same thing as the previous graph and the descriptions of points A, B, and C still apply. As you go from left to right following the arrow, the “doses” of environmental challenges challenges (food (fo od and exercise in our example) example) increases. • Point A represent r epresentss malnutri malnutrition tion (food) (foo d) or lack of activity activity (exercise). point B r epresent beneficial • The “just right” ri ght” (hormet (hor metic) ic) doses of point beneficial amounts amounts of of nutrition and exercise. Moving out of the green zone to the right, you find point C. • Point C represent repr esentss too too much exercise (overtraining) o r too much food foo d (over eating).
There is a proper dose for food and exercise for each individual that maximizes favorable adaptation without taking other external sources of environmen environmental tal stress s tress — such as sleep deprivation or psychological stress—into account. If we take into
account these other external stresses, things can change... A bad night of sleep, a stressful day at work, or a period of financial problems, add to “environmental stress.” This decreases the ideal “hormetic window” for things like certain types of food and exercise because of the additional stresses on the body. What may be a good “dose” of food and exercise while on a week long vacation may not be right when facing a deadline at work with poor sleep .
This is your hormesis hor mesis arr ow after after a couple co uple of nights of bad sleep sleep and and wor wor k str str ess. In this case, just a little exercise will put you in the green zone of hormetic dose. If
we did the same dose of exercise right now as we did last week (B surrounded by the yellow box) when we were sleeping well and on vacation, we would find ourselves in the “overdose” zone. In other words, the dose of exercise that was beneficial for us last week will be too much this week because of the poor sleep and job stress. A smaller “dose” of exercise this week will be the beneficial dose.
COACH’S CORNER: We need to be aware of o f all the pitfalls and landmines that can dr dr ag us o ut of o ur “hor metic metic dose”—sleep deprivation, deprivation, intense intense and and prolonged pro longed psycholo psychological gical str str ess, starvation, starvation, gluttony gluttony,, too much or too litt l ittle le exercise to name just a few. Hormesis is a delicate gossamer strand, a fragile state. External External str str esses will will r ip us out of the pr pr ogr og r ess zone in a matte matterr of hours ho urs —a night nig ht of bad sleep, s leep, a super supe r -stressf -str essful ul day at wor k, a perio per iod d of financial fina ncial problems, pro blems, beatin beating g yourself to a pulp in training then starving starving or stuffing stuffing yourself. It is difficult diff icult to t o stay in the t he “hormetic zone.” zone .” But if we are able to ride the razor’s edge and stay in the zone, we are rewarded with tangible physical gains: measurable decreases in body fat, an increase in lean muscle mass, health, wellness, energy, improved stamina, and dramatic improvements in every definable athletic benchmark. benchmark. It all can be ours and this book shows shows you precisely how to attain att ain and maintain the t he hormetic zone—the zone— the requisite requisit e precursor to all tangible physical progress. progress. In elite eli te athletics athl etics,, the combination of perfect training traini ng combined with perfect eating, plentiful ple ntiful rest, copious amounts of organic, nutri ent dense foods, and stress-free living all combine to create a synergistic zone of progress. progress. The key is i s to balance the components. components. It is better to have a little of all the t he interrelated elements elements and disciplines than a whole lot of one or two at the expense of the others.
TECHNICAL NOTE: The graphics depicted on the previous pages show adverse effects at low doses and high doses, with “beneficial” effects seen in moderate doses (the green part of the curve or arrow). Classically, hormesis as described in toxicology shows beneficial effects at low doses with adverse effects at higher doses. The classical hormesis gr aph differs fr om o urs because we we are ar e extendin extending g the the hor mesis concept to to include lifestyle factors such as nutrition, stress, and exercise—not just looking loo king at chemical chemical exposure. With our expansion of the hormesis concept to lifestyle factors, we see adverse effects eff ects at both very low doses (sedentary lifestyle, under-eating, etc.) as well as high doses (overtraining, overeating, etc.), with a beneficial beneficial mo derate dose. In an upcoming section we will discuss the concept of the “stress cup” and allostasis. These ideas explain how something can be good for you one day when your overall stress is low, and bad the next when your stress is high. Up to this point, we have talked a great deal about “stress.” Let’s dig a little deeper into the concept of stress, especially how your brain deals with stress—a.k.a. the threat response.
CENTRAL THEMES PART IV:
STRESS AND AN D THE RESPONSE RESPONSE TO THREAT
One of the brain’s major roles is to protect us from harm. A hard-wired system lives in the brain and expands to the body. This system responds to external and internal threats, is crucial to our survival, and has been finetuned during the development of the human species. Why is this important and why is it a central theme in a health and fitness book? Just as we we must learn lear n the science of the body we need need also learn lear n about the the brain. br ain.
COACH’S CORNER:
The brain can be an individual’s best friend or worst enemy. The goal is to use the untapped powers-of-the-mind to amplify our training and nutr nutr itional effo ef forr ts. How do we harness the mind? How do we make it an ally instead of a hindrance? The first step is to understand how it works— fro m a scientific perspective. perspective. Stress is a killer. ki ller. Liter Literally. ally. Too much stress is i s the Black Black Plague o f the modern era. Everyone is mentally stressed trying to cope with life. Stress also kills progr pro gr ess. No matter matter how intense intense the the training, or strict and pristine the the nutri nutrition, tion, if you ar e over-stressed over -stressed you will will “go “g o catabolic” catabolic” and no prog ress is possible. possible. Our distant ancestors’ brain circuitry was hardwired to instantaneously respond to real or perceived threats from the environment. Dubbed “fight or flight,” this instinctive reaction was critical for survival. Ingrained deeper and deeper with each passing generation, the “fight-or-flight” response was inserted deep into our collective psyche. Early man had to respond to various “threats” including...
• • • •
Predators Unfriendly Unfriendly neighboring neighbo ring t ribes Competit Competition ion for fo r resources Periods Periods of scarce scarce food foo d
• Environm Environmental ental stresses such as heat and cold • Injury Injury and infectious infect ious disease disease In modern moder n society so ciety,, humans are ar e faced with a differ ent set of “threats.” “threats.”
• Stressful Stressf ul work envi environm ronments ents • Traffic • Financial problem pro blemss • Disruption Disruption of o f circadia circadian n rhythm (artifi (art ificial cial light light at night night,, poor po or sleep, shift work) • Processed Pro cessed food foo d supply supply • Enviro Environm nment ental al t oxicants oxicant s (chemical (chemicals, s, pollut pollut ion) • Chronic disease The differences between the threats to modern and primitive man may see very obvious to us, but in our brain’s hard-wired threat response system they are treated t reated equally equally, and elici elicitt t he same same threat t hreat response.
Your brain treats both types of threats in a similar manner. In an escape from immediate danger, a “bear threat” is actually preferable to the stress from a “traffic threat.” Daily low-level chronic stresses such as traffic can add up to cause real health problems. We are wired to deal with the bear using a short-term threat response, but are not as suited to handle long-term stress associated with things like daily traffic. The big difference between primitive and modern “threats” is that primitive threats were mostly temporary and short-lived, while modern threats are often continuous and long-lived. The same brain-based threat response system that allowed our distant ancestors to adapt, survive, and get stronger works overtime every day with modern humans. Working the threat response system overtime has a very real r eal impact on our o ur health.
Chronic stress and threat response has been linked to the following diseases:
• • • • • • •
Heart disease Type II II diabetes High High blood bloo d pressure Aut Aut oimm oimmune disease disease (see the t he gut chapter) chapt er) Depression Chronic pain Cancer
QUICK FACT: Humans are not equipped to effectively deal with the the chro nic threats rampant in modern society, and it is evident in the overall poor state of public health.
YOUR BRAIN ON “THREAT “THREAT”” Anything in your environment that the brain perceives as a threat will trigger a physiologic stress response. The racing heart, jitteriness, and hyper-alert state we have have all experienced after after being star star tled by by a loud noise noi se or narr owly avoiding a car accident, is the stress/threat system in action. At the primal level, the system’s job is to prepare you to fight or flee fr om danger. There are two main components to this “fight or flight” system, the autonomic nervous system (ANS) and the hypothalamic-pituitary-adrenal axis (HPA axis) . Both components work together to prepare the brain and body to deal with the threat and to recover afterwards. Once a threat is perceived, the autonomic nervous system is responsible for the immediate preparation to deal with the threat.
I. THE AUTONOMIC A UTONOMIC NER N ERVOUS VOUS SYSTEM SYSTEM T he (ANS) (ANS) operates without conscious control. The ANS operates on autopilot so that that you you do not no t have have to to think about about raising your heart rate or moving mo re blood blo od to muscles during a threat. It happens automatically thus the name “autonomic.” There are three main par ts of this system system but only the the first fir st two two are of primar y impor tance tance
to our discussion discussion o f the threat threat response.
• T he Sympat Sympathet hetic ic Nervous System Syste m (SNS) is the “flight or fight” part of the autonomic nervous system (ANS). This is the system responsible for increasing your heart rate when when you are star star tled, tled, perceive danger, danger, or o r in response r esponse to to exercise. T he SNS SNS stim st imul ulates ates t he “fast pathway” that produces chemicals to give you energy and increase your heart rate during danger. Adr Adr enalin (epineph (epinephri rine) ne) is one of the chemicals produced by the adrenal gland when danger stimulates the immediate threat response by the brain. Another chemical similar to adrenalin called norepinephr norepinephr ine is also pr oduced. When the SNS is dominant, processes like digestion, rest and recovery are put on hold; you do not need need them them or want want them them while while fighting or running for fo r your life. The main job of o f the SNS SNS during a threat response is to pr ovide energy to maintain the the high hig h states states of alertness aler tness and increased muscle activity necessary to survive “fight or flee” threats. T he SNS has (prim ( primaril arily) y) inflamm inflammato at o ry act ions and should should only o nly be periodically dominant domi nant to respond r espond to to danger. “r est and digest” system • T he Parasympathet Parasympathetic ic Nervous Nervous System (PNS) is the “rest that counteracts the SNS. SNS. This system br ings your heart r ate down after after the danger danger has passed, passed, allows for movement of food foo d thr thr ough the intest intestines ines during digestion, digestio n, and is associated asso ciated with with a calm, r elaxed state. state. The PNS PNS system is cr itical for the the recovery r ecovery process. pr ocess. The PNS PNS allows your bo dy to to r ecuperate ecuperate and prepar preparee to successfully face ano ther threat thr eat in the future. future. The PNS has (primarily) antiinflam inflamm mator at oryy actions act ions. We want the PNS to be dominant most of the time.
QUICK FACT: Our distant ancestors lived the majority of their lives dominated by the “rest “r est and digest” parasympath par asympathetic etic system. Their sympathetic sympathetic systems sprang into action only when a threat appeared. Stressed out modern man lives his life dominated domi nated by the the SNS. SNS.
KEY POINT: The sympathetic and parasympathetic systems are both operating to some degree at all times. Environmental signals determine which system is dominant at any particular time. third d part of the the autonomic autonomic nervous • T he Enteric Enter ic Nervous System Syste m (ENS) is the thir system (ANS) (ANS) that that controls contro ls your yo ur gastroi gastr ointest ntestinal inal tract tr act (the (the gut). It is sometimes so metimes called the “second brain” due to the huge amount of nerve cells associated with this system. We will discuss this system in depth in the gut chapter.
II. THE HYPOTHALAMIC-PITUITARY-ADRENAL AXIS The (HPA) is the second component to the stress/threat system. It is responsible for the slow pathway in the response to threat, and releases various hormones to support suppor t the the threat response. r esponse. The fir st part of o f the HPA HPA axis is the hypothalamus. hypothalamus.
—HYPOTHALAMUS —HYPO THALAMUS Central to the brain’s threat response system is the hypothalamus—a tiny area located at the base of the brain. If you drew a line starting at the bridge of your nose and went straight backwards into your head, you would run into the hypothalamus. This area of the brain is only about the size of an almond, but packed into that little control rol center for how we respond to stresses perceived from space is the central cont our environment. The hypothalamus regulates many processes crucial to our survival:
• Sleep-wake cycle (circadian (circadian rhythm) rhythm) in response respo nse to t o light • Hunger • Thirst • T hermoreg hermoregul ulation ation (main (maintt aini aining ng a constant const ant body tem t emperature) perature) • Signals for fo r reproduct repro duction ion (making (making babies!) fli ght response • Fight or flight You can see from the vital processes the hypothalamus controls, it is logical that it is the part of the brain responsible coordinating the stress response. The hypothalamus is responsible for initiating both the immediate threat response through the autonomic nervous system and the delayed response through the HPA
axis.
—THE PITUITAR PITUITARY Y GLAND GLAND In response to environmental stress, the hypothalamus releases hormones that travel to another tiny structure “hanging” just below the hypothalamus in the brain called the pituitary gland. The pituitary pituit ary gland acts like a relay station, taking signals fr om hormones hor mones released r eleased by by the the hypothalamu hypothalamuss and making its own hormo nes in response to these signals. The stress hormones produced by the pituitary gland then travel outside of the brain down to the adrenal glands.
—THE ADRENAL ADRENAL GLANDS GLANDS Your adrenal glands sit on top of each of your kidneys and are about the size of your thumb. The adrenals are the third partner in the hypothalamic-pituitary-adrenal (HPA) axis. The adrenals secrete various hormones and chemicals in response to both the slow and fast stress r esponse pathways. pathways.
—HORM —HO RMONES ONES PRIM PRIMAR ARY Y FOR FOR THREA THREAT T RESPONSE: RESPONSE: Cortisol is released in response to stress signals from the slow pathway. Cortisol provides the fuel to help the body recover from the threat and helps control inflammation inflammation fro m the threat threat response. r esponse.
Epinephrine (adrenalin) and norepinephrine are released in response to stress signals sig nals fr om the immediate, fast pathway pathway..
THE HPA-A HPA-AXIS: XIS: HYPOTHALAMUS-PIT HYPOTHALAMUS-PITUIT UITARY ARY-ADRENA -ADRENAL L • FAST PATHWAY:
This pathway is triggered immediately after a threat is sensed by the brain. It bypasses the pituitary and sends a direct signal to the adrenals to produce epinephrine (adrenaline) and norepinephrine. This pathway immediately puts you in an alert state state,, and gets you ready to “fight” or “flee” from fro m danger.
• SLOW PATHWAY: This pathway is also triggered by threat but responds slowly, signaling the adrenal gland to secrete cortisol. Cortisol helps you recover from the threat after it has passed.
MEDICAL MEDICAL CONNECTION: C ONNECTION: Prednisone is the pharmaceutical equivalent of cortisol and works using the same mechanisms in the body. body. Predniso ne is used in mo dern medicine medi cine to control inflammation in many different diseases such as severe asthma and autoi autoimmune mmune diseases. Well-known side effects of chronic prednisone (and other similar medications) use is i s fat gain, muscle wasting, bone weakening, and psychological side effects such as agitation. High levels of cor tisol from fr om chronic chr onic stress/threat act activat ivation ion can result r esult in the same side effects as daily prednisone use.
ANCIENT PHILOSOPHY MIRRORS MODERN SCIENCE The Chinese philosophical concept of yin and yang mirrors the interaction between the sympathetic (SNS) and parasympathetic (PNS) systems very well as it relates to the stress/threat system. The yin/yang graphic has become a universal symbol for good reason; it is an overarching concept that describes our natural world from large-scale ecology to molecular biology. We can use the yin/yang concept to illustrate the importance of balance in the autonomic nervous system between the SNS and the PNS. Prolonged Prolonged activation activat ion of the stress/threat stress/t hreat system syst em leads to dominance by the SNS
and wear and tear on the body and brain.
ANS ANS balance is cr ucial to health.
HEAL HE ALTH TH EFFE E FFECTS CTS OF THE STRESS/THREAT STRESS/THRE AT SYSTEM
The sympathet potential to pro duce high levels sympathetic ic nervous nervous system syst em has the potential of inflammation and oxidative stress, potentially causing significant wear and tear o n our body and brain. br ain. Optimally, the the SNS SNS should only o nly be dominant for short shor t periods o f time. In addit addition ion to responding to threats threats and challenges, the SNS is also purposefully invoked during intense physical training. For many of us, our sympathetic nervous system is always always on, ramped r amped up, up, agitated, agitated, and and frazzled fr azzled from fro m responding r esponding to chro nic stress situatio situations. ns. Chronic over-stimulation of the SNS results in chronic inflammation. The parasympathet parasympathetic ic nervous system syst em is associated with calm, relaxed centeredness, and has anti-inflammatory effects. Bodily functions o ccur optimally when operating in PNS. We want to cultivate the PNS and have it maintain dominance most of the time. Prolonged Pro longed activation activation o f the HPA axis can lead to abnor abnor mally high cor tisol levels. Cortisol is an essential essential part o f the recovery from fr om threat and plays plays vital rol r oles es in our o ur body. Moder n stresses keep our o ur HPA HPA axis threat system
on longer that it was designed, leaving us awash in cortisol. This damages the brain, wastes wastes muscle, weakens weakens bones, and promo pr omo tes fat accumulation accumulation resulting in poor health. health.
KEY POINT: The sympathetic “flight or fight” nervous system (SNS) generally has inflammatory effects. The parasympathetic “rest and digest” nervous system (PNS) generally has anti-inflammatory effects. Low levels of continued cont inued SNS activity can lead to chronic inflammation, inflam mation, and is a key driver of chronic diseases such as heart disease, diabetes, high blood pressure, and cancer in modern society.
Poor health and disease are the result of this imbalance—dominance of the SNS over the PNS. Many modern humans live in a constant state of low level “flight or fight” in response to modern “threats,” with very few of these threats being a true immediate danger to life and limb. The following point needs repeating; the brain will trigger the threat response to both internal threats from within the body and external threats from the environment.
• Internal threat thre at:: swollen fat cells cells in an obese individual individual causing inflammation. • External t hreat: stressful st ressful work environm environment. ent. • Internal t hreat: hreat : bact bacterial erial infection infect ion or injury injury.. • External t hreat: processed pro cessed food foo d causing causing inflam inflamm mation at ion and oxidative stress. • Int Int ernal t hreat: rumin ruminat ation ion and worry worry causing chronic psycholog psychologica icall stress. • External t hreat: consistent consist ent overtrai overt raini ning ng from “boot “boo t -camp -camp beat down” exercise programs. • Int Int ernal t hreat: inadequ inadequat atee sleep. sleep. This is i s just a handful of o f examples that can activate activate the the brain’s br ain’s thr thr eat response. respo nse. You will learn more about all of these threats as you continue your training. Notice that
inflammation and oxidative stress from internal and external threats such as obesity and processed food can stimulate the threat response. In turn, the threat response of the “flight or fight” system (SNS) can cause inflammation and oxidative stress. This creates a vicious cycle that leads to poor health. In the upcoming in-depth training on Chronic Stress, we will show you the damage to your body and brain that results from the cycle of inflammation and over-activation of the stress/threat system. You will also get defensive tactics to break the cycle and restore balance to the system and to your health. This very brief overview of the stress response system sets the stage for how threats from our environment and from within impact our health. On any given day, each of us has a specific capacity for dealing with internal and external sources of stress. This capacity is what we call your “stress cup,” the amount of stress you can handle on any given day. The next section expands the “stress cup” idea using the scientific concepts of allostasis and allostatic overload , which are foundational to the Str Str ong Medicine view of health and disease.
CENTRAL THEMES PART V:
ALL AL L OSTAS OSTASIS: IS: MY CUP RUNNE RUN NETH TH OVER…
Unlike the meaning of this phrase in the biblical context, we will use it in reference for a way to visualize our bodies’ capacity for stress, a.k.a the “stress cup.” You really do not want to routinely overfill this cup, as you will soon see. The scientists who study the adaptation of the human body to stress call this adaptation process allostasis . This word literally means achieving “stability through change.” Put more simply, the human body always wants to achieve balance with with the envir environment*, onment*, and does so by changing changi ng and adapting. If something in our environment (such as strength training) tries to disrupt this balance, the body will adapt to meet the challenge, changing to be in a new balance with the environment (in this example becoming physically stronger in response to lifting weights).
QUICK FACT: *As a reminder, we define environment as our food and water intake, air quality, quality, physical activity and lifestyle. lifes tyle.
KEY QUESTION: How is the concept of allostasis different than hormesis?
Answer: Allostasis Allost asis is i s the physiologic physi ologic mechanism mechanis m by which hormesis operates.
What does that mean? • Hormesis occurs when when an environmental environmental stressor produces a “positive adaptatio adaptation” n” or beneficial effects eff ects in the the body. • Allostasis is how the beneficial effects (adaptatio (adaptations) ns) actually happen inside the body to achieve achi eve stability with with the envir environment. onment. Many of us have felt a sense of euphoria or wellbeing after intense physical activity. Those in the endurance sport community call it the “runners high.” This sensation is really a protective response to stress by the release of natural mor phine-like phine-like compounds called endorphins. Endorphin release is part of allostasis—in this case, the brain is attempting to decrease pain during intense physical stress. Allostasis is responsible for other adaptations/responses seen in response to various vario us types types of environmental environmental stress:
• Release Release of st ress hormones such as cort isol and epinephrine epinephrine by t he brain brain and adrenal glands in response to stress in all forms. • Increase in in muscle size in in response to t o weight traini t raining. ng. • Increased Increased cardiovascul cardiovascular ar fitness in response to t o exercise. • Stimul Stimulat atin ingg the t he ant ant ioxidant ioxidant prot ection ect ion system when when exposed exposed to t o free
radicals.
QUICK FACT: When the environmental challenges are in a high enough dose and frequency fr equency to to co nsistently nsistently overl o verload oad the body’s ability to to adapt, t he body body
starts st arts t o break down from “wear “wear and tear” and disease disease is the t he result result . These adaptations through allostasis allow you to better cope with the demands of any future future environment envir onmental al challenges and/or and/or serve an immediate need need for survival as part of the “flight “flight or fight” response.
FAILURE TO ADA A DAPT PT:: “THE “TH E STRESS CUP” At any one time, your body has an upper limit to the amount of stress it can handle and still produce a favorable adaptive response. This limit or capacity for stress can change dramatically day to day, or slowly over months and years. A night of poor sleep, a couple of fast food meals, traffic during your morning commute, or a demanding boss can reduce the daily capacity for stress. It may be easier to think of this visually using the concept of the “str “str ess cup.” cup.”
THE “STRESS CUP” The entire cup represents your body’s capacity to deal with stress (through
allostasis) allo stasis) on a g iven day. day. In this this example, the enviro nmental str str ess of work, poor sleep, and bad diet fill the cup most of the way, leaving only a little capacity (empty space at the top) top) for f or physical stress such s uch as strength training. Attempting a high intensity workout session—usually a beneficial stressor —on a day da y like this thi s could co uld “over “o verfil fill” l” the “stress “str ess cup” and lead l ead to poor po or adaptation and even illness or injury. When the environmental stressors are greater than the body’s capacity to maintain stability, stability, scientists call cal l this allostatic load or allostatic overload. This overload of the system over time (the overflowing “stress cup”) produces “wear and tear” in the body and over the long-term leads to disease. This wear and tear can express itself as a “broken” metabolism (as in diabetes) or physical physical degeneration leading to pr emature emature aging ag ing and poor poo r health. health.
THE OVERFLOWING OVE RFLOWING “STRESS “STRESS CUP” CUP” This is what happens happens when attempting attempting a high intensity wor wor kout when your “str “str ess cup” cup” is almost full fr om wor k str str ess, bad bad diet and poo poorr sleep. Exercise is usually a good thing, but you need to decrease “the dose” of exercise on a day like this this day to to prevent your your “str “str ess cup” from overflowing overfl owing like in the the picture. picture. The overflowing over flowing “stress cup” is called allostatic overload.
QUICK FACT: The end result of allostatic allostatic overload over load is incr eased chronic inflammation damage to your body and brain. and oxidat oxidat ive ive stress, st ress, which which cause damage Allostatic Allostatic overlo ad represent r epresentss the health health consequences consequences of mor e stress (of (o f all types) over time than your body and brain can handle—your “stress cup” is constantly constantly overflowing. overfl owing. As you “pour” different differ ent stresses stresses into into your yo ur “stress cup”, your body bo dy and brain brain r eact and adapt to the stress through the process of allostasis. As long as you do not exceed the capacity of your cup, your body and brain will survive and thrive in response to stress. I know what you’re thinking, “I’ve got too much stress in my life. I’ll avoid exercise so I don’t overfill my ‘stress cup’.” This is a really bad idea because the complete lack of exercise will make your “stress cup” smaller , leaving you less able to to handle handle other stresses str esses such such as injury, poor diet, diet, poor sleep, and and wor wor k stress.
QUICK QUICK MEDICAL MEDICA L NOTE: We can measure the results of allostat allo static ic overl o verload oad with medical tests tests such as: • • • • • •
Blood sugar tests tests for diabetes diabetes Lipid panels panels for heart heart disease risk ri sk Thyroi Thyr oid d testing testing Adr Adr enal stress indexes indexes for problems with with cor tisol C-reactive C-reactive prote pro tein in (a marker of inflammation) inflammation) Heart Rate Variabi ar iability lity
We will g o over some of these in detail detail in i n the “Stuff “Stuff You You Can Measure” chapter. chapter. Just know that that conceptually, conceptually, we we are ar e really r eally measur ing the markers marker s
or how our body is not adapting well to the of allosta allo static tic overload— or environment over time. Lack of exercise will figuratively reduce your “stress cup” from a 24-ounce cup to a 12-ounce 12-o unce cup. The smaller your cup, the more easily it will overflow, r esulting esulting in allosta allo static tic overlo ad and health health problems.
KEY POINT: It is very important to remember that a lack of stress—such as sedentary
behavior—can just as easily cause allostatic overload as well! Again, these stresses are necessary for a healthy body, and it is no surprise that arthritis and degenerated joints seen in middle age often accompany poor muscle mass and and weak weak bones from fro m lack of physical training training and activity.
Regular Regular exercise can increase increase the size of your “st ress cup”!
SLOW THE HAN SLOW H ANDS DS OF TIME: “SUPER“SUPERSIZE” YOUR “STRESS CUP” A natural part of aging is the gradual “shrinking of our stress cup.” As we age, we do not heal or recover from physical stresses or illness as well, and are generally less l ess resilient resili ent than than we were were as children or young adults. adults. The good news is that we can significantly slow the “shrinkage rate” of our “str “str ess cups”, cups”, and and armor armo r ourselves our selves against stress into into o ld age. The “stress cup” can be “emptied” with stress reduction techniques such as the breathing exercises, mindfulness techniques, physical exercise, and the nutritional appr appr oaches we will will cover co ver lat l ater er in the the book. boo k.
Those with a history of poor nutrition, exercise, and lifestyle habits will see a dramatic increase in the size of their “stress cup” as they adopt the comprehensive approach to health and wellness outlined in Strong Medicine.
THE GOOD NEWS: The size of your yo ur “stress cup” can be be increased over time through smar t training, adequate sleep, good nutrition, and the use of stress reduction techniques. We will slow the aging process by “supersizing” your “stress cup”.
In this this example, the str str esses of poor poo r sleep and bad diet have have been reduced through lifestyle change. There is still some work stress, but we now have a large lar ge empty space that can be filled with intense intense training traini ng without overfillin overfillingg our “st ress cup”.
THE FUTURE OF MEDICINE? In our opinion, the concepts of allostasis and allostatic overload are the best way to view chronic disease as a whole. High blood pressure, diabetes, high cholesterol, obesity, and mental health problems such as anxiety and depression are all examples of the body’s failure to adapt to environmental stresses such as chronic stress, poor diet, and lack of physical activity. It is well known that these diseases diseas es often occur
together—which is no surprise if you view them all as results of allostatic overload, overfilling your “stress “stress cup.”
We need to stop treating these diseases as individual issues to be treated with drugs. Instead, the lifestyle should be aggressively modified to reduce stress, eat well, and exercise more. If you are unwilling to do this, you are doomed to take an ever-increasing number of drugs in an attempt to artificially control your body’s attempt to achieve stability in a poor environment of fast food, inactivity, and high stress. None of the chronic diseases listed above have ever been cured by drugs, only partially cont co ntrr olled at best. Let us eliminate the causes instead of treating the symptoms. The body has an incredible potential for self-healing. Given the right inputs of good food, exercise, and stress r eductio eduction, n, it knows what what to to do. do .
USE IN DAILY LIFE Using the visual concept of the “stress cup”, you can discover your individual daily limits and proper “doses” of the various environmental inputs of food, training, and lifestyle that lead to beneficial changes for you. What works well for you may not work well for your family members, neighbors, o r co-workers, co-wor kers, and vice-versa. vice-versa. You You will make mistakes in the the pro cess of experimentation with this concept, just don’t let your “stress cup” consistently run over. The rest of this boo k will give gi ve you the too tools ls to pr event event allostatic allostatic overlo o verload ad and the chr chr onic diseases di seases that go with it.
SPOTLIGHT ON A SCIENTIST: The work of Dr. Bruce McEwen inspired this section of Strong Medicine with his foundational work on allostasis and allostatic overload. His contributions contributions to this this ar ea of r esearch have been been monumental. monumental.
“MILITARY INTELLIGENCE” INT ELLIGENCE” (REFERENCES): Bohacek Bohacek J , Gapp K, Saab BJ & M ansuy ansuy IM. Transgenerational Transgenerational e pigeneti c eff ects on brain brain functions. functions. Biol Psychiatry 73 (2013): 313-320. Calabrese Calabrese , V. et al. Cel lular stress responses, hormetic phytochemicals phytochemicals and vitagenes i n agi agi ng and longevi ty, Biochim Biophys Acta 1822 (2012): 753. Pharm De s 16 (2010): 877. Calabrese, V. et al. The hormetic role of dietary antioxidants in free radical-related diseases, Curr Pharm Natl Acad Sci USA 109 (2012): 5995. Cohen, S. S. et al. Chronic stress, glucocorticoid receptor resi resi stance, stance, i nflammation, anddisease ri sk , Proc Natl Neurosci 15 (2012): 689. Davidson RJ , McEwe n BS. Social Social i nfluences on neuroplastici neuroplastici ty: stress and andinterve ntions to promote promote we ll -bei ng, Nat Neurosci Fairfie ld KM . Dail y multivi tamin tamin supple ments ments did not not reduce risk for major CV eve nts nts over > 10 ye ars ars i n men, men, Ann Intern Med 158 (2013): JC2. Ganzel BL, M orris PA. PA. Wethington, E. Al lo stasis andthe huma human n brain: Integrating Integrating model s of stress f rom the the soci al and li fe sci ences, Psychol Rev 117 (2010): 134. Gol dstein DS. Adrenal Adrenal responses to stress, Cell Mol Neurobiol 30 (2010): 1433. Gomez-Pinilla, F. The influences of diet and exercise on mental health through hormesis, Ageing Res Rev 7 (2008): 49. Goto S, Radak Radak Z . Hormeti c effe cts of reactive reactive oxyge n species by exercise : a vi ew f rom animal animal studie s for successful successful aging in huma human, n, Dose Response 8 (2009): 68. Jo seph PG, Pare Pare G , Anand Anand SS. SS. Expl oring ge ne-e nvironment rel rel ationships in cardiovascular cardiovascular dise dise ase, Can J Cardiol 29 (2013): 37. Li G, He H. Hormesi s, all ostatic bufferi bufferi ng capacity and and physi ol ogi cal mechanism mechanism of physi cal activ activ ity: a new new theoreti c framewo framewo rk, Med Hypotheses 72 (2009): 527. Environ Microbiol 73 (2007): 572. Mae ta K, No mura mura W, Tak Tak atsume atsume Y, Izawa S, I noue noue Y. Green tea pol yphenol yphenol s function function as prooxidants prooxidants to activate oxi dative dative -stress- responsiv responsiv e transcription transcription factors in ye asts, Appl Environ Mansuy IM , & M ohanna S. S. Epig eneti cs and and the the H uman uman Brain: Brain: Where N urtur urturee M ee ts Nature. Nature. Cerebrum 2011(2011): 8. McEwen BS. Sleep deprivation as a neurobiologic and physiologic stressor: Allostasis and allostatic load, Metabolism 55 (2006): S20. McEw en BS. Central Central e ff ects of stress hormones hormones i n heal heal th and anddisease: U nderstanding erstanding the protectiv protectiv e and damaging damaging ef fe cts of stress and stress mediators, Eur J Pharmacol 583 (2008): 174. McEw en BS. Brain Brain on stress: how the social environment gets under the sk in, Proc Natl Acad Sci USA 109 Suppl 2 (2012): 17180. McEwen BS, Getz L. Lifetime experiences, the brain and personalized medicine: an integrative perspective, Metabolism 62 Suppl 1 (2013): S20. McEw en BS, Wingfi el d JC. What is i n a name? Integrating homeo stasis, all ostasis andstress, Horm Behav 57 (2010): 105. Menendez JA, et al. Xenohormetic and anti-aging activity of secoiridoid polyphenols present in extra virgin olive oil: A new family of gerosuppressant agents, Cell Cycle 12 (2013): 555. Muscatell KA, Eisenberger NI. A Social Neuroscience Perspective on Stress and Health, Soc Pe rsonal Psychol Compass 6 (2012): 890. Novak ovi c B, Saffery R . The i mportan mportance ce of the intrauteri ne environment in shaping shaping the the human human neonatal epi genome, Epigenomics 5 (2013): 1. Metab (Lond) 6 (2009): 16. Nunn Nunn AV, Bel l J D, Guy GW. Life style -i nduced uced metabol metabol ic i nfle xi bili ty and and accel accel erated agei agei ng syndrome: drome: i nsuli n resi stance, stance, frie ndor foe?, Nutr Metab (Lond) Pathol (2013). Ogino Ogino S. e t al. Mol ecular ecular path pathologi ologi cal cal epidemiology of epigenetics: emerging i ntegrat ntegrative ive science science to analyze analyze environment, environment, host, host, and and disease, disease, Mod Pathol (2013). Pace Pace TW, Hu F, Mi ll er AH. Cyto k ine- ef fe cts on gl ucocorticoi ucocorticoi d receptor receptor function: function: rele vance vance to gl ucocorticoi ucocorticoi d resi resi stance stance and and the pathoph pathophysi ysi ol ogy and treatment of major depressi depressi on, Brain Behav Immun 21 (2007): 9. Pick eri ng AM, Voj tovi ch L, Tower J A, Davi es KJ . Oxidative stress adap adaptation tation with acute, chronic, and repeated stress, stress, Free Radic Biol Med 55 (2013): 109. Pie tsch K, et al . Hormeti ns, antioxi antioxi dants dants and andprooxi prooxi dants: dants: def ini ng quercetin-, caffe ic acid- androsmarinic rosmarinic acid-medi ated li fe exte nsion in C. el egans, Biogerontology 12 (2011): 329. Puterman E, et al. The power of exercise: buffering the effect of chronic stress on telomere length, PLoS One 5 (2010): e10837. Radak Z , Chung HY, Kol tai E, Taylor AW, Goto S. Exercise , oxi dative dative stress and and hormesi s, Ageing Res Rev 7 (2008): 34. Ri stow M , Schmeisse Schmeisse r S. S. Extending lif e spanby increasing oxidative stress, Free Radic Biol Med 51 (2011): 327. Ri stow M , Z arse K. How i ncreased ncreased oxidative stre ss promotes promotes l ongevi ty and and metaboli metaboli c heal heal th: The concept concept of mitochondrial hormesi s (mitohormesis), Exp Gerontol 45 (2010): 410. Speci Speci ale A , Chirafisi J , Saij a A, & Cimi no F. Nutriti Nutriti onal antio antio xi dants dants and adap adaptive tive cel l responses: an update. date. Curr Mol Med 11 (2011): 770-789. Webster AL, Yan MS, M arsden PA. Epige netics and card cardio io vascular vascular dise ase, Can J Cardiol 29 (2013): 46. Ye Y, Li J, Yuan uan Z. Eff ect of antio antio xi dant dant vitamin supple mentation on card cardio io vascular outcomes: a meta-analysi s of randomize d controll controll ed trial s , PLoS One 8 (2013): e56803.
BASIC TRAINING II:
NUTRITION NUTRITION AND AN D METABOL METABOLISM ISM 101:
You are now starting Part II of your Basic Training. Gaining a strong foundation of knowledge with these concepts will protect the Strong Medicine trainee from being led astray by the avalanche of misinformation in the popular media. This knowledge will insulate you from fad diets and outright propaganda by special interests trying to gain financially from your ignorance. Mastering this section will give you the tools to analyze nutrition from its very foundations, allowing you to pierce the fog of the “dietary war.” Much like placing raw ore in a blast furnace to make steel, our body is made to take pristine natural foods and use our metabolic “furnace” to produce energy and keep us in optimal o ptimal health. Also like the steel making process, impurities in our food supply have consequences to the quality of the end product—or in this case, our health. Nutrition has become a controversial subject. It is ironic that what we eat as human beings—a central element of our successful development as the dominant species on the planet—has somehow “suddenly” become controversial in the modern age.
The fact that this chapter (or the entire book for that matter) has to be written puts some perspective on how far we have fallen from the ancient synergy of food and metabolism metabolism enjoyed by our ancestors. ancestors. We have strayed so far from eating food in its most natural form, unadulterated by modern processing and additives, that our bodies have not had time to fully adapt to many of the chemical concoctions sold to us as “food.” The health consequences of this failure to adapt (allostatic overload) are readily apparent in the true modern epidemics o f diabetes, obesity, obesity, heart disease, and cancer. This chapter will give you a basic “first principles” education in nutritional science, and background on how human metabolism is supposed to work when in harmony with our environment. Given that that over 2/3rds of o f the population population is i s obese o bese or overweight, and diabetes rates continue to climb to epic proportions, a “normal” human human metabolism metabolism is becoming increasing r are in mo dern society. society. There are several fundamental flaws in the current “official” food and exercise recommendations—lack of a scientific foundation, and poor communication. Many of these nutrition recommendations are based on shaky science. They are built on a “house of cards” with a poor foundation. It is also very rare to see a basic explanation of why the nutrition recommendations are made.
Many people will actually stick to lifestyle changes if they understand what is happening inside their bodies because of lifestyle choices such as poor nutrition. Many public health authorities do not give people enough credit for their intelligence and capacity for understanding. The public usually is not the problem, the message is the problem. We need to educate the layperson on the “whys” in a way that that does the science justice, but is understandable. We We need to build a scientific foundation to evaluate any nutritional recommendations dispassionately to see if they pass the “sniff-test.” Following the mission of this book, this chapter will attempt to explain the science in an understandable manner, while maintaining the careful balance between complexity and over-simplicity.
“It can scarcely be denied that the s upreme upreme goal of all theory is i s to make the irreducible basic elements as simple and few as possible without having to surrender the adequate representation of a single datum of experience.” (Everything should be made as simple as possible, but no simpler.) —Albert Einstein Einst ein 1933
BASIC TRAINING II:
NUTRITION NUTRITION AND AN D METABOL METABOLISM ISM 101: INTRODUCTION
WHA WH AT IS IS “GOOD” NUTRITION? N UTRITION? We all have our own ideas of what we consider to be good nutrition, even if we are not currently eating that way. But what are these ideas based on? Are they based on what we we hear and see in i n the popular popular media? Are they based on advice fr om health professionals—our doctors and dietitians? Are they based on official government recommend reco mmendations? ations? How How about advice advice from fr om friends fri ends and family member member s? For most of us, it is usually some combination of “all of the above”. And more often than not, the advice we hear is contradictory. What and who do we believe? This last question is often the one people struggle with the most, and is the reason “fad diets” are everywhere. There is always a new “lose weight quick” scheme that people latch onto in desperation, hoping that this will finally be the miraculous answer to their quest for a healthy body.
WHY WH Y DO ALL A LL DIETS DIE TS FAIL FAIL IN THE LONG-TERM? Diets fail—this has been proven time after time. They all seem to work in the short-t shor t-ter erm, m, but after after a while, once enthusiastic enthusiastic participant par ticipantss find themselves back to to where wher e they wer weree in the beginning, beginning , and sometimes even worse!
ISSUES WITH CURRENT NUTRITIONA NUTRITIONAL L SCIENCE: SCIENCE: Unfortunately, when you peel back the layers to find the underlying basis for current nutritional recommendations—the basic principles on which they are founded—you find yourself in a sketchy place, far from solid, unbiased science. Surely the Dietary Guidelines from our government are based on the latest and greatest cutting-edge science, right? There are four major problems with modern nutr nutr ition r esearch and practice:
I. FIR FIRST ST PRIN PRINCIPLES? CIPLES? One major problem is that current nutritional science has no underlying guiding principles at its foundation. Physics, chemistry, biology, and geology, all have universal principles such as mathematics, relativity, quantum theory, and the periodic peri odic table of the elements, as foundat fo undatio ions. ns. In In the sciences, these these foundations ar e the basis for formulating and testing theories, through the design and performance of experiments. We will refer to these universal principles as “first principles” in this this boo k.
After reading through countless journal articles on nutritional research, the underlying first principles from which to test theory and perform research seemed to be largely absent. One would think that foundational disciplines of physiology, biochemistry, biochemistry, and even even anthro anthropolog polog y would be very useful in info rming rmi ng nutritional theory and clinical practice, but they are often ignored. When we actually peeled the layers of this onion back even more, we found that modern “official” nutrition recommendations by professional medical organizations and government agencies sometimes contradict the basic scientific principles pri nciples on o n which they they should be based.
equatio ns descr ibe how ho w electrical electr ical and magnetic mag netic fields fi elds Maxwell’s Equations —these equations inter inter act and form for m the the basis for all modern moder n technolog technology y using electri electricity city and and magnetism. I had to derive deri ve these as part of an exam in physical chemistry back in college. Truly first principles, but a painful experience at the time!
II. STUDY DESIGN Most nutr nutr ition r esearch involves “observational data,” which really boils down to study participants reporting what they eat to researchers on questionnaires . How many of us are truly honest about what we really eat when asked, especially by a researcher, or can even recall what we ate weeks and months ago? Do the questionna questionnair ires es allow for differences in food quality in research? For example, example, does red meat fro m a grass-fed g rass-fed cow have the the same biochemical biochemical composition, compo sition, fat profile, pro file, and nutritional value as a cow raised in a feedlot on pesticide-laden grains? Does this make a differ ence when we we claim that r ed meat is bad? Nutrition research that mimics the methods used in physical sciences—tightly controlled variables free from external influences called confounders —is nearly near ly impossible to perform. This is largely due to the expense and logistics associated with with a study follo fo llowing wing these standards. standards.
TECHNICAL NOTE: Observational Obser vational studies can be very useful to gener ate hypotheses hypotheses that can later later be test tested ed mor e rigo r igorr ously, ously, but one should be very car eful when when using observational results to make nutrition recommendations. How many contradictory studies have you seen? It seems like every year a study comes out saying “eggs ar e bad,” bad,” only to have another another say “eggs are good.” These studies are based on observational data, so these associations need to be tested. Often, good first tests for observational study findings are: 1. What are the the proposed pro posed physiolo physiolo gical or biochemical mechanisms mechanisms behind the the findings? finding s? 2. Does the the finding make sense from fro m what what we know about molecular mol ecular biology o r biochemist biochemistry? ry?
Unfortunately these questions are not answered before the results are released released to t o t he medi media, a, who once agai ag ain n confuse t he general public public about whether whether or not they should should eat eggs! egg s!
III. RED REDUCTIONISM UCTIONISM Another problem rampant in nutritional research and recommendations is “reductionist nutritionism.” For example, we know that food “X” has health benefits. We also know that compound compo und “Y” is present in fo od “X”. Therefo r e we can isolate iso late “Y” and test it (and maybe even make a supplement). The problem with this approach to food research is that other unknown factors present in food “X” are likely working with compound “Y” to give the health benefits. Isolating “Y” and using it as a supplement most often will not yield longterm benefits, and may even be harmful.
QUICK FACT: Nutritional supplement sales are a multi-billion dollar industry in the U.S. alone!
IV. GROUPTHINK “If fifty million people say a foolish thing, it is still a foolish thing.” —(Anatole France)
Groupthink is a phenomenon in which groups of people try to minimize conflict when coming to a collective decision and course of action on a given topic. Controversial issues are avoided, and opinions and/or thoughts outside the current norm nor m are not broug ht up or addressed. Independe ndependent nt thinkin thinking g is subtly discour discouraged aged in favor f avor of gr oup conformi confo rmity ty.. This is very much like the peer-pressure to conform that we experienced as teenagers. This type of peer-pressure can continue into adulthood in the form of groupthink, and unfortunately is often rampant in the government and medical communities. When we we hear nutr nutr itional infor mation mation fro m “fitness “fitness experts,” experts,” media, gover nment or physicians, we tend to blindly accept the information as true. Few among us have the knowledge or background to critically examine “settled science” and treasured dietary orthodoxies. It becomes nearly impossible to discover dietary information that is sound from a scientific perspective. Misinformation rules the day as profit becomes inexorably intertwined with knowledge. knowledge. Misinfor Misinfor mation mation and sometimes outright pr opaganda comes in i n a variety var iety of forms fo rms and result r esultss in conflicting and confusing infor mation: mation:
1. Special Special interests interests push push bogus dogma to sell their product pr oductss for financial financial gain. 2. Official r ecommendations ecommendations from fro m go vernment agencies are often influenced influenced by special interests, creating conflicts of interest. 3. Well-meaning organizations and health care providers cling to outdated
information. They are too intimidated to take a second look at established dogma, for fear of o f being ostracized or called “quack “quacks. s.”” 4. Groupthink Gr oupthink is rampant and pro fitable. The basic training that follows will give you the knowledge to critically examine nutrition advice and recommendations so you will not fall prey to misinformation from bad science and outdated paradigms.
NO DIETS HERE! The Str Str ong Medicine appro approach ach for healthy healthy eating eating is r elatively elatively simple; eat food in its natural form, from local sources, as unprocessed as possible, with an emphasis on food quality. We could sum up our entire nutritional philosophy with that sentence. We contend that the primary reason for the obesity and diabetes epidemic in “modern” society is processed food from the industrialized food manufacturing and distribution system. Most of us no longer get our food from the local farmer, but from cardboard cardboar d and plastic plastic packages. “Eat food in its natural form” is easy to say, but we will get into a more detailed definition of that statement, and what it means for your health using the relevant basic biochemistr biochemistr y and physiolog y. When people know why they are doing things, behavioral changes seem to stick longer, and we are after a long-term sustainable lifestyle change. Diets do not work long-term; they never have, and never will. Because Because of the shor shor tcoming tcomingss in most mo st nutrition nutrition research, r esearch, we we will rely r ely on the “first principles” approach, using the the found fo undations ations of biochemistry biochemistry and human human physiology physiolog y as a lens to view nutrition. We combine this view with what we have observed in the eating habits of traditional cultures not largely impacted by “Western dietary habits.” These traditional traditional cultures are relatively free o f chro nic disease. disease. This seems to to be the the most rational approach.
BASIC TRAINING II:
NUTRITION NUTRITION AND AN D METABOL METABOLISM ISM 101: MACRONUTRIENTS
The best place to start with the science of nutrition is to understand the three major building blocks of foo d, otherwise otherwise known known as macronutrients:
I. Carbohydrates II. Protein III. Fat It is crucial to understand macronutrients from a biochemistry perspective. These major building blocks of food are broken down and processed through chemical reactions in the body. Carbohydrates, protein, and fat are natural chemicals, and as chemicals, their specific s pecific structu str ucturr es determine how ho w they they react in the body. The varied chemical structures of the many different types of fat allow them to function very differently from each other. Lumping them all together as “fat” when we discuss nutrition and health misses the huge diversity of structure and function found within this group. Outdated generalizations such as “carbs are bad” or “fat is bad” are complete nonsense when you look at macronutrients chemically. To make educated decisions,
it is imperative to understand the biochemistry involved when looking at food labels in the supermarket.
CARBOHYDRATES Many people think of carbohydrates as bread, pasta, bagels, and potatoes. Carbohydrates include much more than this and are generally divided into 3 main categories: sugar, starch, and fiber.
SIMPLE SUGARS SUGARS AND AN D STARCH STARCH:: Glucose is an example of a simple sugar. It is a single molecule called a monosaccharide; mono mo no = one o ne and saccharide saccharide = sugar.
Above are the actual chemical structures for glucose, fructose, and sucrose. To avoid seeing these chemical structures over and over, we will only show them once. We will represent r epresent them them as circles and triangles from fr om this point for ward. ward. Strings of glucose are connected in chains with branches to make starches. Starches are found in bagels, bread, pasta, roots, and tubers (i.e. potatoes). Starches are called “polysaccharides.” Poly=many, saccharide= sugar. The simple sugars are connected by “bonds,” shown in green in the diagram below. Glucose (circles) linked tog togeth ether er to for fo r m starch. starch. These bonds link the glucose together, and the specific type of chemical bond is
one that our body has the machinery to cut . This cutting process is part of digestion, and and allows us to br eak starch starch into single singl e glucose molecules to use as fuel.
KEY POINT: Note that bagels, bread, pasta and other processed starchy foods are really just fiber fi ber and lar ge colle co llectio ctions ns of o f gluco g lucose. se. The next common simple sugar is fructose, another single molecule monosaccharide. But, the body handles it QUITE differently than glucose. Fructose is found fo und in fruit in varying quantit quantities, ies, and large larg e amounts are found fo und in high high fructose fructo se corn syrup. Fructose can only be used in the liver. The liver turns fructose into glucose or makes it into fat . It also makes the liver a “glucose sponge” and greatly accelerates liver absorption o f glucose. g lucose. Fructose Fructose consumed daily in high amounts amounts can cause big problems in certain situations we will discuss later. People who eat processed foods daily are getting much more fructose (usually in the form of high-fructose corn syrup) than their bodies bo dies can handle effectively. effectively.
DIGGING DEEPER: How to Make a Fatty Liver
High fructose intake is a great way to make a fat-filled liver. It is not fat pr ime example example of this this in the diet that makes the liver li ver fatty. Foie Foie gras is a prime fact in action. To make foie gras, ducks are consistently force fed corn so their livers rapidly fill with fat. This happens because the large amount of sugar (especially (especially fruct fr uctose) ose) in cor co r n is converted to fat in the the liver.
In humans, other factors are involved with fatty liver disease, but high fructose consumption consumption is i s a majo r contributor. contributor. Alcohol Alcoholic ic fatty fatty liver disease produc pro duced ed fro m high levels l evels of alcoho l consumption consumption used to be the number number one cause of fatty liver disease. The new reigning champion of the fatty liver is non-alcoholic fatty liver disease (NAFLD). One cause of NAFLD NAFLD is thought thoug ht to to be hig h fructose fr uctose intake—with intake—with high fructose cor n syrup (HFCS (HFCS)) being a major contributor contributor since it is an ingredient ingr edient in most pro cessed foods. Soda and other other flavored flavor ed drinks with with high amounts of HFCS are thought to be a major factor in the development of NAFLD in kids. NAFLD in children was unheard of
until unt il t he early 1980’s. 1980’s. To be clear, clear, t he problem is the huge amount amount of fructo se in the diet from processed processed foods fo ods and drinks. drinks. The amount amountss of fructose fruct ose found f ound in fruits and vegetables is easily handled by the liver, as long as processed food foo d is avoided. avoided.
Sucrose, another simple sugar, is a double molecule (disaccharide: di=two, saccharide=sugar) made by sticking one glucose and one fructose together (from our previous pictur pictur e, a circle and a triangle stuck stuck together). together).
Sucrose is known to most of us as table sugar, the “white stuff”. When we eat sucrose, it doesn’t stay together long. Our body rapidly breaks down the sucrose double molecule to individual individual molecules mo lecules of g lucose and fructose.
FIBER Strings of glucose and other monosaccharides (such as fructose) can be linked together with with specific types types of o f bonds bo nds that we do not have the machinery to cut . These strings are known as fiber —polysacchar —pol ysacchar ides (“many sugar sug ars”) s”) that we cannot canno t br eak down directly for energy. It is the third type of carbohydrate.
This gr aphic r epresents epresents a small piece piece of fiber showing strings of o f glucose (circles) (cir cles) connected by bonds (shown in red). Humans Humans do no t have the the machinery machiner y (enzymes) to break down fiber into glucose because the connecting bonds are chemically Note that certain types types of o f fiber fi ber may also different different from fro m t he bonds found in starch st arch. Note be str str ings of fructose (triangles instead instead of circles). cir cles). Fiber is found in various plants and is generally favorable for your health. Here again, the devil is in the details: all fiber is not the same. From a health and nutrition perspective, fiber is best classified by the degree that the specific fiber can be fermented.
Fermentation: Over one trillion bacteria are in your colon and have the machinery to break the bonds in fermentable fiber. They feed on the sugars that are released, and secrete “waste” products in the form of short chain fats, butyrate and ropionate. This process is how certain types of fiber are fermented. These short chain fats are t he primary that line the the colon (colonocytes). primary energy source for cells that Check out the gut chapter for more on fermentation.
KEY POINT: New r esearch esear ch has shown that that colon colo n cells begin beg in to die without adequate adequate supplies of bacteria-produced fats. Butyrate and propionate also have antiinflammator inflammato r y and anti-cancer pr oper ties. And by the the way, way, t hey are are saturated fats. Here is another hole in the “saturated fat is bad for you” argument ar gument that we will will get to in i n the fat sectio section. n. This is why fermentable fer mentable fiber fiber is “good “go od for you”. you”.
HEAL HE ALTHY THY WHOLE WH OLE GRAINS? GRAIN S? A major problem—and point of confusion for the public—is that nutrition and medical experts generally don’t know the difference between fermentable fiber and non-fermentable fiber. They lump both types together as “good for you” which is factually false—the fiber found in many grain products (especially wheat) is poorly fermentable. Bacteria cannot break down wheat fiber very well and will not produce significant amounts of the beneficial short chain fats as the “waste” product pro ductss r esponsible for the the health health benefits benefits of o f fiber.
THE TAKE-HOME TAKE-HOME MESSAGE: The next time you see something advertised as “high in fiber”, ask if it is fermentable or non-fermentable. Vegetables and fruits are the best source of fermentable fiber. Grain-based fibers are less fermentable and thus less desirable fr om a health health perspective. perspective. Along Along with with being full of glucose,
gr ains (for the the most part) do not have the the highly fermentable fermentable type type of fiber we need for health benefits. Stick wit wit h fruit fruit s and veggies for fo r your fiber!
PROTEIN Of all the macronutrients, patients and clients ask the most questions about protein. How much should I eat? When should I eat it? What sources are best? This section will help answer some of those questions. Of course, we’ll start with the biochemistry biochemistry first. fir st. Protein is comprised of chemicals called amino acids that are linked together to for m chains. The general gener al amino acid structure is shown in the followin follo wing g gr aphic. In the picture, N represent r epresentss nitrogen, nitrog en, C represent r epresentss carbon, O r epresents epresents oxygen, o xygen, and H represent repr esentss hydro hydro gen.
The bond shown in red in the pictur pictur e below is the “link” (called (call ed a peptide peptide bond) that joins jo ins 2 amino am ino acids. This Thi s “linking “li nking”” proc pr ocess ess happens hundreds hundr eds of o f times, times , creating
the long chains of amino acids that make up a protein.
The “R” in the squares represents chemical “side groups.” These side groups (also called R-gr oups) are what what make make one amino acid different from another. another. There
are 20 standard amino acids used to build proteins, and each has a different side group. The side groups have different chemical properties: some are attracted to water (called polar or hydrophilic), some are repelled by water (called non-polar or hydrophobic). Some have positive charges and some have negative charges.
WHY DOES THIS REALLY MATTER? These different chemical chemical properties pro perties of the side gr oups determine determine how each amino acid reacts to water (remember, we are mostly made of water) and how they react to other side chains in the string. For example, two positively charged side groups will repel each other, while a positive side chain and a negative side chain next to each other in the string of amino acids will attract each other. Because Because pr pr oteins are strings string s of amino acids, the the specific or der and type type of amino acids in the strings will cause the string to behave in different ways. Long strings of amino acids will fol d to become specific shapes shapes of three-dimensional three-dimensional pro teins. teins. For example, a group of non-polar (water repelling) amino acid side chains will attempt to position themselves as far from water as possible. Imagine a droplet of oil put in a glass of water. The oil will stay in drop form and “keep away” from the water instead of dissolving in it. So a group of non-polar (water repelling) amino acid side chains will make the string of amino acids fold in such a way that they are kept on the inside of the 3-dimensional protein structure when it folds, and away fro m water. water. Conversely, a polar (water attracting) amino acid side chain will “want” to be positioned in the three-dimensional protein structure so that it is in contact with the surr ounding water. water. Think of pouring po uring alcohol (a polar substan substance) ce) in a glass o f water. water. It readily dissolves due to the attraction of alcohol molecules to water.
WHY WH Y IS THIS RELEV RELE VAN ANT? T? The preced pr eceding, ing, r elatively elatively long -winded -winded discussion discussion sets the stage stage fo r the the following fo llowing point: Because each protein protei n has a unique order of specific specif ic amino acids linked in the string, stri ng, all with wit h different diff erent chemical c hemical properties, properti es, all of the t he proteins protei ns in our body have a unique shape once folded, and thus a unique function.
Some proteins are enzymes—biologic machinery that help vital chemical reactions happen in the body (such as the production of energy). Some proteins are
hormones hor mones like insulin that that are crucial cr ucial for a pro perly functioning functioning metabolism. metabolism. Other Other protein pro teinss are structural structural and form for m the the scaffolding for our cells.
STRUCTURE STRUCTURE = FUNCTION FUN CTION
Many readers will be interested in the muscle proteins actin act in and myos myosin in which allow muscle contraction contr action to take place. Actin Actin and myosin each have a unique order of amino acids in their chains that make them fold a certain way as 3-dimensional proteins. This folding gives them the unique shape to perfor m their their function. function.
ESSENTIAL? Now that we have established the structure of proteins from amino acid building blocks, and the importance of amino acids to body function, it is a good time to talk about “essential” and “non-essential” amino acids. Of the 20 standard amino acids, nine of them are essential. Essential just means that your body must get these nine amino acids from the diet . The other 11 are of course necessary for you to live, but they can be manufactured within the body. All of the the preceding discussion o f protein pr otein biochemistry biochemistry was was leading up to the follo wing wing key point:
KEY POINT: To manufact manufacture ure all of o f the the required requir ed proteins for proper pro per functioning, functioning, your
body must get the nine essential amino acids from your diet in the
correct amounts to support your activity level. A deficiency in an essential amino acid will lead to sub-optimal protein synthesis. There won’t be enough essential amino acid building blocks in the the corr cor r ect or der in the the chains chains for the the proper folding, for mation, mation, and function of the crucial proteins when your body needs them—especially in times of environment envir onmental al stress. For example, let us say you were fighting off an illness and your body needed to generate a large immune response. The immune cells especially need certain essential amino acids called “branched-chain” amino acids to generate the special immune proteins pr oteins they need to to fig f ight ht the the infection. If your diet is deficient in some of these amino acids, there will not be enough on hand to generate the large amount of immune proteins needed, and you will not be able to fight the infection as well as you otherwise could with adequate essential amino acids from your diet. diet.
THE NINE ESSENTIAL AMINO ACIDS T he nine essential essent ial amino amino acids are histidine, isoleucine, leucine, lysine, methionine, phenylalanine, thr thr eonine, tryptophan, tr yptophan, and and valine.
PROTEIN QUALITY The resistance-based exercise programs that are a central pillar of the Strong Medicine approach require high quality protein beyond the recommended daily allowance (we will get to this soon). The quality of a protein food is generally graded on its ability to deliver the full complement of the nine essential amino acids when eaten. Animal-based foods are
high quality proteins because they contain all nine essential amino acids in high amounts. Many individual plant-based proteins are often lacking in relative amounts of one or more of the essential amino acids to support heavy resistance training or other high intensity intensity exercise. A sedentary vegetarian will motor along fine (from a protein perspective) with plant-based protein. It is important for vegetarians engaged in resistance training to make use of more than one source of plant protein, as one incomplete plant-based protein will have the essential amino acid that another is lacking. Using multiple plant-based proteins this way is called eating “complimentary proteins” and can be a useful strategy for vegetarian lifters to get enough protein without without having having to consume an inor dinate dinate amount of calories. calor ies.
ONE-STOP SHOPPING FOR ESSEN ESSENTIAL TIAL AMINO AMIN O ACIDS
Ounce for ounce and calor calor ie for calorie, calor ie, nothing nothing can beat an animal animal source sour ce of prote pro tein in for a person engaged in regular strength training. The nutrient density of these proteins is of course enhanced in wild game or pastured pastured (g rass-fed) animal produc pro ducts. ts.
HOW MUCH MUCH PROTEIN PROTEIN DO D O I NEED? NEE D? The current official recommendation for minimum daily protein intake for “healthy people with moderate physical activity” is 0.8 grams per kilogram of body weight (0.8 g/kg). This recommendation is from the Institute of Medicine, Food and Nutrition Board and uses the concept of nitrogen balance to arrive at this number. Remember from the previous discussion of protein biochemistry that the core amino acid molecule contains nitrogen as part of its structure (some amino acid
side chains have additional nitrogen). Amino acids from protein are our body’s primary source of nitrogen, and our kidneys kidneys are in charge o f get g ettin ting g rid ri d of the the excess nitr nitr ogen og en we we do not no t use. use. The rat r atio io betwe between en intake intake of nitro nitro gen (fr om prote pro tein) in) and excretion of nitr nitr ogen og en by the the kidneys kidneys is called the nitrogen balance. Zero balance occurs when the intake of nitrogen is equal to excretion of nitrogen . Positive nitrogen balance occurs when the intake of nitrogen is larger than excretion, and is seen during anabolic states (building processes with overall body protein gain) in the body. Negative nitrogen balance occurs when we lose more nitrogen from excretion than we take in from diet, and is seen during catabolic (over all pro tein tein loss seen in muscle wast wasting). ing). states (overall
QUICK FACT: The official recommenda reco mmendations tions of 0.8g/kg 0.8g/kg/day /day are made to achieve zer zer o nitrogen balance in the average adult. The Food and Nutrition Board does recognize that individuals have different needs and preferences with diet and activity activity and set an upper limit li mit of pro tein intake intake to 2.5g/kg 2.5g/kg /day without without any identifiable medical risk. Going by the official recommendations, the average 70kg (155 lbs.) male would fall into a range of protein intake from 56 grams to 175 grams per day. That is a huge r ange! So how do I decide how much I need? Many factors come in to play when deciding how much protein you really need, including age, type and amount of physical activity, activity, and under underlying lying medical issues. iss ues.
PROTEIN PROT EIN NEED N EEDS S DIFFE DIFFER R BY AGE AND AN D PHYSICAL ACTIV ACTIVITY ITY The dietary signal for muscle building is supplied by the nine essential amino acids. As we age, we do not respond as well to the anabolic, muscle-building signal
provided by the essential amino acids obtained from protein in our diet. Because of this, intake of protein higher than the 0.8g/kg body weight is recommended as we start pushing middle age and may be especially valuable for those past retirement age. Regular resistance training, coupled with adequate protein intake has shown to be incredibly effective in stimulating the muscle-building pathways in older trainees, and preventing preventing muscle wastin wasting g (sarcopen (sarco penia) ia) seen in old o ld age. This age gr oup should shoot for 1-1.5g/kg body weight as long as they have no pre-existing kidney
disease.
TECHNICAL NOTE: The signaling pathw pathway ay for this this is mTOR (mechanistic (mechanistic target targ et of r apamycin apamycin —for —fo r mer ly known kno wn as mammalian mammal ian targe tar gett of r apamycin). apamyci n). mTOR is the main part of the the signaling chain that that dri drives ves anabolic anabolic (building (building processes pro cesses)) and is stimulated by essential essential amino ami no acids.
QUICK QUICK MEDICAL MEDICA L NOTE: There is absolutely NO evidence that higher intakes of protein CAUSE kidney dysfunctio dysfunction n or o r disease. However, However, those that have kidneys that that are not working 100% (known as insufficiency) from other causes DO need to monitor protein pro tein intake intake closely and should wor wor k with with their their doctor in determining safe amounts.
No sarcopenia here—adequate protein and resistance training can stave off age r elated muscle wasting wasting When trying to build muscle mass with resistance training, most people will need significantly more protein than 0.8g/kg/day. This is highly individual based on your training volume and intensity, so you will to experiment with it to see how much is optimal for you.
OTHER REASO REA SONS NS FOR INCREASED PROTEIN Protein intake above the recommended 0.8g/kg/day has other advantages not related to nitrogen balance. Protein has positive metabolic effects, especially if you are overweight. Protein sends signals to the brain that you are full much more effectively than carbohydrates (or fat).
The effect of this signaling to the brain is called satiety . Studies have shown that eating eating 30 grams gr ams or gr eater eater of o f prote pro tein in in the the morning r educes educes total total calorie calori e intake intake for the rest of the day. This effect can help you control calorie intake without being hungry. Higher prote pro tein in intake intake will also minimize any lean muscle loss when losing excess body fat as calorie intake naturally decreases due to satiety. Take heed, all of you “bagel and orange orang e juice for breakfast” breakfast” people! You’ll be hungry by mid-morning...
FATS Fat is a favorite subject, partly because there is so much controversy and misinformation surrounding this macronutrient. Let us look at fat from a biochemist’ biochemi st’ss perspective per spective first, fir st, then then deal with with the controversy. contro versy. Fats—or according to chemists, “lipids”—are an incredibly versatile and essential group of chemicals with hundreds of functions in the human body.
TECHNICAL NOTE: Fats Fats are really r eally a subgro subgro up of a larger gr oup of chemicals classified classified as lipids. Other non-fat lipids include: waxes, sterols, phospholipids, and fatsoluble vitamins. Just a few functions of o f fats:
• Energy storage • A major com co mponent po nent of o f cell membranes embranes • Essential Essent ial for fo r proper brain brain development development and nerve function funct ion • Proper Pro per lung lung function and prevention of lung lung coll co llapse apse • Crucial for fo r inflam inflamm mato at o ry response respo nse and imm immunity unit y cell signaling/communication A complete chapter on fats is well beyond the scope of this book. Instead we will concentrate on fats in the diet, beginning with classifying the three major types of fats:
• Saturated fat • Monounsaturated fat • Polyunsaturated fat
I. SATURATE SATURATED D FA FAT T “THE HORROR! THE HORROR!” Just like the plot from Joseph Conrad’s book, we will now venture into The Heart of Darkness, the world of saturated fat. All drama aside (somewhat), it is evident in the repeated official recommendations and relentless marketing campaigns, that the idea of saturated fat as a villain of the nutritional world is very widely accepted. Somehow the visual of saturated fat “clogging” arteries has taken hold in our collective consciousness. The demonization of this type of fat has reached a quasireligious fervor in the dogmatic proselytizing of mainstream nutrition and medical professionals. There has even been collateral damage caused by this message to basic scientist scientistss (who should r eally know bett better) er) performi perfo rming ng r esearch.
Let us take a deep breath, a step back, and look at saturated fat from a dispassionate scientific perspective.
CAUTION, CA UTION, CHEMISTRY CHEMISTRY LESSON LESSON AHEAD! A HEAD! So what does “saturated” mean when we talk about fat? As we will see in the diagrams below, saturated just means that the molecule of fat has the maximu amount of hydrogen atoms possible. Using a tree-branch analogy, everywhere there could be a leaf, there is a leaf. Before we go any further, let us establish a very basic chemistry rule regarding the carbon atom. This rule guides the maximum number of hydrogens (amount of fat. saturation) possible for a fat.
carbon atom can only for fo r m 4 bonds RULE: Each carbon
KEY POINT: The single bond chain is a very important feature in the saturated fatty acid for a couple couple of r easons. easons. 1. The single bond “backbone” gives gi ves the chain flexibility flexibil ity.. 2. There Ther e are ar e no double bonds in the chain, making saturated fats
resistant to free radicals. We will discuss the implications implicatio ns of these two two facts very so on. Single fat molecules, called fatty acids, are just long chains of carbon linked together. The head of the fatty acid is called the alpha end. The alpha end has oxygen oxyg en molecules mo lecules attached, attached, which makes this this end attract fatty att ract water. water. The tail of the fatty
acid molecule is called the omega end. The length of the tail all the way to the omega end only has carbon and hydrog en, making making this end repel water. The long chains of carbon on a saturated fat have only one single bond connecting each of the carbons to each other. This fact is important because of our two bond bo ndss are left left open on most most of t he rule of o f four total total bonds per per car bon atom— atom— two carbons in the chain for hydrogen to bond. The omega carbon can actually bond thr thr ee hydro hydro gens.
This is a 12-carbon saturated fat called lauric acid. Notice that every grey carbon atom has four fo ur bonds (even the alpha carbon carbo n because the the double bond bo nd counts as two two bonds). The all-single-bond carbon backbone gives the chain flexibility. This flexibility means that when when a bunch of o f saturated fatty acids are ar e together, tog ether, the the tails can “bend” to for m close clo se associations with with their their neighbors. neig hbors. These close associations are why saturated fats are solid at room temperature (but they they are all al l liquid li quid at body temperature).
TECHNICAL NOTE: For all of the biochemists out there, I realize I have represented the carbon chain of the fatty fatty acid in the diagr am as a straig s traig ht line. In reality reali ty,, the carbon chain looks like a series seri es of “zigzags” due to to bond geomet geo metrr y. Representing the bond geometry accurately in a picture complicates the visual greatly, so it is simplified above to teach the concept. Now that you know what a saturated fat is from a biochemistry perspective, we will discuss the basic ways to classify the various saturated fats. You will see that even small changes in the chain length make a huge difference in how each type affects our body functions. You will also see how ridiculous it is to make generalized statements about saturated fat and health, without discussing the specific types of saturated fat involved.
CLASSIFICATION BY CHAIN LENGTH chain length lengt h A general way to classify saturated fats (and other fats as well) is by chain of the carbon “backbone”. 1. Short-chain saturated fats have backbones t wo to five five carbons carbons long. 2. Medium-chain saturated fats have backbones six to 12 carbons long. 3. Long-chain saturated fats have backbones longer than 12 carbons. We are going to profile fats from each of these three classifications, so you can see the huge differences in function among them, while keeping in mind that they
are all saturated fats.
Profile of a
short-chain saturated fat.
BUTYRIC ACID (BUTYRATE) From Fro m the diagram, you can see butyrate butyrate (also called butyric butyric acid) is a four carbon car bon saturated fatty fatty acid. Butyr Butyrate ate has some very ver y interesting actio ns in our body: body: • It is the the major majo r product of fiber fermentation by the gut bacter bacteria. ia. • Butyr Butyrate ate has ver very y potent potent anti-inflammatory properties. • Butyr Butyrate ate has powerful power ful anti-cancer effects through epigenetic mechanisms. • Butyr Butyrate ate has been used in conjunction conjunctio n with with modern moder n cancer cancer treatment tr eatment techniques (photodynamic therapy) on certain types of brain tumors, killing more cancer cells. • Butter Butter is i s about 3% butyrate, butyra te, and is the the best direct dietary dietary sour ce (fermentation (fermentation o f fiber is the best best indirect source).
LAURIC ACID (LAURATE)
Profile of a medium-chain saturated fat. From Fro m the diagr diagr am, you can see see laurate (also called lauric acid) is a 12 carbon car bon saturated fatty fatty acid. Laurate has the the follo fo llowing wing effects in the body: • Comprises Compr ises about 6% of the fat content in human breast milk. • Potent antibiotic actions against bacteria and viruses. • As a medium-chain trig lyceride, lycer ide, laurate laur ate is used as an alternate fuel source in the brain, showing pro mising r esults esults treating epilepsy and and degenerative degenerative brain disor ders such as Alzheimer’s dementia. • Increases high density density lipopr lipo protein otein (HDL (HDL)) associated cholesterol cholester ol,, which may decrease risk from fr om developing heart disease.
• As a component of medium-chain tr tr iglycer ig lycerides, ides, lauric acid in the diet has been shown to aid significantly in weight loss . • Coconut oi sour ce of lauric acid, which which comprises about o il is a gr eat source 50% of the fat content in coco nut oil.
DIGGING DEEPER: Medium-Chain Fats and Metabolism
Coconut Coco nut oil: an excellent source sour ce of medium chain chain fats Medium-chain fatty acids in the diet are metabolized metabol ized much differ ently than than long-chain fatty acids. The medium-chain fats, in the form of mediumchain triglycerides, are taken direct directly ly to t he liv liver er after they are absor bed in the intestines. intestines. In In the liver they are r apidly metabolized metaboli zed for energy use in t he body. The long-chain fatty acids are absorbed in the intestine and travel in the lymphatic system. They have a much higher chance of being stored in fat cells before g etting etting to to the liver for energy use. This may be why medium-chain triglycerides have been used successfully as a dietary supplement for body fat loss. They are able to bypass the fat storage storag e sites sites and ar ar e used directly for energy product pr oduction. ion. Additionall Additionally y the medium-chain fats do not need the specialized fat transporter (carnitine-acylcarnitin (carnitine-acylcarnitinee translocase) to get into the mitochondria (the place in the cells where energy production takes place)
that long-chain fats need. This fact allows rapid entry of medium-chain fats fats into the the mitochondria for fo r energy product pr oduction. ion.
PALMITIC ACID ACI D (PA (PA LMITATE) LMITATE)
Profile of a long-chain saturated fat. From the diagram, you can see palmitate (also called palmitic acid) is a 16 fatty acid. Palmitate has has the following foll owing characteristics character istics and carbon saturated fatty effects: • It is the the primar pr imar y fat stored sto red by by the body in fat (adipose) tissue. • High amounts in fat cells are inflammatory. • It is the the primar y saturated saturated fat used in research studies . • Activates Activates an inflammator y response by immune system. • High levels of palmitate increase increase insulin insulin resist resistance, ance, contributing co ntributing t o diabetes. • Palmitate levels are higher hig her in the fat content of grain-fed animals .
WHAT WH AT IS A TRIGLYCER TRIGLYCERID IDE? E?
Triglycerides are simply three individual fatty acids linked together at their “alpha” ends by another carbon backbone (made from glycerol). T he t riglycerid riglyceridee form fo rm is the way fats fat s are stored st ored in fat cells. cells. This form of fat is also what we measure in doctor-ordered blood tests (see the Analytics chapter). The graphic above shows three separate lauric acid molecules (twelve carbon saturated fatt fatty y acids) joined together by a three carbon carbo n glycero l backbone. The ar ea shaded in pink is where the three separate separ ate fatty fatty acids are joined jo ined to to the glycerol to make a tr tr iglyceride. iglycer ide. We are going to profile another long-chain fatty acid just to show you the difference two extra carbons in the backbone makes, concerning how the fat “behaves” in the body. Make sure you compare the 16 carbon palmitic acid to this next long-chain long- chain fatty acid.
STEA STEARIC RIC ACID (STEARAT (STEARATE) E)
Profile of a long-chain saturated fat. From Fro m the diagram, you can see stearate stearate (also called steric steric acid) is an 18
fatty acid. Althoug Although h differ ing in length leng th by only two two carbon saturated fatty carbons, car bons, stearate behaves very differ diff erently ently than than palmitate: palmitate: • Stear Stear ic acid has has been shown to to beneficially reduce blood clotting and may decrease the risk of heart disease. • Unlike palmitic acid, stearic acid has no bad effects on insulin resistance or development of diabetes. • Stearic acid does not promote inflammation in fat cells. • Stearic Stearic acid tr tr iggers igg ers the deat death h of breast cancer cancer cells in laborator y testing. • Grass-fed Gr ass-fed beef is a good go od source of stear stear ic acid. acid. Comparing the 16-carbon saturated fat palmitic acid, with the 18-carbon saturated fat, stearic acid, there are substantial differences in potential health effects for each.
FIRST PRINCIPLES-BASED PRINCIPLES-BA SED SPECULATION: I think there is a reason why palmitic acid in high amounts in particular can trigger an inflammatory response in the body. As we will discuss in the chapter chapter o n obesity obesi ty,, palmitate is the specific type of fatt f atty y acid the body makes and stores in fat cells. When fat cells become overloaded, the immune cells cells are ar e trigg ered as a warning r esponse to to the body that that something “bad” is happening (in this case obesity). The immune cells cells trigg er an inflammatory r esponse, and an an overlo aded fat cell is considered an overall “threat” to the body as a whole. Because palmitate is generally the specific type of fat stored by the body in fat cells, high amounts in the diet can trigger the immune system, mimicking the threat of the palmitate-overloaded fat cell. It is interesting that the same specific molecules (called toll-like receptors) that that palmitat palmitatee trigger trig ger s for the the inflammator inflammator y response, r esponse, are in the same family that the immune system uses to recognize pathogenic bacteria as “threats.”
WHY HAVE WE BEEN TOLD THAT SATURATED FAT IS BAD? I think the reason for the “saturated fat is the devil” messaging stems from combination of bad science, politics (big shock!), and groupthink. I encourage you to read Gary Taubes’ outstanding book Good Calories, Bad Calories. Mr. Taubes does a masterful job in chronicling the origins of the current campaign against saturated fat. Just a cursory review of the differing effects of the many different types of saturated fat on the previous pages should be enough for us to stop lumping all saturated fats together as a harmful, homogenous, “artery-clogging” substance. This type of fat should be regarded with a bit more nuance and thoughtfulness. To be fair, there are many scientific studies showing that saturated fat causes inflammation and disease in animal models. However, there is a pretty good reason why we see so many scientists coming to this conclusion. In 2012, a group of scientists showing a high amount of critical thinking published an article in the American Journal of Physiology, Endocrinology, and Metabolism, showing that a large majority of scientific studies on saturated fat used only palmitic acid when testing the effects of saturated fats on animals and cultured human cells. To make matters worse, it was found that many of the authors of these studies then generalized their results to all saturated fat, even though only palmitic acid was used. We have shown you in previous pages that palmitic acid can indeed be inflammatory in the right circumstances, and may be associated with health problems. But, the effects of palmitic acid certainly cannot be generalized to all
types of saturated fat. This type of bad science just reinforces the collective groupthink that all saturated fat is “bad”. This information is taught to doctors and dietitians who unfortunately do not question the science. Again, public health suffers at the hands of bad
science science and groupt g roupthi hink. nk. We have spent this much time discussing saturated fat for a reason. We have to change the public health message that all saturated fat should be avoided. Most saturated fat is a necessary and beneficial macronutrient for optimum health, and was an essential part of our distant ancestors’ diets. The next time a health care provider or well-meaning acquaintance tells you to avoid saturated fat, I encourage you to first respond, “What
specific type of saturated fat are you asking me to avoid?”
After the likely quizzical look, hopefully a mutually-beneficial and educational conversation can occur.
II. MONOUN MON OUNSA SATURATED TURATED FAT (MUFA) Now that you know what “saturated” means, discussing monounsaturated fats should be a bit easier from a biochemistry perspective. Remember that each carbon atom can only form four total chemical bonds. With a monounsaturated fatty acid, two of the carbons in the “backbone” are joined by a double bond, instead of a single bond. This double bond ties up two bonds out of the total of four that each carbon atom can for m.
You will notice that the carbons on the right have lost the bonds on top due to the double bond. Adding the top facing bonds on the picture in the right would give five total bonds per carbon, violating the four bond rule. This matters because when we add a double bond to a fatty acid carbon backbone, we cannot get the maximum amount of hydrogens on the fat. Thus it is no longer “saturated” with hydrogens, but “unsaturated” because of one double bond. Mono=one, so we call this type of fat a monounsaturated fatty acid (MUFA). The “kink” in the chain from the double bond is important for the function of monounsaturated fatty acids. When a large amount of monounsaturated fats are lined up together, the angle of the “kink” does not allow them to get very close l ess densely packed when when in a gr oup. It It woul would d be like trying to together, so they are less bundle a bunch of bent sticks. sticks. This is why olive oil, a primarily monounsaturated oil, is liquid at room temperature, rather than solid like the saturated fats which are able to group together more closely.
OLEIC ACID A monounsaturated fatty acid
CHARACTERIS CHA RACTERISTICS TICS AND HEAL HE ALTH TH EFFE EF FECTS CTS OF MUFA MUFA Oleic acid, an 18 carbon monounsaturated fat, is the primary dietary MUFA and has generally positive health effects: • May help help reduce blood pressure pressur e and and car car diovascular diovascular r isk. • It is the the crucial fat for proper pro per cell membrane funct function. ion. • It is the main fat of the Mediterr Mediterr anean diet, diet, gener ally consider ed healthful. • High levels of MUF MUFA are ar e found in olive olive oil o il,, avocados, avo cados, macadamia nuts, lard, lar d, and beef tallow. tallow.
THE DOUBLE BOND: BOND : UNSATUR UNSATURA ATED FAT’S ACHILLES ACH ILLES HEEL HE EL Remember Remember our o ur discussion discussion o f fr ee radicals and oxidative oxidative stress in the Central Themes chapter? Free radicals are the unstable molecules with an unpaired unpaired electron, lo oking to take take another another electro electro n from fr om anywhere anywhere to complete the pair. Free radicals are attracted—like moths to a bright porch light—to light—to any source sour ce of electrons. electro ns.
It turns out that double bonds are a particularly attractive source of electr electr ons, like bloo d in the wat water er to a fr ee radical shark. Free r adicals will will “steal” an electron electro n from fr om the double bo nd in an unsaturated unsaturated fatty acid, turning the fat into a free radical in the process. The newly created fatty acid free radical r adical is a “lipid peroxide”. Imagine a newly created lipid peroxide, formed from an unsaturated fat previously just minding its own business as part of a cell membrane. The free r adical lipid pero pero xide will will then find its own source of electro electro ns to steal, likely from a neighboring unsaturated fat in the cell membrane. This creates a chain reaction in the cell membrane called lipid peroxidation, and if not stopped, leads to widespread destruction of the cell membrane and deat deat h of t he cell cell. Double bonds can also lose electrons when subjected to heat, light, or left in the open air, thro through ugh pro cesses called photo-oxidation and
autoxidation. Oxidized fats are damaged fats and free radicals themselves. You You certainly cer tainly don’t want to to eat any of these oxidized fats, f ats, and should not cook with unsaturated unsaturated fats for health it is why you should health reasons. This is the main reason fried fr ied foods foo ds are bad for you. Eating Eating damaged unsatu unsaturated rated fats fats fro m high heat cooking coo king or processing pro cessing is like importing
oxidative stress into your body.
Remember that saturated fats do not have any double bonds in their back-bone, and are relatively resistant to oxidation at high heat. This is why saturated fats don’t “go rancid” like other fats and why they have a long shelf life. There are tons of health benefits to foods containing high monounsaturated fats. Just make sure you store them away from light and heat and don’t routinely cook with them.
STRONG MEDICINE TACTICS: Cook mostly with saturated fats such as coconut oil to avoid fat oxidation and impor impor tin ting g fr ee radicals into into your body body..
III. POLYUN POLYUNSA SATURATE TURATED D FA FAT T (PUFA) You already know what “unsaturated” means, so this will be easier. A polyunsaturated fatty acid (PUFA) is simply a fatty acid with more than one
double bond. The two main types of polyunsaturated fatty acids we will cover are the omega-3 and the omega-6 fatty acids. In our original diagram of a fatty acid, remember that we called the “head” the alpha-end, and the “tail” the omega-end. When we name polyunsaturated fats, they are named for the position of the first double bond from the om o mega end.
ESSENTIAL” FATTY ACIDS:
Only two fatty acids are kno wn to to be “essential” for fo r humans. Essential Essential means that we have to to g et these these fats fro m the diet, diet, as our bodies cannot canno t make them from other fats. This is similar to the concept of essential amino acids we discussed in the protein pr otein section. Both essential essential fatt f atty y acids are ar e of the polyunsatur polyunsatur ated type. type. These two essential fats are: car bon omega-3 o mega-3 polyunsaturated polyunsaturated • Alpha Linolenic Acid Acid (ALA), an 18 carbon fatty fatty acid that is fo und in many seeds, no tably flaxseed. po lyunsaturated fatty fatty acid • Linoleic Acid (LA), an 18 carbon omega-6 polyunsaturated that is fo und in many vegetabl veget ablee oils such as safflower, safflower, grape seed, corn, and soybean oils. These two essential fatty acids are important building blocks for other fats, but you only o nly need a little ALA and LA in your diet to satisfy the
body’s requirem re quirement ent.. Following the Strong Medicine Medi cine dietary diet ary prescripti presc riptions ons will ensure adequate amounts am ounts of both ALA and LA.
Although we need relatively little polyunsaturated fats in our diet, they have a profound influence on our health. We’ll start with a little background on the two main types of PUF PUFA, dietar dietary y sour ces and health effects.
OMEGA-3 OMEGA-3 FATT TTY Y ACIDS AC IDS You probably have heard a lot about the beneficial effects of the omega-3s. It seems food manufacturers are putting them in all kinds of processed foods, even milk and ice cream. It is important that we discuss the science behind the health claims before you buy these products thinking that you are doing something good for your health.
THE OMEGA-3 OMEGA -3 PUFA PUFA “BIG 3”
The following foll owing ar e the the three most biolo gically impor tant tant omega-3 PUF PUFA in the diet:
The 18 carbon omega-3 o mega-3 pictured pictured o n the the • Alpha Linolenic Acid Acid (ALA)— The previous previ ous page pag e and one of o f the two two essential fatty fatty acids. Flaxseed and flaxseed flaxseed oil are probab pro bably ly the best best known known food foo d product pro ductss containing containing high amounts of o f ALA. ALA. Thi s omegao mega-3 3 PUFA PUFA is 20 carbons • Eico Eicosapent sapentaenoic aenoic Acid Acid (EPA)— This long and is one of the main fatty acids found in “oily” fish (salmon, tuna, sardines). DHA is the lo ngest chain o f the • Docosahexaeno Doco sahexaenoic ic acid (DHA)— (DHA)— DHA omeg om ega-3 a-3 PUFA at 22 carbons in lengt length h. It is also found in oily fish and fish oil. o il. DHA DHA has been shown to be especially especiall y impor impo r tant in brain br ain health, especially especially in the the developing br ains of children. Research on omega-3 PUFAs have shown numerous positive health effects in recent years against ag ainst the the following foll owing diseases:
• • • • • •
High High blood bloo d pressure Diabet Diabetes es t ype II Heart arrhythmia Cancer Cancer (certai (cert ain n t ypes) High triglycerides Osteoporosis
They have also been found to be beneficial in the following areas:
• Reducing chronic chro nic inflamm inflammation at ion • Optim Opt imizing izing brain developm develo pment ent in children children • Neurodegenerat Neurodeg enerative ive disorders in in t he elderly elderly EPA EPA and DHA seem to be the omega-3 superstars superst ars for health benefits, benefit s, more so than ALA from recent research.
WHAT WH AT IS AN A N “OILY “OILY FISH”? FISH ”?
Oily (or fatty) fish are those that carry fat in their flesh and gut, as opposed to “white” fish that have their fat located primarily in their liver. Oily fish usually swim in the water column away from the bottom of the sea. White fish are usually bottom dwellers. Oily fish include species such as salmon, tuna, sardines, and trout.
WHERE WHE RE DO THE OMEGA-3 PUF PUFAS COME FROM?
The beneficial omega-3 PUFA found in fish and animal foods originally come from land plants and tiny water-based plants called algae. This is why why when when choosing fish and land animal animal flesh for fo r food, foo d, it is extr extr emely important to know the diet of these animals before assuming any health benefits. In the wild, fish get their omega-3 from the food chain, starting with aquatic aquatic plant-like species such as algae alg ae (a type of phytoplankton). phytoplankton). Algae are eaten by krill (a tiny crustacean), and krill are eaten by small fish (and larger fish as well). The smaller fish are then eaten by the larger fish. In
this way way,, the the or iginal ig inal omegao mega-3 3 PUF PUFA produced pr oduced by algae alg ae are ar e now in the fish you eat. It is well-established that fish traditionally high in omega-3 such as salmon, have almost no useable omega-3 when when raised r aised in fish farms, eating processed fish feed. Wild game and domesticated herbivores such as cattle have significant amounts of omega-3 from the plants they eat. Meat from grass-fed cows has almost almo st twice twice the omeg a-3 PUFA PUFA than cows that that are g r ain-fed in feedlots.
STRONG MEDICINE TACTICS: To maximize maxim ize omegao mega-3 3 PUFA PUFA in your yo ur diet, eat wild-caught oily fish and rass-fed ed animals. animals. meat from g rass-f
OMEGA-6 OMEGA-6 FATT TTY Y ACIDS AC IDS do ublee Chemically, the the omegao mega-6 6 fatty acids are ar e simply sim ply PUFAs PUFAs that that have their their first doubl bond six carbons carbons fro m t he “tail,” or omega end. end.
This seemingly small chemical difference from omega-3 PUFAs results in very big differ ences ences in how omega-6s o mega-6s differ in function function within within our body. body. Omega-6 PUFAs PUFAs are cr ucial to the follo wing wing processes pro cesses::
• • • •
Inflam Inflamm mato at o ry process of o f wound healing healing Regulating Regulating bloo blood d coagul coag ulation ation Stimul Stimulat atin ingg growt g rowth h of cells cells and repair repair processes Proper Pro per funct functioni ioning ng of the t he im immune system syst em
WHERE WHE RE DO THE OMEGA-6 PUF PUFAS COME FROM?
Omega-6 Omeg a-6 PUFA PUFA are ar e found fo und in high hig h amounts in nuts, seeds, as well as vegetable and seed oils. They are also present in animal-based foods, but like omegao mega-3 3 content in animal pro ducts, the amount of omegao mega-6 6 PUF PUFA is dependent dependent of the type type of foo d the animal animal itself i tself is eating. Western estern diets high in pr ocessed food foo d contain large amounts amounts of omega-6 PUF PUFA, mostly from fro m the ro utine utine use of industr industr ially processed pr ocessed seed oils such as sunflower, safflower, soybean, and corn-derived oils. Herbal oils such as evening primrose and borage oils are also good sources. Grain products also contain significant amounts of omega-6 PUFA. People in modern moder n societies have have significantly increased their their omega-6 PUF PUFA content compared compar ed to ancestral diets and the the diets of traditional traditio nal cultures. As As we will see, this incr ease is no t without without potential potential health consequences.
It is unfortunate that the omega-6 PUFA have recently been demonized in nutr nutr itional cir ci r cles in a similar si milar way to to saturated s aturated fat. fat. We need to dig a little deeper and use some critical thinking thinking before befor e pronouncing pro nouncing a sentence sentence on omega-6. While it is true that the large amounts of omega-6 many of us are consuming in processed food from added industrially produced vegetable and seed oils can be problematic from a health standpoint, balanced dietary intake of omega-6 from natural whole food sources is an important part of our diet and necessary for optimal health.
THE OMEGA-6 OMEGA -6 PUFA PUFA “BIG 3”
The following foll owing ar e the the three most biolo gically impor tant tant omega-6 PUF PUFA from the diet:
• Linoleic Acid (LA) is the 18 carbon omega-6 found in many vegetable oils such as safflower, safflower, grape seed, corn, and soybean oils. • Gamma Gamma Lino Linolenic lenic Acid (GLA) (G LA) is another 18 carbon o mega-6 with with one mor e double bond bo nd than than LA. LA. Unlike most omega-6, om ega-6, which have inflammator inflammato r y actions, GLA can have anti-infl anti-inflammator ammatory y effects. Direct dietary sources include: evening primrose oil, borage oil, and
blackcurrant seed oil. • Arachidonic Arachido nic Acid (AA) is a 20 carbon carbo n omega-6 which is very very impor i mportan tantt in the the inflammator inflammator y response and repair processes pro cesses (such as muscle tissue build buildin ingg in response response t o weight weight t rainin raining). g). It is also very impor i mporta tant nt in gr owth owth and repair o f nerve cells. Dietary Dietary sources so urces are ar e primarily from synthesized from fr om animal products such as meat and eggs. It can also be synthesized LA, so vegetarians are usually not deficient. We need to have a relative balance of omega-3 to omega-6 in our diets, and for
many of us currently eating processed foods, this means reducing omega-6 intake and increasing omega-3 intake.
INVESTIGATE YOURSELF! Read the the labels on o n the food yo u buy at the grocer gr ocer y store. stor e. You will be surprised surpr ised how often you will will see vegetable and seed seed oils (high in o mega6) listed in the ingr edients. They seem to be in ever ything, ything, and ar e the primary reason why many of us have an unbalanced dietary intake of omega-6 fatty acids. The balancing of omega-3 and omega-6 will happen naturally and without supplementation if you stop eating processed foods and focus on high quality whole food sources. The following section will discuss why balancing omega-3 and omega-6 intake is so impo rtant. rtant.
THE OMEGA-3/OMEGA-6 BALANCE The omega-3 and omega-6 PUFA act as building blocks for a group of messenger molecules called eicosanoids. These messengers are central to how the body creates and controls inflammation. The eicosanoids go by names such as prosta pro staglandins, glandins, prostacy pr ostacyclins, clins, thromboxane thrombo xane,, and leukotr leukotr ienes. In general (there are exceptions), the omega-3 PUFA are building blocks for eicosanoids that have anti-inflammatory actions which control the body’s inflammator inflammator y response. Overall, the omega-6 PUFA are building blocks for eicosanoids with inflam inflamm mator at oryy actions act ions such as wound healing and the immune response.
Having Having a balance of the the anti-inflammat anti-inflammator or y and inflammator inflammator y eicosanoids is very importa impor tant nt for optimum funct function ion of o f our body systems. systems. When we are injured, or are fighting a viral or bacterial infection, we need the inflammatory eicosanoids (derived from omega-6 PUFA) for wound healing or mounting a strong immune response. The anti-inflammatory eicosanoids (built from omega-3 PUFA) are there to calm down the inflammation as the injury is healing or after the infection has been dealt with.
KEY POINT: If we we don’t have enough o mega-6 PUFA PUFA to act as building blocks bl ocks fo r inflammator inflammator y eicosanoids, we we won’t be able to to r ecover fr om injury, i njury, rebuild muscle after after a workout, or fight off infection. If we we don’t have enough o mega-3 PUFA PUFA to act as building blocks bl ocks fo r antiinflammator inflammator y eicosanoids, eicosanoi ds, acute acute inflammation will become chronic inflammation. Our immune system may become overactive, and we won’t be able to to control cell gr owth owth well, which which is a factor contributing contributing to cancer. The high intake of o mega-6 from fr om processed pro cessed food has shifted the the balance balance in many of us decidedly towards an excess of omega-6, promoting a general low-level chronic inflammatory state in our body. Remember the diagram below from the intro intro ductory ductory section section on inflammation inflammation and oxidative oxidative stress:
It is no surprise that as processed food intake (high omega-6) increased in the 20th century (even more in the 21st), the incidence of chronic diseases such as cancer, heart disease, diabetes and obesity have increased incr eased as well. The high intak i ntakee of omega-6 from vegetable and seed oils in processed food may be a primary contributor. It also makes sense that supplementation with fish oil (high omega-3) has shown in many studies to be effective in treating some of these chronic diseases.
PUFA COMPETITION A major way that omega-3 and omega-6 PUFA work is through their incorporation into the cell membranes of all cells in the body. Once in the cell membranes, they can then be the building blocks for the eicosanoids as previously discussed.
co mpete pet e for fo r placement placement in the t he cell mem membranes, branes, The omegao mega-3 3 and omeg a-6 PUFA PUFA com so having a balance of the two in the diet is important. An unbalanced diet, heavy in omega-6 will result in a disproportionate amount of omega-6 placed in the cell membranes, essentially outcompeting the omega-3 by sheer numbers. This leads to an unbalance unbalanced d pro duction duction of larg e amounts of inflammatory eico sanoids due to to the the high amo unt of omega-6 o mega-6 PUFA PUFA in the cell membr anes.
TECHNICAL NOTE AND RESEARCH UPDATE:
Recent studies have shown that omega-3 PUFA also directly affects the gene expression o f inflammatory messengers messenger s by inhibiting inhibiting their for mation mation in the cell. This effect on r educing educing inflammat i nflammation ion is i s separate fro m omega-3’s role as a building building block of anti-inflammatory anti-inflammatory eicosanoids.
You can see fr om the graphic gr aphic that the the essential fatty acids ALA and LA are ar e converted co nverted into into their their “big brother” br other” omega-3 omeg a-3 and omega-6 with with conversion conversio n enzymes. enzymes. The omega-3 and omega-6 conversion conversio n pathwa pathways ys share the same conversion enzymes. This is impor tant tant because because if you have an excess of dietary o mega-6, the the conversio n enzymes will be busy converting the LA omega-6 and won’t have room to convert the ALA omega-3 to the highly beneficial EPA and DHA. It is also very important to note that the conversion from ALA to EPA and DHA is est imated ated t hat o nly nly 5% of diet dietary ary ALA ALA is converted t o EPA very inefficient. i nefficient. It is estim and DHA. If you add in a bunch of LA omeg a-6, then due due to competition co mpetition with the the shared conver sion sio n enzymes, very ver y little ALA is co nverted to EPA EPA and DHA DHA (now less than 5%). You can bypass the poor poo r conversio conver sion n by eating EPA EPA and DHA DHA directly dir ectly from fr om fatty fatty fish, but this is obviously a problem for fo r veget veg etari arians ans who try to get all of their omega-3 in the form for m of ALA ALA from fr om sources so urces like flaxseed. flaxseed.
TECHNICAL NOTE: The preceding graphic was simplified significantly, and left out an
important omega-6 called dihomogamma linolenic acid (DGLA). It is synthesized synthesized fr om GLA and is made m ade into AA. DGLA is interesting i nteresting as an omeg a-6 in that it has anti-inflammatory properties. The conversion graphic highlights the problems encountered with shared conversion enzymes for omega-3 and omega-6 PUFA. As noted, strict vegetarians and vegans can have a hard har d time gett g etting ing enough enoug h EPA EPA and DHA—w DHA—which hich is critical cr itical to health—due to the poor conversion of ALA. This is especially problematic if the same vegetarian or vegan is taking in a high amount of omega-6 PUFA at the same time.
QUICK QUICK MEDICAL MEDICA L NOTE: DHA DHA is especially especiall y impor impo r tant for brain br ain function. A full 40% o f the cell membranes of nerve cells ar e comprised compri sed of DHA. DHA. DHA is especially important for children with developing brains, and elderly with potentially degenerating brains. Women of reproductive age show an increased incr eased efficiency over o ver men m en for converting conver ting ALA to EPA EPA and DHA. DHA. This makes sense, as they would need to pro vide plenty of DHA DHA to a developing developing fetus fetus for fo r brain development during during pregnan preg nancy cy.. Children do not have this conversion advantage, so it is extremely important that kids get adequate EPA and DHA. Enforcing a strict vegan lifestyle o n a child and neglecting neg lecting adequate amounts of DHA, DHA, can lead to developmental problems if not supplemented.
SUPPLEMENTATION? Given what we know about competition for membrane placement and competition for conversion enzymes, the better approach to balancing omega-3 and omega-6 would be to decrease the amount of omega-6 in the diet and increase the omega-3 fro m whole whole food, fo od, high quality quality sources.
Supplementing omega-3 using fish oil capsules, while you continue to eat high omega-6 omega-6 processed pro cessed food, foo d, has a couple of disadvantag disadvantages es in our opinion: opinion:
• This approach appro ach is trying to to directly dir ectly outcompete the high om omega-6 ega-6 with high omega-3 intake. The human body only needs small amounts of both omega-3 and omega-6, so this has a potential to overwhelm the system. • Omega-3s are still still polyunsat polyunsaturated urated fats, fats, and prone pro ne to oxidation oxidation and free fr ee radical formation because of the multiple double bonds. The process of extracting and stor stor ing fish fi sh oil leaves these these fragile fragi le double bonds exposed to to heat and light, creating omega-3 free fr ee radicals. Free radicals, omega-3 or not, are not good go od things things to import impor t into into your body. body. Similarly, the omega-6 extracted in industrial processes to form vegetable and seed oils, also have the potential to form significant amounts of fatty acid free radicals!
QUICK QUICK MEDICAL MEDICA L NOTE AND AND RESEARCH UPDATE: UPDATE: Recent research has starting to link an unbalanced omega-6 to omega-3 ratio (o ne that that is high in o mega-6) to an increased incidence incidence of o f allergies and asthm ast hmaa. This makes sense as high levels of omega-6 lead to increased inflammatory eicosanoids and over-active immune systems. Balancing your omega-6 and omega-3s may help decrease decrease the severity severity of aller gy symptoms and asthma.
Maintain the balance for your health
STRONG MEDICINE TACTICS: To balance omega-3 and omega-6 PUFA, decrease high omega-6 processed pro cessed vegetab vegetable le and seed oils, and increase whole whole foo food d sources sour ces of omega-3 such as wild caught fish and products from pastured animals eating their natural diet.
TRANS FATTY ACIDS (TFA) Trans fatty acids, or “trans fats” as you may have heard them called, do exist in small amounts in natural foods, but it is the TFA produced by man-made processes that have negative effects on o ur health. Chemically, the concept of TFA is relatively simple. As you now understand the chemistry of the double bond, the following shouldn’t make your eyes glaze over too much. There are two types of double bond configurations in fatty acid carbon chains. The most common configuration which occurs in almost all fats is called “cis.” The configur ation ation which is relatively rare in i n nature nature is called “trans.” Cis and trans simply describe where the hydrogens are positioned on the double bond. This positioning changes the structure of the fat considerably, and we have previously discussed how important structure is to function in the body. Small changes in structure can change function dramatically.
The cis configuration config uration has the hydro hydro gens on the the same side of the the double bond.
The trans configuration config uration has the the hydro hydro gens on the opposite side of the double bond.
This seeming small change change in the the double bond configur ation profoundly pro foundly changes changes the way way trans fatty fatty acids o perate in the body. body. As most trans fats in our food supply are not products of nature but man-made,
our bodies treat them as foreign invaders and the result is increased inflammation and oxidative stress. With this effect in mind, it comes as no surprise that routine intake of trans fat has been linked to diseases associated with chronic
inflammation and oxidative stress such as heart disease, diabetes, cancer, and neurodegenerat neurodeg enerative ive diseases such s uch as Alzheim Alzheimer’ er’ss dementia. This is the 18 carbon cis monounsaturated mo nounsaturated fat, oleic acid. This is i s the same healthhealthpromoting fat found in olive oil we discussed earlier. Notice that the hydrogens on either side si de of the double bond bo nd are o n the same side. Also notice no tice the the kinked shape this this cis double bond gives the tail.
This is the 18 carbon trans monounsaturated mo nounsaturated fat, elaidic acid. Other than the configuration of the double bond, it is chemically identical to oleic acid. Notice what the tr tr ans double bond bo nd does to the kink in the tail, tail, r esulting in a “str aighter” aighter ” carbon backbone. This structural change makes all the difference in the world to the body, as as elaidic acid is a well-known well-kno wn tr tr ans fat linked to diseases such as cancer and heart disease in humans.
INVESTIGATE YOURSELF!
Did you know that according to the Food and Drug Administration, a food manufact manufacturer urer can claim “zero trans fats” fats” if there are less than 0.5 grams of trans fat per serving size in the product pro duct?? If something has hydro hydro genated genated or partially hydr hydr ogenat og enated ed oil of any type type listed listed among the is some am amount of t rans fat present , despite any ingredients, t here is claims to the contrary.
WHERE DO TRANS FATS COME FROM?
In the early 1900s it was discovered that you could make liquid oils solid, by putting them through a process called hydrogenation. Hydrogenation is a process in which hydrogen is added through a catalytic reaction to unsatur unsatur ated fatty fatty acids. Unsaturated Unsaturated vegetable oils o ils can be produced pr oduced much mor e cheaply cheaply than than animal-based animal-based fats fats for use in cooking coo king and as foo d additives. As you now no w know, know, unsaturated fats have double bo nds, leaving them susceptible susceptible to o xidation when left out in the the open or o r in stor age. You You may have have heard of o f fat going go ing “r ancid”—t ancid”—this his is the result of o xidation xidation o f the double bonds in i n unsaturated fats.
Food manufacturer manufacturer s had the the idea of artificially adding hydrog ens to to the the unsaturated vegetable oils, making them saturated (or at least more saturated) and thus resistant to “going rancid.” This extended shelf life and created cr eated an inexpensive long lo ng lasting l asting fat f at that that wouldn’t go bad. Vegetable shorte shor tenings nings and margar ine are examples of “foo ds” made made using this process pro cess of turning liquid vegetable vegetable oils int i nto o pr oducts oducts that that are solid at room temperature. Unfortunately, the process of hydrogenation alters many of the unsaturated fat’s double bonds, turning them from the natural cis configur ation ation to the rare trans configuration config uration that that our bodies are not equipped to process. During the 1950s and 1960s, hydrogenated vegetable fats became more widely used than the traditional animal fats of lard and tallow for cooking and food ingredients. It is quite interesting that heart disease, formerly a relatively rar e health health problem, pro blem, increased dramatically dramatically during the the same time period as the widespread use of hydrogenated and partially hydrogenated vegetable and seed oils. Hydrogenated and partially hydrogenated vegetable oils are industrial concoctions not found in nature—enough said.
STRONG MEDICINE TACTICS: Eliminate any food or foo Eliminate food d product containing containing hydr hydr og ogenat enated ed or partially hydro hyd ro genat genated ed vegetab vegetable le or seed oils (including (including soybea so ybean n oil) fr om your diet. Read your labels!
TECHNICAL NOTE: There ar e some naturall naturally y occurr ing trans fats in animal-based animal-based foods that that
have not shown to have bad health consequences. One of o f these is vaccenic Vaccenicc acid aci d acid found in dairy products, as well as human human breast br east milk. Vacceni is converted into into a highly beneficial gr oup of fats known known as conjugated linoleic acid (CLA). CLA has been shown to have anti-cancer properties Aside from fro m and has shown promise as a weight loss aid for humans. Aside being formed from vaccenic acid, CLA can also be found directly in milk and meat meat from fro m pastured pastured (grass-fed) (g rass-fed) animals. We have spent a disproportionate amount of time discussing fats, but hopefully it was time well spent. If you are interested in further study into the world of fat, an excellent book boo k is “Know Your Your Fats,” Fats,” by Mary Enig, Enig , PhD. Now get ready to dive headfirst into the basics of human metabolism. We have to know how the flesh machine is supposed s upposed to function to understand the the consequences co nsequences and causes causes of a broken br oken metabolism. metabolism.
“MILITARY INTELLIGENCE” INT ELLIGENCE” (REFERENCES): Astbury Astbury SM, Corfe BM . “U ptak ptak e and metaboli sm of the short-cha short-chain in fatty acid butyrate, utyrate, a criti cal revi ew of the li terature,” terature,” Curr Drug Metab 13 (2012): 815. Nutr 93 (2011): 684. Astrup Astrup A, et al . “T he role of re ducing intake s of saturated saturated fat in the the preventio n of cardio vascular vascular disease : where does the e vi dence dence stand in 2010 ?” Am J Clin Nutr Baer DJ, e t al. “W hey protei protei n but not soy protein suppleme ntatio ntatio n alte alte rs body body wei ght and and compositio n in free- li vi ng overwei ght and and obese adults,” J Nutr 141 (2011): 1489. Bake wel l L, Burdge Burdge GC, Cal der PC. Poly unsaturated saturated fatty acid concentra concentratio tio ns in young men andwome n consuming consuming their habitual habitual diets, Br J Nutr 96 (2006): 93. Benjami n S, S, Spener F. Conjugated li nolei c acids acids as functio nal nal f ood: an insi ght into their health benefi ts, Nutr Metab (Lond) 6 (2009): 36. Brenna JT. Eff ici ency of conversion of al pha-l inol enic acid to long chain chain n-3 fatty acids in man, Curr Opin Clin Nutr Metab Care 5 (2002): 127. Childs Nerv Syst 28 (2012): 1723. Bueno-Carrazco Bueno-Carrazco J, e t al. Sodium butyrate butyrate increases the ef fe ct of the photodyna photodynamic mic therapy: therapy: a mechanism that that invol ves mo dulati on of ge ne expressio n and dif fe rentiation i n astrocytoma astrocytoma cell s, Childs Nutr Dev 45 (2005): 581. Burdge Burdge GC, Calder PC. Conversi on of alpha-l alpha-l inol enic acid to lo nger-chain nger-chain poly unsaturated saturated fatty acids in human human adults, Reprod ults, Reprod Nutr Burdge Burdge GC, Calder PC. Di etary alpha-l alpha-l inol enic acid and and heal th-related outcomes: a metaboli c perspecti ve, Nutr Res Rev 19 (2006): 26. Calde r PC. Branched-chain Branched-chain amino aci ds and immunity, J Nutr 136 (2006): 288S. Calder PC. Me chan chanisms isms of actio n of (n-3) fatty acids, J Nutr 142 (2012): 592S. Calder PC. Long-chain fatty acids and inflammation, Proc inflammation, Proc Nutr Soc 71 (2012): 284. Calde r PC, Yaqoob P. M arine om eg a-3 f atty acids and coronary heart heart dise ase, Curr Opi n Cardiol Cardiol 27 (2012): 412. Nutr 61 (2010): 653. Cle gg M E. M edium-chain edium-chain trigl ycerides are advant advantageous ageous in promoting promoting we ig ht lo ss although although not benef benef ici al to exe rcise performance, Int J Food Sci Nutr Inflammopharmacology 16 (2008): 216. Covas MI . Bio active e ff ects of ol iv e oi l phenoli c compoun compounds ds in humans: umans: reduc reduction tion of heart dise dise ase factors and oxidative damage, damage, Inflammopharmacology Dale y CA, Abbott A, Doyl e PS, Nader GA, Larson S. A revi ew o f f atty acid acid profi profi le s and and antioxi antioxi dant dant content content in grass-fe grass-fe d and andgrain-fe d bee f, Nutr J 9 (2010): 10. 48, 612 (2012). Donohoe, D. R . et al . The Warbu Warburg eff ect dictates the the me chan chanism ism of butyrate-medi ated histone acetyl ation and and cel cel l proli fe ration, Mol Cell 48 Evans LM, Co wey SL, Sie gal G P, Hardy Hardy R W. Stearate Stearate prefe rentiall y i nduces uces apoptosi apoptosi s in human human breast breast cancer cancer cel ls, Nutr Cancer 61 (2009): 746. Gol omb BA, Die tary fats and and heart heart disease- -dogma chall chall enged?, J Clin Epidemiol 51 (1998): 461. Kang Kang J X, Li u A. The role of the the tissue omega-6/omega-3 f atty atty acid ratio ratio in regulating tumor tumor angioge nesis, Cancer Metastasis Rev (2012). Clin Nutr Nutr 55, 88 (2001). Kel ly F D, et al. A ste aric acid-ri acid-ri ch diet i mprove mprove s thrombogenic thrombogenic and atherogenic atherogenic risk factor profi le s in heal heal thy male male s, Eur J Clin Kie colt-Gl aser JK, e t al. Omega-3 fatty acids, acids, oxi dative dative stress, and andle ukocyte tel omere l ength: A random randomiz iz ed controlled controlled trial, Brain Behav Immun 28 (2013): 16. Kuipe rs RS, e t al. Saturated fat, carbohydr carbohydrates and cardi ovascul ar di sease , Neth J Med 69 (2011): 372. Leonel A J, A lvarez-Le ite JI , Butyra Butyrate: te: impli cations cations for intestinal intestinal function, function, Curr Opin Clin Nutr Metab Care 15 (2012): 474. Liu YM, Wang HS, Medium-chain Triglyceride Ketogenic Diet, An Effective Treatment for Drug-resistant Epilepsy and A Comparison with Other Ketogenic Diets, Biomed J 36 (2013): 9. Loef M, Walach H. The omega-6/omega-3 ratio and dementia or cognitive decline: a systematic review on human studies and biological evidence, J Nutr Gerontol Geriatr 32 (2013): 1. Metabolism 47 (1998): 529. Louheranta AM, et al. A high-stearic acid diet does not impair glucose tolerance and insulin sensitivity in healthy women, Metabolism 4 Mak i KC, Slavin J L, R ains TM, & Kris-Etherton PM. PM. Limi tations tations of observationa observationall evi dence: dence: impli cations cations for evi dence-ba dence-based sed dietary dietary recommendations. ations. Adv Nutr 5 (2014): 7-15. Me ij er K, de Vos P, Prie be MG . Butyrate Butyrate and other short-cha short-chain in fatty acids as modulators of immunity: what rele vance vance f or health?, Curr Opin Clin Nutr Metab Care 13 (2010): 715. Nutr Metab 58 (2011): 66. Me nsink RP, Di etary Fatty acids and and cardiovascular heal heal th - an ongoing controversy, Ann controversy, Ann Nutr Mo zaff arian D, Wu J H. Omega-3 f atty acids acids and and card cardio vascular vascular disease: e ff ects on risk risk factors, mole cular cular pathways, pathways, and cli cli nical eve nts, J Am Coll Cardiol 58 (2011): 2047. Thromb (2013). Ohira H, et al . Butyrate Butyrate A ttenuates ttenuates Infl ammation and Lipol ysi s Ge nerated nerated by the Interactio Interactio n of Adipocytes and and Macropha Macrophages, ges, J Atheroscler Thromb (2013). Page KA, et al . M edium-chain fatty acids acids i mprove mprove cognitiv e f unction in i ntensiv ntensiv el y treated type 1 diabetic patients and and support in vi tro synaptic synaptic transmissi transmissi on dur during ing acute acute hypoglyce mia, Diabetes 58 (2009): 1237. Vitro (2013). Paskova L, e t al. Di ff erent eff ect of sodi um butyrate on cancer and and normal prostate prostate cel ls, Toxic ol In Vitro (2013). Nutrients 4 (2012): 1868. Pham Pham TX, Lee J . Di etary regulation of histone acetyl ases and and deacetylases f or the the prevention of metaboli c dise ases, Nutrients Chem (2013). Porter NA. A Pe rspectiv rspectiv e on Free Radical A utoxidation: The Physi Physi cal Organic Chemi stry of Pol yunsatu yunsaturated rated Fatty Aci d and andSterol Peroxi datio datio n, J Org Chem (2013). Psomiadou E, Tsimidou M. Stabili Stabili ty of virgin ol ive oil . 2. Photo-oxidation Photo-oxidation studies, studies, J Agric Food Chem 50 (2002): 722. Ranall Ranall i A, F errant errantee M L, De Mattia G, Costantini Costantini N. Analyti Analyti cal cal evaluation evaluation of virgin ol ive oil of f irst and and second extraction, extraction, J Agric Food Chem 47 (1999): 417. Ri zos E C, El isaf M S. Current Current evidence andfuture perspective s of o mega-3 polyunsatur polyunsaturated ated fatty acids for the the preventi on of cardio vascular disease , Eur J Pharmacol 706 (2013): 1. Ri zos EC, Ntz ani ani EE , Bik a E, Kostapan Kostapanos os MS, El isaf M S, Associatio n betwee n omeg a-3 fatty acid acid suppleme ntatio ntatio n and and risk of majo r card cardio vascular vascular dise dise ase eve nts: a systematic revie w and and meta-analysi s, JAMA 308 (2012): 1024. Ro el ofse n H, Priebe M G, Vonk Vonk R J. T he interaction of short-cha short-chain in fatty acids wi th adipose adipose ti ssue: rele vance vance fo r preve ntion of type 2 diabetes, diabetes, Benef Microbes 1 (2010): 433. Russo I , Luciani A , De Cicco P, Troncone Troncone E, Ciacci C. Butyrate Butyrate atte nuates l ipopoly saccha saccharide-i ride-i nduced uced i nflammation i n intesti nal nal cel ls and and Crohn’s mucosa through rough modulati modulati on of antiox idant def def ense machinery, machinery, PLoS One 7 (2012): (2012): e328 41. ASEB J 14 (2000): 2380. Saemann Saemann MD, e t al. A nti-i nflammatory ef fe cts of sodium butyrate butyrate on huma human n monocytes: monocytes: potent inhibiti on of I L-12 and and up-regulatio n of IL- 10 produc productio tio n, F n, FASEB Nutr Food Res 53 (2009): 315. Schnei der C. An upd update ate on products products and mechani sms of l i pid peroxi dation, Mol dation, Mol Nutr Segain J P, et al . Butyrate Butyrate i nhibi ts infl ammatory ammatory responses through through NFk appa appaB B inhibiti on: impli cations for Crohn’s dise ase, Gut 47 (2000): 397. Nutrigenet Nutrigenomics 6 (2013): 1. Shaw Shaw B, et al . Indivi dual Saturated and Monounsaturated saturated Fatty Acids Trigge r Disti nct nct Transcriptional Transcriptional Ne twork s i n Dif fe rentiated 3T3- L1 Preadipocytes, J Nutrigenet Med (Maywoo d) 233 (2008): 674. Simopoulos A P. The i mportanc mportancee o f the o mega- 6/omeg a-3 f atty acid ratio ratio in cardio vascular vascular dise ase and other chronic chronic diseases, Exp Biol Med (Maywoo World Rev Nutr Diet 102 (2011): 10. Simopoulos AP. Importanc Importancee of the omega-6 /omeg a-3 balance balance i n heal heal th and anddisease: evol utionary utionary aspects of die t, World Mol Neurobiol Neurobiol 44 (2011): 203. Simopoulos AP. Evol utionary utionary aspects of die t: the omega-6 /omeg a-3 ratio and the brain, brain, Mol Nutr 91 (2010): 535. Siri- Tarino Tarino PW, Sun Q, Q, Hu FB, K rauss RM . M eta-analysi s of prospective cohort cohort studie s eval uating uating the associati on of saturated saturated fat with cardiovascular cardiovascular dise ase, Am J Clin Nutr Stanhope hope KL , et al . Consuming Consuming fructose-swe ete ned, not gl ucoseucose- swee tened, beve beve rages increases visce ral adiposi adiposi ty and and li pids and anddecreases insulin sensiti vi ty in ove rwei ght/obese ght/obese humans, mans, J Clin Invest 119 (2009): 1322.
Sun Sun LB, et al . Serum palmi palmi tic acid-ol ei c acid ratio ratio and and the the ri sk of coronary coronary artery artery dise ase: a case-control study, J Nutr Biochem 22 (2011): 311. Teres S, et al. Ole ic acid content content is responsible f or the the reductio reductio n in blo od pressur pressuree i nduced uced by oli ve oi l, Proc Natl Acad Sci USA 105 (2008): 13811. Lipids 40 (2005): 1229. Tholstrup T. Influence of stearic acid on hemostatic risk factors in human humans, s, Lipids Tsuji H, e t al. D ie tary medium-chain medium-chain triacylgl ycerol s suppr suppress ess accumulation accumulation of body body fat i n a double ouble -bli nd, control control le d trial trial in healthy men and and women, J Nutr 131 (2011): 2853. Vi nolo M A, e t al. Suppr Suppressi essi ve e ff ect of short-chain short-chain fatty acids acids on production oduction of proinfl ammatory ammatory medi ators by by neutroph neutrophil il s, J Nutr Biochem 22 (2011): 849. Voon PT, Ng TK, Le e VK , Nesaretnam K. Di ets high in palmiti c acid acid (16:0), lauric and myristic acids (12:0 + 14:0), or ol ei c acid acid (18:1) do do not alter postpran postprandial or fasti ng plasma plasma homocysteine and infl ammatory ammatory marke rs in Nutr 94 (2011): 1451. healthy Mal aysian adults, Am ults, Am J Clin Nutr Waterman Waterman E, Lock wood B. Active components and and cli nical appli appli cations of oli ve oi l, Altern Med Rev 12 (2007): 331. Endocrinol Metab 302 (2012): E1. Watt Watt MJ , Hoy AJ, Muoio DM, Coleman RA. Disti nct nct roles of specifi c fatty acids acids i n cellular processes: processes: impli cations cations for i nterp nterpreting reting and and reportin reporting g e xperiments, xperiments, Am J Physiol Endocrinol
BASIC TRAINING II:
NUTRITION NUTRITION AND AN D METABOL METABOLISM ISM 101: META MET A BOLISM BOL ISM BASICS BAS ICS
Any discussion about human metabolism is quickly lost in the incredible complexity of this dynamic self-regulating system. Whole academic textbooks are written on the subject and are still lacking in some way. We will greatly simplify the discussion by focusing on overarching ideas and concepts. Essential details will emerge.
ENERGY AS CURRENCY Metabolism is the production and utilization of energy from the foods we eat. Foods and beverages are converted into the fuel needed to run the human body. The human body uses a specific molecule as its energy currency. Everything revolves around making and breaking down this molecule for energy. We make money and we spend money o n essential needs. It It is the same with ener gy—we manufacture and distribute, or “spend,” our available energy on the body’s essential needs. This molecule of energy currency is known as adenosine triphosphate (ATP). Our body and brain control the metabolism. Think of metabolism as your home
thermostat: optimally, we want a fast metabolism. Through the skilled blending of intense exercise and certain power-packed nutrients found in regular food, we can “amp up” or accelerate the metabolism. We want to raise our metabolic thermostat. A morbidly obese individual has a snail-paced metabolism while a super active ten-year-old boy will have a blast-furnace metabolism. The obese person’s slow metabolism is very efficient in its use of fuel. The burning hot metabolism of the lean and athletic youngster is a raging bonfire; a bonfire craves big logs (lots of food/fuel) to stay raging. We seek to build the metabolism, raise our home thermostat, build a metabolic bonfire, and inefficiently burn a lot more fuel (calories). The body has an innate wisdom and preferentially sends macronutrients to where they are most needed on an immediate basis. The metabolism regulates how much of each nutrient needs to be present at any one body location at any one time. You will learn how different types of food stimulate different hormones, which in turn control what type of fuel is used to make energy—fat or carbohydrate.
META MET A BOLISM BOL ISM CONCEPTS CON CEPTS The following are overarching ideas we will use to help you understand metabolism:
The brain is an energy and glucose hog.
1. The T he brain brain is an “energy hog ” and requires requires glu g lucose. cose. The average human brain weighs about three pounds. For a 170-pound person, the brain represents less than 2% of total body weight, but uses 20% of total daily body energy. The brain is also very particular about which type of fuel it uses. Most of the brain requires glucose to function. In a pinch the brain can use ketones as an alternate fuel.
CENTRAL CENT RAL THEMES THEMES CONNECT CONNECTION: ION: Because the the brain brai n requir r equires es glucose gl ucose as br ain fuel to make m ake ATP ATP,, when when bloo d glucose starts to drop, the brain quickly notices and signals the body to produc pro ducee more mor e glucose, or it generates generates a “sugar “sugar craving” so you will consume more glucose. In the “Chronic Stress” chapter, we will further discuss the hypothalamus and its role as the master regulator of the stress/threat stress/threat r esponse. The hypothalamu hypothalamuss is also a regulator r egulator of metabolism metabolism and hunger which ensures the brain receives a consistent supply of glucose. Low glucose in the brain is considered a “threat.” Perceived threat in the brain (in this case low glucose) is central to controlling our metabolism.
2. The T he liver liver is the t he glucose “banker” The liver r eceives eceives signals from fr om the br br ain to to keep bloo blood d sugar at a (relatively) (relatively) constant constant level. level. The liver will stor e glucose gl ucose when when dietary dietary levels o f carbohyd carbo hydrate rate are high. The liver r eleases glucose when when dietary intake is lo w. All the liver ’s actio actions ns are ar e done to maintain mai ntain adequate adequate levels of glucose gl ucose and keep the brain happy. happy. In times of starvation (i.e. radical calorie-restricted diets) the liver will make glucose from amino acids either from protein in the diet, or more often from “muscle cannibalism” when the body breaks down its own muscle tissue, strip mining it for amino acids.
Making glucose from amino acids stolen from protein is called gluconeogenesis gluconeogenesi s (gluco=glucose, neo= new, genesis= make). With prolonged starvation, the liver acts like the Federal Reserve and will print money (make glucose from amino acids derived from muscle) and put that energy currency into immediate circulation.
TECHNICAL NOTE: Gluconeogenesis actually happens all of the time, especially during the night as we sleep. As long as you have adequate adequate protein pr otein in your yo ur diet to to provide pro vide amino acids, the the process pr ocess will have minimal impact on your skeletal muscle. Muscle wasting happens in times of starvation/calorie r estrictio n without without adequate adequate protein pr otein intake.
3. Skelet Skeletal al muscl musclee has a large capacit capacit y to t o store st ore glu g lucose. cose. Muscle can store five times more glucose (as glycogen) than the liver. The caveat with glucose stored in muscle—when glucose goes in, it cannot come back out. The muscle holds onto glucose gl ucose in case it needs needs to to use it for a “flight or fight” response, such as running away from fro m a bear at full speed. speed. Fat cannot fuel this type of extreme muscular effort, so the muscles store large amounts of glucose in case it is needed as a survival mechanism. Muscle will not
and cannot share this stored glucose with the brain (even under starvation We will use this fact to our advantage advantage by implementing im plementing intense exercise exercis e conditions). We to create a large glucose “sink” in the muscle. Stay tuned for more on this topic.
TECHNICAL NOTE: Red Red blood bloo d cells are unable unable to use fat for an energy source so urce because they they do not have have mitochondria. They can can only use glucose g lucose for energy.
4. Our body runs more efficiently on fat but will use glucose first. Fat is the most efficient energy source for most of the body. Even our muscles use fat as their their primar y energy source so urce while at rest. Our o r gans and tissues tissues will will use
glucose befor e using fat for energy if i f we eat glucose in i n the the diet. When glucose is scarce, the body seeks to horde its dwindling glucose supply and shifts into a burn-fat-for burn-fat-for -fuel metabolic mo de. Using Using fat f at when when glucose is low spares glucose
for use by the t he brain brain (and red-bloo red-blood d cells). cells). 5. High High levels levels of glu g lucose cose in the t he bloo blood d are toxic. t oxic. Glucose is inherently toxic. Excess glucose promotes inflammation and oxidative stress. The metabolism of glucose for fo r energy cr eates eates free r adicals. Glucose “sticks” “sticks” to to pr oteins in the the blood and in the cells lining the blood vessels. This results in advanced glycation endproducts (AGE).
AGEs promote inflammation and oxidative stress. Our bodies are always detoxifying AGEs. The body is designed to clear low amounts of AGEs, produced by normal blood glucose levels, but is overwhelmed if blood glucose levels stay high. Several Several mechanisms keep keep blood bloo d glucose levels in the the “goldilocks” “go ldilocks” r ange, not too high, not too low, just right.
Large increases i ncreases in dietary dietar y glucose will be moved out of the blood to be used for energy (or stored in cells) by the actions of insulin. Controlling the interaction between glucose and insulin—and its overarching relationship with inflammation— is one key to mastering mastering body composition.
storage age 6. Fat cells cells are energy st orage orag e facilities. facilities. Fat cells (adipocytes) are energy stor facilities that dot the bodily geography. Excess energy is highly prized by the human body and is derived from dietary fat and dietary carbohydrate. Excess carbohydrate (glucose, fructose) intake will be stored in the liver and in the skeletal muscles. When the liver and skeletal muscles are filled to overflowing, the excess glucose is sent to fat cells and converted to fat for storage. Glucose is converted to to fat in fat cells for a couple of r easons: • The glucose has to go somewhere, as it is toxic toxic in the the blood bloo d stream at high levels. If the liver and muscles are “full” and the rest of the organs are using all they need, fat becomes the only place left for storage.
• Fat is over twice twice as energ y dense as carbohydr car bohydrates ates and pro tein. Fat contains 9 calories calor ies per gr am while while carbohydrate or prote pro tein in contains contains 4 calor ies per gr am. A pound of carbohydrate contains 1800 calories while a pound of fat contains 4100 calories. calor ies. You can store stor e mor e energy energ y in less space by conver conver ting ting glucose to fat. Fat from the diet which is not used for energy is stored directly in fat cells. How much dietary fat is stored depends on the current energy needs of the body and the level of certa cer tain in hormones hor mones in the bloo blood d stream.
7. The body uses both glucose and fat for energy. How much of each is used at any one time depends on o n the body’s energy needs, activity levels, the relative intensity of the activity and the brain’s requirement for glucose. The balance between between the use use of glucose gl ucose and fat (as fuel) i s called the “Randle Cycle.” Philip Randle first described the process in the early 1960s.
TECHNICAL NOTE: The body is always using both glucose and fat as fuel. The hormones insulin, glucagon, glucago n, and and growt gr owth h hormone hor mone determine determine the pr pr opor tions of glucose and fat used for energy. For example, high insulin levels mean very little fat will be burned for energy, and the body will use mostly glucose. gl ucose. It It is impor impo r tant to note that 100% fat or 100% glucose gluco se is never burned at any one time.
Mitochondri itocho ndria: a: the
cell’s power station. Mitochondriaa are ar e tiny powerho powerhouses uses 8. Mito Mitochondria chondria are the t he “energy facto ries.” ries.” Mitochondri residing inside each cell in your body. body. Mitochondria Mitochondria br eak down carbohydrates, carbohydrates, fat and protein. Mitochondria generate energy in the form of ATP. The number of mitochondria per cell differs differ s depending depending on o n the type type of tissue and varying needs for energy. Cells that have a high requirement for energy, such as those found in the liver, brain, and muscle, can have thousands of mitochondria in each cell.
Oxygen must be available for the mitochondria to make energy.
KEY POINT: Mitochondri itocho ndriaa can only make ener gy (ATP) (ATP) when oxyg en is available. available.
9. Much Much more more energy energ y can be generated generat ed from glucose glucose in the presence of o xygen. A full-speed sprint can only last for a matter of seconds. During a sprint, the body cannot cannot pro vide oxygen to the muscle muscle cells fast enough enough to allow glucose gluco se to be fully oxidized. Glucose will start breaking down in the cell, outside the mitochondria. A small amount of energy can be extracted without oxygen. pro cess of breaking Anaerobic (literally “without oxygen”) glycolysis is the process down glucose for energy. • Only a very small amount of energy energ y (ATP) (ATP) can be gener ated with glycolysi gl ycolysis. s. The end product of glycolysis is lactate. Lactic acid ‘build-up” often occurs during intense exercise. Lactic acid is the end product of breaking down glucose for energy without without any oxygen present. present. • If you slow down the sprint, spr int, to allow allo w oxygen oxyg en to arr ar r ive in the muscle cells, some som e of the breakdown products of glucose can now enter the mitochondria. With an infusion of oxygen, the the body is able to make significantly more mor e energy energ y.
The above picture represents a cell in your body. The internal parts of the cell are suspended in cytosol, the liquid inside the cell that is similar sim ilar to the water inside a water balloon. The mitochondria (not (no t drawn to to scale) are r epresented epresented in purple and suspended in the the liquid cytosol. cytoso l. You do not need to know the technical technical names listed in the picture, pictur e, just fr om glucose g lucose in the the cytoso cytosol. l. follow the arrows from When there is no oxygen present (anaerobic), the breakdown breakdown of glucose stops at lactate, and only two AT duced. AT P are pro duced. breakdown pro duct duct of g lucose When oxygen is present (aerobic), ( aerobic), the breakdown can enter enter the the mitochondria, leading to pr oduction oduction o f 38 AT AT P from one glucose molecule!
10. Burni Burning ng fat requires requires the t he presence of oxygen. oxyg en.
From the above picture, you can see that fat (triglyceride) is broken down into three separ ate 16 carbon palmitat palm itates es in the cytoso cytoso l, and must enter enter the mitochondria to be used as energy. Remember that since mitochondria must have oxygen to generate energy, fat can only be be burned burned in t he presence of oxygen oxyg en (called an aerobic process). The payoff is worth it, as one 16 carbon palmitate fatty acid can generate 104 ATP!
Because it uses both fat and glucose to generate ATP in the presence of oxygen, oxyg en, you can see why aerobic aerobic exercise exercise can be sustained for so so long (as ( as in a maratho marathon). n).
DIET, HORMONES, AND THE RANDLE CYCLE With the previous 10 concepts in mind, let us figure out how it all works when applied to daily life.
The preceding diagr am simplistically simplistically summarizes the metabolic metabolic r esponse to to food foo d intake. We will plug in some details in different situations to help deepen your understanding using 10 central concepts as a guide. A high carbohydrate meal plugged into the “FOOD” box has a specific reaction.
CASE 1: HIGH H IGH STARCH/SU STARCH/SUGAR GAR MEAL ME AL Foods containing pro cessed flour are starches (example: (example: bagels) bagels) and are quickly quickly bro ken down down to to lar ge amount amo untss of g lucose by digestion. digestion.
The larg e amount of glucose pr oduced by by digestion (of a bagel) causes causes a reaction by the pancreas. The pancreas is situated near our digestive tract releases and when when large larg e amounts of glucose g lucose are ar e present, t he pancreas releases
insulin. “st oragee and build buildin ing” g” hormone. It has the following actions Insulin Insulin is a “storag in the body:
• Insulin Insulin allows allo ws entry of glucose gl ucose into cells. The glucose gluco se is used as an energy source so urce or o r stored. Insulin Insulin can be be thought of as a “gate-keeper” “gate-keeper” for fo r glucose. Without insulin, glucose (in most circumstances) can’t gain entry into the cells and stays in the bloodstr blo odstream. eam. Insulin Insulin is the mechanism used by the the body to to clear larg e amounts amounts of glucose g lucose fro m the the bloodstream. • Insulin Insulin increases incr eases glycogen synthesis synthesis from fro m glucose. • Glycogen is the the stor stor age for m of glucose and chemically chemically looks a lot like a starch. Glycogen synthesis is the process of taking excess glucose and storing it as glycog en. The liver and skeleta skeletall muscle store most of the the body’s glycogen. Glycogen is stored and ready to be broken down into glucose gl ucose when needed. • Insulin Insulin increases incr eases fatty fatty acid synthesis synthesis and storage stor age (making and stor stor ing fat). When the body has had its fill of glucose, and the liver is full of glycogen, glycog en, the the liver will become a fat-pro ducing ducing factor factor y. This can result in “high triglycerides” on a blood test at the doctor’s office. Fat produced by the liver along with dietary fat will be stored under the influence of insulin. • The machinery machinery (enzymes) (enzymes) for fat product pro duction ion and stor stor age is tur tur ned on by insulin. Any Any fat eaten eaten while insulin is i s high hig h will be shuttled off to fat storage depots instead of being used to make energy. Insulin decreases fat
breakdown and and turns turns o n the the machinery machinery for product pro duction ion and storage stor age of o f fat.
Insulin also turns off the machinery for “burning” fat. • Insulin Insulin increases incr eases protein pro tein synthesis synthesis and is a potent potent stimulator for f or building building pr otein and and muscle from fro m amino acids. • Insulin Insulin stimulates cell gr owth and division, divisio n, and and creates an envir environment onment favorable for new cell gr owth. owth.
Large amounts of insulin prevent fat from being used as a fuel. If you cannot effectively utilize fat for fuel it remains stored in unattractive places. Insulin is an essential hormone, crucial for growth and building processes pro cesses while while maintaining maintaining optimal bloo d sugar levels.
CASE #1 High insulin levels decidedly tip the balance in favor of “burning” glucose as a fuel for energy product pr oduction ion and stops fat f at from being burned for energy. The large larg e insulin release from fro m a bagel and orange juice meal will clear glucose fr om the the blood bloo d very r apidly (unless (unless you have diabetes diabetes)) and often “overshoo ts,” ts,” resulting in a r apid dro dro p in bloo bloo d sugar that that tri trigg ggers ers symptoms such as fatigue, difficulty diff iculty concentrating and hunger. It is no wonder wonder that that people people who eat this this type type of meal for breakfast (or a variation with with toast, toast, or cereal) will o ften be be hungry by mid mo rning.
QUICK QUICK MEDICAL MEDICA L NOTE: A condition called reactive reactive hypoglycemia is fair ly common commo n condition in which high carbohydrate meals produce an excessive insulin response. It is easily treated by modifying the diet to include more protein and fat in each meal, and significantly less starchy carbohydrates and sugars.
KEY POINT: Any meal based on processed starchy carbohydrates (with little protein or fat) such as pasta and bread will have the same effect on insulin insuli n and will larg ely stop stop fat from being used for energ y. With insulin insulin and glucose available in lar ge amount amo untss after a hig h carb meal, other other or gans in the body body that that do do not no t have have to to use glucose g lucose for energy will use glucose, as it is available and plentiful. Once insulin insulin clears much of the glucose lo ad from fro m the bloo bloodst dstrr eam, insulin levels will start to fall. Once insulin levels begin to fall, fat can start to be burned as fuel. The faster insulin is able to do its job and dispose of the glucose (shutt (shuttling ling it into cells for stor stor age or using glucose for energy) the faster faster insulin levels fall and normalize. Insulin sensiti se nsitivity vity is how well well insulin is able to to “trig ger ” entr entr y of glucose gl ucose fro m the the bloodstream into the cells.
INSULIN SENSITIVITY
A helpful way to to think about insulin sensitivity is to visualize vi sualize your yo ur house as a cell in i n the body. body. The street str eet and dr dr iveway outside your house is the bloo dstream. Let Let us say that that you are hosting a party and want want to to impr i mpress ess your fr iends with with a new electro electro nic front fro nt doo doorr to your house. ho use. To really r eally “class up” up” your party, party, you also hir e a doorman doo rman to activate activate your your front fr ont door by pushing a button when guests arrive to let them in your house. The doorman (playing the part of insulin) will look for your arriving guests (guests (g uests are glucose) g lucose) and meet them them at the the door. doo r. He He will push the button button of your newly newly installed installed electr electr onic doo r and the the door will open to let your guests inside your yo ur house. If If the button button works wor ks as it should when pressed, the door will open and let your guests in immediately. Let us say for some reason the button stops working well, and now takes 10 pushes before the door will open and let your guests in. As you throw large, lar ge, lavish l avish parties par ties with a huge guest list, li st, the the delay caused by the button button not wor wor king well well causes a line to to form fo rm o utside utside of your fr ont doo doorr and guests waiting in the driveway (just like glucose in the bloodstream waiting waiting to enter the cell). The button activating your door has lost its sensitivity to the doorman pressing press ing it. This is i s what happens in your body when sensitivity sensitivity to insulin is lost, leading to increased glucose in the bloodstream, and eventually diabetes. When the insulin sensitivity of a cell is low, it takes much longer for the “triggering” process to work. When a person (who is diabetic) is not sensitive to insulin, glucose is delayed from entering the cell and stays in the blood stream.
As long as there are high amounts of glucose in the bloodstream, insulin levels will not fall. The longer insulin is around, the less fat will be burned for energy. The loss of insulin sensitivity, also called insulin insulin resistance resist ance leads to diabetes.
CASE 2: LOW STARCH STARCH/HIGH /HIGH PROTEIN PROTEIN MEAL MEA L Let’s Let’s take take a loo k what what happens happens when we plug this meal into o ur “foo d box”. The lettuce lettuce wrap is car bohydrate, bohydr ate, but but has no starch to speak of. o f. The lettuce carbohydrate component is mostly the indigestible fiber called cellulose. We can’t extract glucose from cellulose because we don’t have red)) connecting the the “machinery” to dig est the the chemical bonds bo nds (in red glucose.
Since no glucose gl ucose is released fro m cellulose digestion, there there is no insulin
response to the lettuce wrap component. These particular particular tacos tacos ar e made with with gr ass-fed beef, beef, so they have have a good go od amount of pro tein tein that that will will be broken br oken down dur dur ing digest dig estion ion int i nto o amino acids. Amino acids stimulate the pancreas to secrete a hormone called
glucagon.
Glucagon has actions actions opposite to those those of insulin as far far as glucose is concerned:
• Glucago Glucagon n breaks breaks down down glycogen stored st ored in t he live liverr to release release dietary glucose is lo w (not eating eating starchy starchy carbohydrate car bohydrates) s) glucose. When dietary glucagon glucago n is r eleased to to break down stor stor ed glycogen. glycog en. The body seeks to to release glucose into the bloo bloodst dstrr eam to to preven pr eventt bloo bloo d sugar fr om becoming too low. low. o n gluconeogenesis— gluconeog enesis—th thee liver is i s the glucose “banker” “banker” • Glucagon turns on and when glucose starts to run out of stored glycogen, the liver starts to “print money” by making making glucose g lucose from fr om amino acids using the the process pro cess of gluconeog enesis. enesis. The liver uses amino acids to to make mor e glucose—this glucose—this amino acid derived der ived glucose can then be released into the blood stream. The brain is an “energ “energ y hog” and has has a heavy demand demand for glucose. When When dietary dietary glucose g lucose sources sour ces such such as star star ch and sugar are lo w, most of our o ur or gans and tissues tissues will will burn fat as an energy source, sparing glucose for use by the brain, glucose-dependent red blood cells and the kidneys. The fat from the beef and avocado (used to make the guacamole) is a good mixture of saturated, monounsaturated, and polyunsaturated (grassfed beef has has a goo g ood d omega-3/omega-6 omeg a-3/omega-6 balance) balance) fats. Fat is “hor “hor monally neutral.” Dietary fat does not stimulate insulin or glucagon.
KEY POINT: Fat alone does not stimulate stimulate insulin or glucagon glucago n release. r elease. Overall, it is neutr neutr al for these these two two hormones. hor mones. Amino Amino acids derived fr om a pr otein meal will will stimulate stimulate a small release r elease of insulin. One of insulin’s actions is to increase protein synthesis, and to assist in the making of protein. This is one reason why elite athletes will consume amino acids post-workout; they want want to to purposefully trig ger the the anabolic anabolic (gr owth inducing) inducing) proper pr operties ties associated associated with with insulin secret secr etion. ion.
KEY POINT: Amino Amino acids from fro m protein pr otein will will stimulate stimulate a small amo unt of insulin release. The carbohydrate present in the the guacamole (fr om the the avocado) is mo stly fermentable fiber, so it will not contribute to release of insulin. The fermentable fiber will feed our gut bacteria. The resulting “waste” product is the beneficial shor s hor t chain satur satur ated fats fats (i.e. butyr butyr ate). The hormonal hor monal r esponse is mostly glucagon with a small amount of insulin —we tip the scales in favo f avorr of burning bur ning fat as fuel instead of o f car bs as fuel. fuel . Without much glucose around, the rest of the body stops utilizing glucose as a major fuel source and goes into fat burning mode. The body seeks to spare spare the glucose given out by the liver for exclusive use by the brain.
CASE CASE #2: Low insulin insulin levels and hig hig h glucago g lucagon n levels decidedly tip the balance balance in favor favor of “burning” fat as a fuel fuel for energy product pr oduction, ion, sparing glucose for fo r use by the brain.
DIGGING DEEPER: Does glucagon directly stimulate stim ulate fat burning? burning? The recent r ecent research resear ch regarding reg arding this this question question has shown conflicting result r esults. s. Some studies have shown that glucagon stimulates a fat releasing enzyme
called hormone sensitive lipase (HSL). But these studies were conducted on fat cells in a test tube. The few studies conducted with humans have shown no no effect of glucago n in direct dir ect stimulat stimulation ion o f breakin br eaking g down fat for energy. There are other hormo ho rmo nes that that definite definitely ly direct dir ectly ly stimulate stimulate fat burning, which we will discuss very soon. As we we have cover ed recent r ecently, ly, insulin stimulates the the machinery machiner y involved in in making and stor ing fat, AND AND inhibits the machinery involved invol ved with with fat burning such as HSL. HSL. Curr ent scientific scientific thoug ht is that that as insulin levels drop, the “brakes are taken” off of the fat burning machinery, allowing fat to be used as energ y. So it seems decreased decreased insulin levels levels are ar e mor e responsible r esponsible for fat burning burning than directly stimulating the effect of fat burning with glucagon. This is still an active area of research. Soon we may know how to better answer this question.
THE INSULIN/GLUCAGON RATIO
In CASE CASE #2 you yo u saw that that ther theree was some insulin insuli n released r eleased by eating our meal, but glucagon glucag on was dominant. do minant. With any given meal, meal , the balance between between the amount of insulin and glucago g lucago n present is known kno wn as the the amounts of insulin will will lead to using g lucose insulin/glucagon insulin/glucagon ratio. r atio. High amounts as an ener ener gy sour ce while while storing fat. When glucagon dominates, glucose will be used by the brain, the liver will break down glycogen to r elease glucose and make make new glucose fr om amino acids, and the rest of the body will switch to fat burning.
Insulin stops glucagon from being secreted by the pancreas. When there are high hig h insulin levels, glucagon levels are ar e usually very low. The reverse r everse is NOT true however, as glucagon itself has NO effect on stopping insulin secretion. A healthy metaboli metabolism sm can negotiat nego tiatee changes in the ratio r atio quickly and effectively in response to food, but with a broken metabolism (diabetes), rapid change is not possible. We’ll cover this much more in the obesity/diabetes chapter.
CASE 3: FASTING Dur Dur ing sleep, insulin levels fall rapidly r apidly after after the the increased blood bloo d glucose (from dinner) has been shuttled out of the blood stream. The falling glucose levels (and insulin levels) levels) tr tr igger igg er r elease of glucagon fr om the pancreas. We know that that glucago glucagon n will release r elease stor stor ed glucose fr om the the liver to feed the brain and red blood cells. We also know that glucagon will prompt the liver to start making making new glucose via gluconeogenesis. Since we are sleeping and have not recently eaten any any pro tein, the the liver would normally use amino acids “stolen” “stolen” from fr om the breakdown breakdown of o ur muscle to make new glucose gluco se to feed the brain. But But there there are ar e mechanisms in place to prevent the loss of muscle while we are sleeping—and any other time we are fasting. Dur Dur ing sleep, our muscle mass is mainly pro pro tect tected ed from fro m amino acid pilfering (to feed gluconeogenesis) by growth hormone (GH).
GH is secreted by the pituitary gland in response to a signal by the hypothalamu hypothalamuss (technically (technically this signal is another hormone hor mone called “g r owth owth hormone hor mone releasing hor mone”). Signals for r elease of GH include… include…
• Fasting • Intensive exercise • Deep sleep
SLEEP SLEE P YOUR WAY THIN THIN?? You can indeed burn your love-handles for energy while you sleep IF you are getting good sleep. Although GH is secreted throughout the day, the larg est amount amount is released r eleased in the the first fir st 1-2 hour hourss of deep sleep. sleep.
GH release is cut back significantly by poor sleep. Bad sleep sleep habits habits can stop st op your yo ur fat loss in itit s tracks! t racks! GH is an interesting hormone because it promotes muscle building through protein synthesis, while at the same time triggering fat breakdown for energy. These effects effects make sense if you view gro wth wth hormone hor mone as a muscle mass protect pr otector or during sleep and other times of fasting. GH is very potent in triggering the breakdown of fat cells for energy. In this way, GH provides the majority of the body with a plentiful supply of energy from fatty acids (fat). The question is, “How does the brain continue getting glucose if growth hormone shuts off the ‘theft’ of amino acids from muscle that would otherwise be used by the liver to make glucose for the brain?”
The liver can make a special kind of fuel called ketones. Ketones are created from fatty acids released by GH while you are sleeping. The brain cannot directly use most fats for energy, but two-thirds of the brain’s energy needs can be supplied by ketones made from fat during fasting and starvation. When the brain starts to use ketones as an energy source, the demand for glucose plummets and muscle tissue (and the body’s reserve storage of amino acids) is spared. GH increases liver gluconeogenesis (making new glucose). However a different sour ce—lactate, ce—lactate, lactic acid—is used.
KEY POINT: Growt Gr owth h hormone hor mone spares muscle fr om amino acid “theft “theft”” by jump-starting jump-starting ketone pro ductio duction. n. The brain br ain can now use ketones and doesn’t need as much glucose. Red blood cells and the inner parts of the kidney both produce energy from glucose anaerobically (without oxygen). They accumulate the lactic acid waste product pro duct and use use it during during fasting fasting for fo r making glucose in gluconeogenesis. gl uconeogenesis.
KEY POINT: When growt gro wth h hormone hor mone is around, ar ound, lactat lactatee is the major major source sour ce of new glucose, sparing amino acids (and sparing sparing your muscle!) muscle!)
CASE #3 REVIEW REV IEW:: • Dur Dur ing an overnig ht fast, fast, the the insulin/glucago insulin/glucago n ratio changes so that that glucagon glucago n is dominant. dominant.
• Most of the body switches switches to fat burning burni ng in order or der to preser ve and and reser ve adequat adequatee glucose for fo r the the brain. • Growt Gr owth h hormone hormo ne accelerate acceleratess fat burning, allowing for the liver liver to make ketones ketones fr om fat f at taken taken from fat cells. cells. • The brain can (mostly) (mostly) use ketones ketones in place place of glucose gl ucose dur dur ing fasting; when when fasting fasting there is also less need for glucose. • Growt Gr owth h hormone hormo ne spares spares prote pro tein, in, and and prote pro tects cts muscle fro m being being broken bro ken down down to to make glucose gluco se during fasting. • The glucose is primar ily made from fr om lactate lactate instead instead of amino acids. acids.
Glucago Glucagon n and Growth Growt h Hormone Hormone work together to burn fat while sleeping
YOUR HORMONES ON DE DESS SSERT ERT
Looking at the the effect of ice cr eam and cake cake from fro m a hor monal perspective perspective is included included to to dr ive home insulin’s insulin’s role r ole as a stor age hor mone. Again, when when large amounts amounts of insulin are trigg tri ggered ered by glucose, g lucose, the the body will store fat and glucose. No appreciable fat burning will take place under insulin’s umbrella.
INSULIN AND CARBOHYDRATES ARE NOT EVIL....
All of this talk about insulin, carbohydrates, and fat storing may give you
the (wrong) idea that insulin and carbs are bad things and need to be avoided at all costs. This view has unfortunately become very popular of late, and misses an impor tant point. Insulin and carbohydrates are crucially important to your health. It is the chronic loss of insulin sensitivity that leads to disease. Once insulin sensitivity is lost, los t, the the ability to handle starchy carbohydr car bohydrates ates in the the diet is compr omised omi sed as we discussed at the end of CASE CASE #1. An example to illustrate this point is the diet of a traditional culture such as the Okinawans. Okinawans. Tr Tr aditional Okinawan O kinawan diets diets consisted co nsisted of 85% carbohydrates, mostly eaten in the form of sweet potatoes. The traditional Okinawans were some of the longest-lived people on the planet, with many in their their populat po pulation ion r eaching eaching o ver 100 years o ld. They were were also lean l ean and relatively free o f chronic chr onic disease. The large lar ge amount of sweet potat potatoes oes definitely caused insulin to rise in their bodies. The key to their success is maintaining insulin i nsulin sensitivity. sensitivity. Do not be in a hur hur ry to blame insulin and carbo carbohyd hydrates rates for insulin resistance, diabetes, and obesity. There are other important factors at play, which we will soon explain. Once insulin comes back down, fat burning for energy can take place again. For someone with high insulin sensitivity, insulin will rise and fall very quickly. Once insulin subsides, fat burning for energy purposes can take place. A metabolically
“broken” individual with poor insulin sensitivity will maintain a relatively high insulin level long after the meal is eaten and will have a hard time burning fat for energy. We will show you how chronic inflammation and oxidative stress from multiple sources can lead to insulin resistance and wreck your metabolism—slowing fat burning to a crawl. A broken metabolism is one of the drivers of chronic diseases such as obesity, diabetes, heart disease, neurodegenerative diseases and even cancer. We will dive headlong into each of these underlying sources of disease now that you have the framework and knowledge to understand what is going on “under the hood.”
“MILITARY INTELLIGENCE” INT ELLIGENCE” (REFERENCES): Textbooks: Frayn KN. M etaboli c Reg ulation, A HumanPerspective, 3rd Editio n, John Wi le y & Sons Sons Ltd, West Sussex, Sussex, U nited Kingdom (2010).
Journals: Rev Endocrinol 6 (2010): 689. Habegger Habegger K M, et al. The metaboli metaboli c actions actions of glucagon glucagon revisite d, Nat Rev Heppner KM, et al. Glucagon regulation of energy metabolism, Physiol Behav 100 (2010): 545. Mo ll er N, J orgensen JO, Eff ects of grow th hormone on glucose, li pid, and protei n metabol ism i n human uman subjects, Endocr Rev 30 (2009): 152. Moller N, et al. Growth hormone and protein metabolism, Clin Nutr 28 (2009): 597. Perea A, Cle mente F, Martinell J. Vil lanueva-Penaca eva-Penacarr rril il lo, M. L., Valverde, Valverde, I., Physiologi cal cal eff ect of glucagon glucagon in human humanisol ated adip adipocytes, ocytes, Horm Metab Res 27 (1995): 372. Lipidol (2013). Stanhope hope KL, Schwarz Schwarz JM , Havel PJ . Adverse metaboli c effe cts of die tary fructose: fructose: results from the recent recent epidemio lo gi cal, cli nical, and and mechanisti c studies, Curr Opin Lipidol (2013). Endocrinol Metab 302 (2012): Vendel bo MH, et al . Insulin resi stance stance after a 72- h fast is associated wi th impaire impaire d AS160 phosphorylati osphorylati on and accu accumulation of l ipid and gl ycogen i n human uman ske le tal muscle, Am J Physiol Endocrinol E190.
CONGRATULATIONS CONGRATULATIONS ON COMPLETING COMPLETIN G STRONG MEDICINE MEDICINE BASIC TRAINING. PREPARE FOR ADVANCED TRAINING; WE ARE GOING TO MEET THE ENEMY...
PART II
KNOWING KN OWING YOUR YOUR ENEMY “If you know the “If t he enemy enemy and know know yourself, you need not fear the t he result result of a hundred hund red battles. batt les. If If you know yourself but not no t t he enemy enemy, for fo r every vict victory ory gained you will also suffer a defeat. If you know neither the enemy nor yourself, you yo u will will succumb succumb in every batt bat t le.” —Sun Tzu, The The Art of War
THE “PENTAVERATE” OF PESTILENCE These are the five enemies producing chronic inflammation and oxidative stress. They are a cabal of health calamity. We have collected ample intelligence on each of these nefarious characters. We will train you t o understand them t hem from fro m t he ground gro und up, up, and wil willl give defensive defensive t actics t o protect prot ect you fro m t heir heir advances. Each Each enemy enemy will will be briefed briefed in the foll fo llowin owingg order: • Gut Inflammation • Obesity and Insulin Insulin Resistance • Chronic Stress • Circadian Disruption We will will discuss discuss “Inact “Inactiv ivity” ity” (#5) (# 5) in Part 3 in our extensi ext ensive ve coverage coverag e of o f exercise. Notice Not ice that no matt matt er the t he specific specific enemy enemy, t he underlyi underlying ng cause of o f most most chronic disease is long-term inflammation and oxidative stress. The Pentaverate works together to cause the diseases listed in the black box. Those listed are only a fraction of diseases thought to be caused by chronic inflammation and oxidative stress.
KNOWING KNOW ING YOUR ENEMY I: I:
THE GUT: GUARDIAN AT THE GATE
Our intestin intestinal al tract will will likely l ikely become become a primar y focus as we learn mo r e about the the underlying causes and treatment of disease in the 21st century. century. Indeed Indeed the last decade has shown shown tremendous tremendous progr pro gr ess in our understand understanding ing of o f just how centr centr al this this or gan system is for maintaining health. The following discussion will be fairly lengthy, but a basic understanding of how the gut works and what happens when its function is disrupted is extremely important to your health. If you want to attain your body composition and fitness goals, go als, you cannot cannot overloo over look k this this section. section. Chronic inflammation of the gut is the first member of the Pentaverate. The intestinal tract (gut) is our first line of defense from outside “invaders” such as pathogenic pathogenic bacteria bacteria and from our modern moder n diet. diet. When the gut defenses are constantly stimulated, they can transform from protectors into agents of chronic disease. We will show you how to stop this insidious process with Strong Medicine defensive tactics. Proceed for in-depth training on the inner workings of the “guardian at the gate.”
GUARDIAN AT THE GATE PART I:
GUT HEAL HEA LTH: FIRST PRINCIPLES PRINCIPLES
A r ecent case study study published in the British Medical Jour nal described descr ibed the results of placing a 6-year o ld boy on a g luten luten free diet after after he was diagnosed diagno sed with type type 1 diabetes (T1D). For those of you that do not know, T1D is an autoimmune disorder in which the person’s own immune system destroys the insulin-producing cells in their pancreas, typically the person will be dependent on insulin injections injections for fo r the the rest of their life. The results of the gluten free diet with this child were remarkable. Within weeks of starting on the diet, he no longer needed insulin injections. Twenty Twenty months after after starting the diet, diet, he still did no t need daily insulin
treatments. Essentially, Essentially, the the gluten g luten free diet put his his T1D T 1D into into r emissio n. T1D is traditionally thought of as an incurable disease, so how was this child apparently “cured” with something as simple as a gluten free diet?
A “FIRST PRINCIPLES” ARGUMENT ARGUME NT THAT INTESTINAL INTE STINAL TRACT HEAL HE ALTH TH IS CRITICAL IN ATTAIN ATTAINING ING OVERA OV ERALL LL HEALTH: • Our intestinal intestinal tr tr act (gut) is wher wheree we absor b nutr nutr ients from fr om the the foo d we eat.
barrier through t hrough which we we “int “int eract” with • The intestinal intestinal tract is the first barrier outsid out sidee environmental environmental inputs inputs of food fo od and wat wat er, er, selectively letting in i n the “good” “go od” envir onmental inputs and keeping keeping o ut the the “bad” inputs. inputs. • This inter interaction action is the fir st oppor oppo r tunity tunity for the body’s defense against agai nst outside bacterial invaders and toxins/toxicants in our food and water. • A large lar ge pr pr opor opo r tion of our body’s body’s immune system is located lo cated in the intestinal intestinal tract. • When the gut immune system system is overactive, over active, bad things can happen. Chronic Chro nic inflammation inflammation is a result of pr olonged olo nged activat activation ion of o f our gut-associated gut-associated immune immune system. This creates chronic inflammation and oxidative stress in the body. • Chronic Chro nic systemic inflammation inflammatio n and the r esulting oxidative stress are ar e the main contributor contributor s to chronic chr onic diseases including cancer, athero atherosclero sclerosis sis and diabetes. diabetes. • The intestinal intestinal tr tr act and brain brai n are ar e closely clo sely connected. Inflammation in the gut is communicated to the brain, creating a body-wide stress response that can wreck our metabolism and ruin our health if left unchecked.
THE INTESTINAL INTESTINA L BARRIER The intestinal tract was designed to maximize absorption within the smallest possible space. The intestinal wall is intricately folded, creating structures called villi. The villi themselves are comprised of individual epithelial cells with their own
folds called microvilli. The “lumen” is the space “inside the tube” of the gut where food passes after digestion. The epithelial cells selectively absorb nutrients— amino acids from protein, glucose and fat—from digested food. The absorbed nutrients are sent into the blood stream, including amino acids, glucose, short and medium-chain fats and in the lymphatic vessels, long-chain fats are absorbed.
This is a close-up view of the epithelial cells (light brown.) Each is connected by tight junctions.(TJ). TJs keep large undigested particles of protein and harmful bacteria from penetrating through to the blood stream. This system allows nutrients (amino acids, sugars, fats) to travel through transporters in the microvilli. The epithelial cell barrier is our first line of defense (The Guardian at the Gate) from harmful things in our diet. We have a system of immune cells just below the epithelial layer (in the lamina propria) to deal with anything trying to bypass the tight junctio junctions. ns.
When the tight junctions fail, this is called intestinal permeability (IP) or “leaky gut.” IP allows harmful bacteria and undigested protein fragments into the lamina propria and the bloodstream. The immune system then launches its response against the interlopers, resulting in
inflammation. The intestines contain most of our body’s total immune system, 70-80% by many estimat estimates. es. This is a strategic strategic location for most of our immune defenses, as it is one of the first places where the inside of our body contacts things we bring in from the outside world—food and water— which may include disease-causing bacteria and viruses. The gut’s immune system is incredibly important for maintaining our health and defending against invaders. First, a brief review of the immune system, then a discussion on how the immune system can get out of control and attack our own body in a process called autoimmunity. Recent research has shown that the gut may be the primary place where autoimmunity is triggered.
IMMUNE SYSTEM REVIEW The immune system is highly complex. We have simplified the concepts considerably. Please reacquaint yourself with the main players of the immune system that we originally introduced in Basic Training. Because the majority of the immune system makes its home in the gut, it is crucial that you retain a basic understanding of how each member contributes to maintaining our first line of defense against threats from the outside world. The members of the gut immune system are tr uly the “guar dians at the gate.” gate.”
INNATE IMMUNE SYSTEM: The cells of the innate innate immune system are like the guar ds at the the castle gate. They will deal with anyone who looks or acts suspicious. This is usually the initial encounter encounter with with bacteria/vir bacteria/vir uses and and “for eign” pro tein tein fragment fr agments. s. Their response is not targeted at specific individuals, but is a general protective response to anything
deemed deemed “for “fo r eign.” eign.”
ADAPTIVE IMMUNE SYSTEM: These assassins are called T-cells and B-cells and once they encounter pieces of a prisoner priso ner caught by the the dendritic cells o r macropha macro phages ges o f the innate innate immune system, system, they “adapt” themselves. They morph and become perfect assassins for this specific type type of pr isoner. They They for m “clones” of themselve themselvess to make an army o f assassins once they have found a specific victim.
T-REGULATORY CELLS, AKA TREG CELLS: Think of these cells as the “hippie” anti-war protestor that helps control the assassins. Treg cells are the peace-loving part of the adaptive immune system and pro duce an anti-infl anti-inflammator ammatory y response. r esponse. We We need a balance between between Tr Tr eg cells cel ls and the assassins to prevent the immune system from attacking our own body tissues in something called autoimmunity.
AUTOIMMUNITY AUTOIMMUNITY AND AN D INTESTINAL INTESTINA L PERMEABILITY Autoimmunity occurs when our immune system (the innate guardians and
adaptive assassins) fails to recognize tissue in our body as “self.” Instead, the immune system gets its wires crossed and recognizes “self” tissue as foreign. As the immune system is designed to protect us from foreign invaders, it attacks and destroys destro ys our own tissue. This can happen in multiple tissue types. • • • •
Celiac disease: cells lining the the intestine intestine are ar e destroyed. destro yed. Hashimoto’s thyr thyr oiditis: oi ditis: the thyroid thyro id tissue is destroyed. destro yed. Multiple ultiple sclerosis: sclero sis: the the “insulation” “insulation” (myelin) (myelin) of our nerves nerves is destr destr oyed. Rheumat Rheumatoid oid arthritis: our joints are destro destro yed.
There are many theories currently being investigated why our own immune system turns on us. Some interesting theories involve the loss of Treg cells (hippies). We We also know that individual g enetics, specifically g enetics of the immune imm une system, play a large role in autoimmunity, but there are environmental “triggers” that jump-start the process. One leading researcher in the field has proposed that a third factor is necessary for the development of autoimmunity, intestinal ermeability. The theory of intestinal permeability as the third factor required for autoimmunity came from studying people with celiac disease. Celiac disease is an autoimmune disease triggered by intestinal intest inal permeability. People with this condition are known to have a much higher incidence of other autoimmune diseases. It is proposed pro posed that that what whatever ever the environmental environmental trigg tr igger—bact er—bacteria, eria, vir us, food particle—it must first come into contact with the immune system for a reaction. Intestinal Intes tinal ermeability allows the contact of the gut immune system with environmental triggers to take place.
KEY POINT: Intestinal permeability may be the third required factor for developing autoimmune disease. Review the graphic from the beginning of this section showing the intestinal barrier. Pay close attention to the tight junctions that prevent undigested food particles and bacterial invaders from penetrating the lining of the gut wall. When the tight junctions fail, things that should not get past the protective gut lining take the
passage that is now open between the intestinal epithelial cells forming the barrier. Failure of the tight junctions is the mechanism behind intestinal permeability (“leaky gut”). When this happens, undigested food particles and bacterial invaders come in contact with with the the immune system guar g uardians dians that are ar e defending the castle wall. The gut immune system is now on alert.
DISRUPTION OF THE BARRIER: CONSEQUENCES AND AN D CLINICAL DISEASE Daily exposure exposur e to things that induce induce intestinal intestinal permeability per meability can lead to: • Chro Chro nic inflammation, inflammation, the the precursor precurso r to to developing developing chronic chro nic diseases—diab diseases—diabet etes, es, obesity, cancer, cancer, Alzheimer ’s dementia dementia and heart hear t disease. • Autoi Autoimmune mmune diseases, which strike stri ke those who have a genetic predisposi pr edisposition. tion. Multiple sclerosis, rheumatoid arthritis, type I diabetes, Hashimoto’s thyroiditis, celiac disease, and Crohn’s disease are just some of the diseases influenced by intestinal intestinal per meability.
In this diagram, the tight junctions have been disrupted, allowing harmful bacteria and undigested protein fragments past the epithelial barrier. The immune system is now activated (red glow) glow) and the inflammatory response is initiated. Chronic intestinal permeability can also lead to reduced numbers of the Treg cells “hippies” and increased numbers of adaptive “assassins.” New science has shown that Treg cells are extremely important in prevention of autoimmunity. Having enough Treg cells is critical for preventing the adaptive assassins from getting getting out o ut of cont co ntrr ol.
Chronic intestinal permeability leads to the “assassins” outnumbering the
“hippies.” This sets the stage for out of control inflammation and autoimmunity because there are not enough hippies (Treg) to keep the assassins in check. We need to maintain the intestinal barrier and prevent chronic intestinal permeability perm eability to maintain a proper pr oper balance between between the “assassins” and the the “hippies.” “hippies.” Too many assassins leads to out of control inflammation and autoimmunity, while too many hippies would leave us vulnerable to invading microorganisms such as bacteria and viruses. When the balance between “assassins” and “hippies” is disrupted, chronic inflammation and autoimmunity are triggered, leading to disease.
Balance Balance prevent preve ntss aut o imm immunity and chronic chro nic inflamm inflammation. at ion. We will show you strategies on how to maintain this balance in upcoming sections, but first we will show you how chronic intestinal permeability (leaky gut) is triggered by components of processed food, stress, and disruption of our normal opulation of gut bacteria.
Recent science supports the idea that although you may have the genetics predisposing you to getting getting autoimmune autoimmune diseases, if your gut immune system system does not come into contact with the environmental trigger, you will remain free of disease.
KEY POINT: Even if you are genetically predisposed to autoimmune disease, avoiding
the the environmental environmental trigger trig ger s will prevent you from fr om developing o ne of these diseases. In the next section, your in-depth training on the causes of gut inflammation will continue. We will identify the environmental triggers of chronic intestinal permeability and train you in defensive tactics to protect yourself from these triggers. This is how we will bring down the first member of the Pentaverate and keep the “Guardian at the Gate” intact, protecting your health from the onslaught of chronic disease. disease.
GUARDIAN AT THE GATE PART II:
TRIGGERS OF INTESTINAL INFLAMMATION
TRIGGERS OF INFLAMMA INFL AMMATION TION Potential triggers for chronic inflammation in the gut leading to disease are the following:
1. Glut Glut en and other ot her diet dietary ary t riggers 2. Stress, the Gut-Brai Gut -Brain n Axis Axis 3. Dysbiosis, Dysbiosis, t he disruption disruption of gut bacteria bacteria
KEY POINT: It is very important to keep in mind that short term increases in intestinal permeability is a normal physiologic mechanism, and is an essential part
of our natural defenses to fight infectious bacteria and viruses in the gut, as well as to clear them from the body (diarrhea). It is only when we have long-term intestinal permeability and inflammation that we run into trouble.
TRIGGER TRI GGER #1: # 1: GLUTEN In Environmental Medicine, we judge the public health impact of potential environmental envir onmental toxins and toxicants on the toxicity of the compound and the potential potential for exposure. With gluten, toxicity will vary depending on the person, but potential exposure is extremely high. Gluten is always potentially problematic. Inflammatory reactions to gluten proteins—found in wheat, barley and rye food products—have received a lot of press over the last couple of years. The gluten family of proteins have become whipping boys in the dietary blogosphere and popular media. Although the demonization of gluten is somewhat justified and is supported by recent research, we need to look at this issue dispassionately. Gluten is an ingredient in countless processed foods (and many other products) so our potential potential for exposur exposuree cannot be underestimat underestimated. ed.
GLUTEN 101 • Gluten is the the main structural pro tein in wheat, wheat, barley barl ey and r ye. Gluten gives gi ves bread products their soft, doughy texture. Extra gluten is often added to make bread and bagels softer. • The toxic components components of gluten prote pro teins ins are called gliadins and and glutenins. glutenins. Proteins are “chains” of amino acids. Different amino acid sequences in the chains determine the shape of the protein, the ease of digestion, and most importa impor tant ntly ly,, their bio logic log ic function.
Amber Amber waves o f inflamm inflammation? at ion? • Parts of the the chains in gliadins gl iadins and gluten gl utenins ins are ar e very resistant to our digestive dig estive “machinery.” Small fragments of these proteins with amino acid sequences containing containing high amount amo untss of proline pro line and glutamine, glutamine, ar ar e responsible for fo r digestive digestive resistance. resistance. Glute Gluten n pro teins teins are ar e called “pro lamins” (proline (pro line + glut gl utamine). amine). • Prolamin Pro lamin protein pro tein fragment fr agmentss can trigg er intest intestinal inal permeability and immune response r esulting esulting in inflammation and oxidative oxidative stress. • Genetic differ ences in our immune systems r esult in individual differ ences in the strength and type of immune response to these prolamin protein fragments. Differing immune responses to gluten create differing classifications of glutenrelated diseases. • Celiac disease is also called gluten gl uten-sensitive -sensitive enteropath entero pathy y. This condition conditio n creates cr eates an innate and and adaptive adaptive immune r esponse. • Gluten sensitivity is an innate, non-specific non-specifi c immune r esponse.
SPECTRUM SPECTRUM OF GLUTEN-RELAT GLUTEN -RELATED ED DISEASE
genetics (and T he spectrum of glutenrelated disorders: your genetics epigenetics) determine the reaction of your immune system to gluten and where you fall on the spectrum.
without any known Between points A and B: People ar e able to eat gluten without adver adver se health health effects. effects. This group gr oup r epresents epresents the majority major ity of us.
Between points B and C: People Peo ple with Gluten Sensitivity. Sensitivity. Those in this range have immune reactions to gluten. The range includes those with no symptoms and a low lo w level of inflammatio i nflammation n to those with substant substantial ial symptoms, including irritable bowel syndrome (IBS). About 20-30% of us fall into this category.
Between points C and D: These people are afflicted with celiac disease. About 1% of the population has celiac disease. di sease. The variance among responses to gluten is largely genetic (and epigenetic). Many of the scientists studying the effects of gluten on health have come to the conclusion that there simply has not been enough time for humans to fully adapt to grains as a food source. Widespread agriculture has only been in existence for 10,000 years—a blip on the histori historical cal radar. Another interesting hypothesis holds that the increase of gluten-related health problems pro blems is in direct pr pr opor tion to to the increase in food pro cessing. Indust Industri rial al foods foo ds are constructed using cheap, subsidized grain containing gluten. The rise in the consumption of these artificial gluten-containing foods mirrors the increase in gluten-related health maladies. Traditional cultures have long used grains without nearly the degree of glutenrelated health problems Western cultures are experiencing. These cultures often prepare their grains using sprouting and fermentation processes that decrease the toxicity of g luten. (see Weston A. Price foundation.) One school of thought holds that genetic modification of grains, most particularly wheat, has changed the protein structures enough to promote an increased immune response.
QUICK QUICK MEDICAL MEDICA L NOTE: Recent Recent research resear ch is finding links li nks to to gluten for a wide range of o f diseases and metabolic disorders:
• • • • • • •
Insulin resistance Leptin Leptin r esistance Hashimoto’s thyroiditis thyroi ditis Neuro Neurolog logic ic diseases diseases Rheumatoi Rheumatoid d arthritis ar thritis Irritab Irr itable le bowel syndr syndr ome Inflammatory Inflammator y bowel disease (Cro hn’s, hn’s, ulcerative ulcer ative colitis) col itis) System Syst emic ic inflamm inflammation at ion st s t arting art ing in the gut may be t he hidden link link to
these conditions.
CELIAC DISEASE DISEASE (CD) This “disease” is not really that rare, affecting as many as 1 in 100 people. It is also under diagnosed. It is estimated that 90% of those with celiac disease are walking around undiagnosed. Undiagnosed children with celiac are short and scrawny for their age and are delayed developmentally. Celiac disease is not so much a disease as it is a mismatch between a person’s genetics and their environment. When the environmental trigger of gluten is removed, most CD patients see complete resolution of their symptoms. • The innate and adaptive adaptive immune systems each contribute contr ibute to the problems pr oblems seen in CD. • The undigested protein pr otein fragments fr agments of gluten proteins pr oteins disrupt disr upt the tight junctions of the the epithelial epithelial barr ier.
• The “innate guar dians” intercept the for eign eig n fragments, fr agments, ingest inges t them and display pieces on their cell surface. Individual genetics determine how these fragments are ar e displayed and the interaction inter action with the T-cell T-cell “adaptive “adaptive assassins”. assassi ns”.
• The adaptive adaptive assassin T-cells T-cells recog r ecognize nize the the displayed displayed gluten fragments frag ments as for eign, and for m clones to specifically r ecognize and unleash unleash their their destructive destructive arsenal. • Unfortuna Unfor tunately tely,, this r esults in the “nuclear option” as far as the intestinal barr bar r ier is concerned. The assassins assassins release large lar ge amount amo untss of inflammator inflammator y cytokines cytokines in response to g luten luten fragment frag ments. s. • The massive cytokine r elease increases incr eases the intestinal intestinal permeability perm eability even further, fur ther, letting letting in i n mor e gluten fragment frag mentss and for eign particle par ticless including bacteria. bacteria. The nuclear nuclear option physically physically destroys the epithelial epithelial barr ier in the process—akin to to an innocent casualty of war. Destruction of the absorptive epithelial barrier r esults in decreased ability abil ity to absor b nutrients in the diet. diet. This leads l eads to malnutri malnutrition tion and “failure “failure to thrive” in gr owing children.
KEY POINT: This process pr ocess will continue as long as gluten is included included in the the diet for this this group of genetically susceptible people. The adaptive assassins are always waiting waiting to pounce on o n gluten gl uten fragments. fr agments. This is i s why even even a tiny bit of gluten gl uten in people with CD CD results in immediate im mediate symptoms symptoms of gastroint gastro intest estinal inal distress and diar r hea. The intestinal permeability and immune response in CD may contribute to the development of a variety of autoimmune and inflammatory disorders often seen in CD patients. These include: • Endocrine diseases Hashimoto’s to’s thyro thyro iditis (mo st dis eases such as type I diabetes, Hashimo common form fo rm o f thyro thyroid id disease), disease), and and reproduct repro ductive ive disorders. disorder s. • Neurologic disorders such as cerebellar ataxia, peripheral neuropathy, psychosis, epilepsy (seizures), autism and migraine headaches. • Autoimmune liver diseases sclero sis and autoimmune autoimmune dis eases such as primary biliar y sclerosis hepatitis. • Anemia, Anemia, osteoporosis, osteopor osis, r heumatoid heumatoid arthritis, autoimmune autoimmune heart disease (myocarditis). • Non-Hodgkin’s lymphoma (a type type of cancer of the the immune system).
Gluten activates activates autoi autoimmunity mmunity (celiac disease) throug thr ough h intestinal intestinal permeability. per meability. Observe the destruction of the microvilli in the epithelial cells (on the right) of the gut lining. The damaged microvilli are now unable to to absor b nutri nutrient entss from fr om fo od.
DIAGNOSIS DIAGNOSIS OF CELIAC DISEASE There is no clear and reliable way to definitively diagnose celiac disease. Intestinal biopsy has been—and still is in current clinical care—the “gold standard.” The tissue tissue sample sample fro m the the biopsy is analyzed analyzed under under a micro scope to look loo k for signs of microvilli damage in the wall of the intestine. The problem lies in the fact that not all CD patients show microvilli damage. The most reliable way to test for a gluten problem is by eliminating it from the diet and monitoring symptoms over a couple of months. months.
RESEARCH UPDATE: Recent r esearch esear ch has shown sho wn that that as many as 50% of patients patients with CD show show
no signs sig ns of micro villi destruction. destruction. This test test still still may be helpful as most CD patients patients show infiltration infil tration o f “adaptive assassin” immune cells into i nto the epithelial cells themselves. These are called intraepithelial lymphocytes, or IEL.
KEY POINT: The most reliable and practical way to determine any type of glutenrelated disorder is to completely eliminate eliminate gluten gluten for a period perio d of time and monitor your symptoms.
GLUTEN SENSITIVITY Gluten sensitivity (GS) is gaining credence as an emerging diagnosis. GS is distinctly different from celiac disease in how the gluten proteins within the body cause cause problems. pr oblems. • The epithelial cells in the small intestine intestine are ar e usually nor mal, without without signs sig ns of micro villi destr destr uction. uction. • The “adaptive “adaptive assassins” of the the immune system system do not appear to to be a key player in GS; but investigations ar e still under way. way. • The non-specific non-specifi c r esponse of the the innate immune system, the “guar dians” system, produces inflammation by secreting cytokines in response to gluten protein pro tein fragments. fragments. • Clinically, this r esponse leads to symptoms of bloat bloatin ing, g, diarrhea, diarrhea, and cramping after exposure to gluten. • These symptoms are ar e often classified classifi ed as irrit irrit able bowel syndrom syndro me (IB ( IBS) S) by the medical medical pr ofession. IBS IBS is a catch-all catch-all diagnosis diagno sis for fo r gastrointe gastro intestin stinal al symptoms symptoms for which a specific cause cannot be found. The current research suggests that GS may be one of the underlying causes of IBS.
Many people have suffered with gastrointestinal symptoms all of their lives without a clear diagnosis. This is very frustrating for most, and most learn to live with it, although the symptoms routinely affect their quality of life. Some of these individuals need to plan their day to ensure they have easy access to restroom facilities wherever wherever they they go. go .
DOC’S RANT: What has has always been inter interesting esting to me is i s that many people suffer ing with IBS-like symptoms will not “give up” foods like bread and pasta, even when given the above information. As we discussed in previous chapters, most glut gl uten-cont en-containing aining gr g r ain pro ducts ducts are not no t nutr nutr itionally dense, dense, and have anti-nutrients. Since we are not missing anything nutritionally by eliminating these products, why do people cling to their grain-based foods? You never hear anyone say, “I won’t give up my m y brocco br occoli!” li!” A few scientists have looked loo ked at this phenomenon and have shown that that some pieces o f the gluten pro tein
may mimic the effects of opiates (morphine-like compounds) in the brain. We have all heard of endor endor phins—our phins—our naturally naturally pr oduced feel-good feel-goo d substances. Some scientists are now referring the specific pieces of gluten proteins as “exorphins,” and think these molecules may be responsible for the the craving so me people have have for gluten-contain gluten-containing ing grain g rain pr oducts. oducts. Most of us do not have celiac disease or gluten sensitivity. However, if you have any chronic gastrointestinal problems such as IBS, reflux disease (chronic heartburn), gallbladder problems, or inflammatory bowel diseases such as ulcerative colitis or Crohn’s disease, gluten may be a significant contributor to these diseases. Gastrointestinal problems often have an inflammatory origin, so why not eliminate a potential source of gut inflammation by eliminating gluten. Without a clear and definitive test for determining whether you have CD or GS, the most rational approach is to eliminate gluten from your diet. How do you feel after a week or a month? Is your heartburn better? Are IBS symptoms decreased? If
you have an autoimmune disease, a glutenfree trial period is a must do. You have nothing to lose (other than bread) and everything to potentially gain. There is no nutritional benefit to eating gluten, and for as many as 30% of us, there are significant health consequences for continuing to eat gluten-containing products.
RESEARCH UPDATE: The focus on gluten in wheat is admittedly a bit reductionist on our part. Gluten is cer tainly potentially potentially pro blematic and the best studied, but but it may not represent the whole story. New r esearch esear ch shows that other luten are ot her protein prot einss in wheat wheat aside from g luten potential culprits in stimulating intestinal permeability and inflammation and may be the underlying cause of problems previously attributed to gluten.
STRONG MEDICINE TACTICS: Eliminate gluten-containing grains for 1-2 months to assess their potential effects on your individual health.
TRIGGER #2: TRIGGER #2 : STRESS ST RESS AND INTESTINAL PERMEA PERMEABILITY BILITY Many of us are familiar with clichéd sayings such as, “I’ve got a gut feeling about this”, “Show “Show some so me intestinal for titude! titude!”” or “Gut it out!” out!” Most of us have experienced exper ienced a “nervous stomach” or “butterflies in the belly” before stressful events. There is very strong scientific and anatomical basis for a gut-brain connection. The intestinal tract has its own nervous system that can operate independently from
the brain. This gut-based nervous system is known as the enteric nervous system (ENS) and has been called our “second brain” by some scientists.
THE SECOND BRAIN The ENS is extensive and contains as many nerve cells as our spinal cord. Like the brain, the ENS has sympathetic (flight or fight) and parasympathetic (rest and digest) systems. These systems can and do operate independently from the brain. Also similar to the brain, the ENS has nerve cells responsible for sensation, controlling muscle movement (peristalsis) and neurotransmitter production. Neurotransmitters are molecules that carry messages between nerve cells. You may be familiar with neurotransmitters such as serotonin (depression) or epinephrine (adrenaline). The ENS alone produces over 30 different neurotransmitters!
DIGGING DEEPER: Enteric Enteric Glial Glial Cells Yet another similar si milar ity between between the ENS ENS and the the brain br ain are ar e the presence o f specialized cells cell s that act in support suppor t of ner ve cells. In In the br br ain these cells are ar e known as astrocytes. astro cytes. These cells have a multitude multitude of functions f unctions and act to r egulate the the function function of nerve cells. Astrocytes Astrocytes are the primar y component of the blood-brain bar r ier. This barrier barr ier is crucial cr ucial in preventing preventing things from fr om g etting etting into the brain that that ar ar e potentially harmful. There are very specific transport systems in the blood-brain blood-br ain barr ier that that only allow certain things things (like (li ke nutri nutrient ents) s) to pass through. The ENS has a cell similar in type to the astrocyte, the enteric glial cells. These cells support the ENS nerve cells and help control gut function. EGCs EGCs are ar e responsible r esponsible for helping helping maintain maintain intest intestinal inal barr ier function function by
reducing intest intes t inal permeabil permeability. ity.
“THE GUT GUT-BRAIN -BRAIN AX AXIS” IS” Even though the ENS can operate independently from the brain, there is a strong communication link between the two, the gut-brain axis. Through this two-way communication network, signals are passed from gut to brain, and from brain to gut. The system of how stress is communicated between the brain and gut explains how psycholog psycholog ical stress can produce pr oduce physical physical symptoms symptoms such as diarr hea. As a system, the gut-brain axis orchestrates processes such as:
• Gastrointestinal function • Appetite Appetite control cont rol • Body wei weight ght control contro l The vagus nerve is the direct connection of the gut-brain axis. The vagus nerve carr ies sensory infor info r mation mation fr om the gut to to the brain. The vagus also controls motor signals for gut muscle contractions.
KEY POINT: Higher levels of parasympathet states) have been parasympathetic ic act ivit ivit y (as in r elaxed states) shown to decrease inflammation, and protect the gut from intestinal permeability. This is how stress reduction can protect your gut. High sympathetic (fight or flight) states reduce parasympathetic signaling leading to increased inflammation and intest you are ar e intes t inal permeabili permeabilitt y. If you “stressed” co nstantly nstantly,, think how this this may affect af fect your gut!
THE BRAIN RESPONSE RESPONSE TO STRESS The vagus nerve is the primary carrier of parasympathetic (rest and digest) signals from fr om the brain to to most mo st of our internal internal org o rg ans, including including the the gut. gut.
During psychological stress or physiological stress (poor sleep, overtraining, etc.) the brain releases a signaling hormone called corticotropin releasing the hypothalamus. hypothalamus. This trig ger s the pituita pituitarr y gland to r elease hormone (CRH) (CRH) fr om the a hormone called adrenocorticotropic hormone (ACTH). ACTH then acts on the adrenal glands to release the stress stress hormo ho rmo ne cortisol. Cortisol is released to combat stress, and decreases inflammation. It does so by depressing the immune system. This process is your body’s way of defending itself after a stressful event. This works well for short-term stresses, but the system breaks down if it is constantly stimulated from a lifestyle of daily stresses. Chronically high cortisol levels lead to weight gain and poor blood sugar control—a risk factor for diabetes. Stress leaves you susceptible to sickness from bacteria and viruses.
THE GUT RESPONSE TO STRESS The “second brain,” the ENS, also releases its own CRH in response to stress signals. The effects are different from CRH released by the brain. This CRH acts directly on immune cells of the “innate guardian” type, the mast cells. Mast cells are known in medical circles as cells that release histamine in allergic reactions. It is now known that mast cells also release a full complement of inflammatory cytokines. These cytokines increase intestinal permeability by altering the
function of the tight junctions shown in the pictures at the beginning of this chapter.
GUT INFLAMMATION FROM STRESS LEADS LEAD S TO TO CHRONIC DIS D ISEA EASE SE
1. Psychologi Psycholo gical cal and/or physical stress leads to high sympathetic sympathetic (fig ht or flight) nervous system activity. 2. The brain brai n r esponds by decreasing decreasi ng par parasympath asympathetic etic (rest (r est and digest) dig est) signaling to the gut by the vagus nerve. 3. Decreased par parasympath asympathetic etic signaling sig naling by the vagus nerve leads to increased intestinal permeability. 4. Incr Increased eased intestinal intestinal permeability permeabili ty activates activates the the gut immune system. system. “Invaders”—foreign bacteria and protein fragments—lead to inflammation. 5. Inflammatio Inflammation n of the the gut leads to impaired functio function n r esulting in symptoms such as diarrhea and bloating. 6. Chronic Chro nic str str ess leads to chr chr onic intestinal intestinal permeability permeabili ty,, which leads to to chronic inflammat i nflammation. ion. 7. Chronic Chro nic inflammation inflamm ation leads to diabetes, cancer, high hig h bloo d pressur pr essuree and heart disease.
Locally in the Gut:
1. Stress Stres s activates the ENS to produce pro duce CRH. CRH. 2. CRH CRH activates activates mast cells that that r elease inflammator y cytokines. 3. Inflammator Inflammator y cytokines disrupt disr upt tight junctions leading to intestinal intestinal permeability. 4. Intest Intestinal inal permeability perm eability leads to inflammatio n. 5. Chro Chro nic stress leads to chronic inflammation. inflammation. 6. Chronic Chro nic inflammation inflamm ation leads to diabetes, cancer, high hig h bloo d pressur pr essuree and heart disease.
STRONG MEDICINE TACTICS: Stress r edu Stress eduction ction is crucial cr ucial to impro ving your gut health health and will will help prevent chro nic disease. Use Use the str str ess reduct r eductio ion n techniques techniques in the Chr Chronic onic Stress chapter.
TRIGGER #3. #3 . DYSBIOSIS: DYSBIOSIS: CHAOS IN THE T HE GUT GUT “ZOO” “ZOO” “This consortium of bacteria contains tenfold more cells than the human body, 100 times the number of genes than the human genome, and has the metabolic capacity of the human liver.”
The quote above is from an article published in 2009 from a very prestigious scientific journal, describing the bacteria that live in our gut. We have known for a long time that vast amounts of bacteria call our gut home, but we are only recently beginning to learn the profound effect they have on our health. The gut really is a “zoo” in the truest sense of the word: • There are approximately approximately 100 trillion trillio n bacteria bacteria in our intest intestines. ines. • There are appr appr oximately 1,000 1,000 separate bacterial bacterial species species capable capable of colonizing the human intestinal tract. • At any one time, a healthy healthy adult has 150 150 to 200 200 of these these bacterial species inside them.
• Which specific species are ar e present pr esent depends on the the human host’s environment. envir onment. A study has recently shown that gut bacteria species in children from rural African communities communities are ar e very different fro m the species species found fo und in European city dwellers. dwellers. Just as a large diversity of species is good for our planet’s ecosystem, a large diversity of bacterial species has been shown to be an indicator of good health in humans. In fact there has been shown to be a direct correlation with loss of gut bacteria diversity and poor health. Sickly and obese people have fewer types of
bacteria in in thei t heirr guts g uts t han healthy healthy people.
DIGGING DEEPER: What is a Microb Microbiome iome?? Many of us have heard the term, human genome. Our genome is simply the total total collectio co llection n of o ur genes. We We each have approximately approxi mately 20,000 20,000 differ ent genes. Each gene repres r epresents ents a message encoded in o ur DNA DNA that when activated, produces a protein of a specific structure and function. These pro teins teins include—among include—among other things—hor things—hormones, mones, enzymes, enzymes, signaling and structural proteins. The metabolic “machinery” in humans is also made from fr om these proteins pro teins encoded by DNA DNA.. The machiner y that creates (and breaks down) carbohydrates, protein, and fat, are all made fro m specific specific genes. The gut bacteria bacteria micro biome, is simply si mply the the total amount of differ ent genes found among the bacteria that live in our intestinal tract. There is a key difference between the human genome and the gut bacteria microbiome: • The human human genome completely completely resides within within a single or ganism—a human. • The gut bacteria bacteria microbiome micr obiome is comprised compr ised of separate separate genes in each each species of bacteria. When we group the species of bacteria together (150200 species in our guts), we then get the total collection of genes known as the the microbio micr obiome me from fr om the populations populations of o f separate bacte bacterr ial species. You and I can have different species of bacteria present in our gut “zoo”, but our gut micro biomes can still be similar to one another, because because
similar genes will be present in a diverse population population o f separate bacte bacteri rial al species. This is why high diversity (many different types) of gut bacteria is impor impo r tant. tant. Sick and obese people have less species, and this this lo wer diversity means that the microbiome in these people is probably lacking some bacterial genes that are important to the person’s health. So now when we refer to the microbiome, you know what we are talking about.
FROM CRADLE TO GRAVE When you were still in your mother’s womb, your insides were a sterile place, free of any bacteria. Bacteria began to colonize your gut during and after the birthing process. Recent science suggests that the time during and immediately after birth is crucial for development of a diverse population of bacteria. Certain practices in Western society affect this process with potentially profoundly negative health consequences. The results of a study in the Netherlands published in 2006 showed that the specific gut bacterial species found in infants depended on a number of factors including: gestational age (how long the fetus was carried in the mother before delivery), type of delivery (C-section vs. vaginal), location of delivery (hospital vs. home), home), type of feeding (br ( breast east milk vs. formula), and antibiotic use. The results showed that infants born at home and breastfed exclusively, showed the highest amount of beneficial gut bacteria and the lowest amount of potentially athogenic bacteria.
Hospitals are certainly appropriate places to monitor delivery of pregnancies. Formula feeding is sometimes the only option and C-sections can be lifesaving. That said, it seems whenever possible and safe, “natural” birth environments and processes promote a healthy and diverse gut bacteria population for the baby. Breastfeeding has been shown to be especially beneficial in this regard. It is thought that the gut bacteria population has matured to mirror that of an adult by three years of age. The first few years of life are crucial for forming a balanced gut bacteria population. The early development of our immune system system during infancy and and
childhood is influenced by gut bacteria composition. Disruption to the normal “balance” of gut bacteria may change the way our immune systems develop, possibly leading to increased susceptibility to:
• Allergic Allergic disease disease such as asthm ast hmaa • Autoim Auto imm mune diseases diseases such as type I diabetes
RESEARCH UPDATE: Some scientists think that early in life, our gut bacteria may “program” our metabolism et abolisms, s, helping determine whether we will develop metabolic disor ders such as obesity o besity or type II II diabetes. diabetes. One scientist scientist suggests sugg ests that that we can help prevent obesity and diabetes diabetes in adulthood adulthoo d by identifying and corr cor r ecting ecting g ut bact bacteria eria imbalance imbalance in early earl y childhood and even during during childbirth!
THE DELICATE DELICATE BALANCE
It turns out that a balance exists between bacteria species beneficial to our health and those that are potentially problematic. In medical lingo, we call the latter “opportunistic pathogens.” They don’t cause problems if there are enough beneficial beneficial (go od guy) g uy) bacte bacterr ia aro und, und, but if the population population of g ood oo d guys is r educed educed for some reason, the opportunistic pathogen bad guys will take over with chronic inflammation as the result.
THE HEA H EAL LTH BENE BE NEFITS FITS OF OF OUR “INTESTINAL TEN TENAN ANTS TS”” The beneficial beneficial species of bacteria bacteria can do g reat things things for fo r us as long as we treat them well. • When we eat eat fermentab fermentable le fiber—fibrous fiber—fibr ous carbohydrate material material mainly fro m fr uits uits and vegetables— vegetables—th thee bacteria bacteria uses the the fiber fo r food, foo d, metabolizes it for us, and produces a “waste” product of antiinflammatory short-chain (SC) fats. Our colon uses SC fat as a primary energy source. These SC fats are powerful and exceedingly effective at reducing inflammation. Short-chain fat boosts the immune system and has been shown to have anti-cancer properties. • Our beneficial gut bacteria detoxi detoxify fy potentially harmful harm ful compounds in our food foo d and wat water. er. • They prevent pr event the over gr owth of infectious “pathog “pathogenic” enic” bacteria. • They are crucial for proper pro per development development of our immune i mmune system. system. • They can help prevent insulin resistance r esistance and and diabetes. diabetes. • Beneficial gut bacter bacteria ia can even even help help pro tect against autoi autoimmune mmune diseases.
DIGGING DEEPER: T-Regulatory Cells and Gut Bacteria New research has shown that beneficial gut bacteria provide the signal for for mation of o f new Treg cells (the “hippies”) in the gut. Remember that the the Treg cells keep the “assassin” T-cells in check, preventing them from getting getting o ut of control contro l and damaging o ur body tissues. tissues. The beneficial gut bacteria need to be present in the proper proper balance to keep the “assassins” and “hippies” in proper balance. This signaling sig naling function function to for m new Tr Tr eg cells by beneficial gut bacteria bacteria may be behind behind the followin follo wing g findings in r ecent ecent research:
• Beneficial gut bacter bacteria ia have been shown shown to to help prevent our immune im mune system system from fr om becoming overactiv o veractive, e, thus thus preventing preventing chronic chr onic inflammatory disease. • Specific types types of beneficial gut bacteria bacteria may pr pr otect against autoimmune disease, including inflammatory bowel diseases such as ulcerative colitis and Crohn’s disease. • People with with inflammatory inflammator y bowel diseases often show a loss of certain types of beneficial gut bacteria. • Beneficial strains of g ut bacteria have been been shown to help maintain maintain our intestinal barrier, protecting against chronic intestinal permeability. • Butyrate produced pr oduced from fro m fiber (vegetables (vegetables and fruit) fermentation fermentation by beneficial gut bacteria makes more Treg (“hippies”) to help contro l T reg cells cells (“hippies”) inflammation.
RESEARCH UPDATE: Deficiencies Deficiencies in beneficial gut bacteria bacteria lead to deficiencies defi ciencies in in Treg cells Recent research has shown that deficiencies in Treg cell populations in humans may predispose us to asthma, inflammatory bowel disease, type I diabetes, and multiple sclerosis.
The impor impo r tance of the balance between between the the “beneficial” gut g ut bacter bacteria ia (green green)) and the opportunistic pathogens (red red)) is illustrated here. Certain types of beneficial bacteria stimulate formation of the Treg “hippies” while the pathogens pathogens stimulate for fo r mation of o f T-cell T-cell “assassins.” “assas sins.” Imbalance Imbalance resulting in an overgrowth of pathogens is called dysbiosis. It can lead to too many assassins around which can cause chronic inflammation. At the same time, too many hippies and not enough assassins can lead to a poor immune response to an infection when necessary. Just like real life, we need both the warriors and anti-war protesters in balance so we do not go too far in i n either either direct dir ection. ion.
THE BALANCE DISRUPTED: DYSBIOSIS TAKES OVER... The term “dysbiosis” refers to any altered state of normal bacteria balance associated with disease. A feature common to all types of dysbiosis is the loss of bacteria species diversity. We need balance between “beneficial bacteria” and “opportunistic pathogens.”
TECHNICAL NOTE: The definition of dysbiosis we are using is greatly simplified. Indeed, recent research shows that there are significant differences in the composition and balance of gut bacterial species between obese
individuals and non-obese no n-obese and between diabetics diabetics and non-diabetics. Classifying Classifying g ut bact bacteria eria as “beneficial” “beneficial” or o r as “oppor tunist tunistic ic pathog pathogens” ens” is not as black bl ack and white in reality r eality.. We We use this distinct dis tinctio ion n to co mmunicate a concept, but it is impor im por tant to note no te that that some bacteria bacteri a associated asso ciated with with inflammation inflammatio n in the g ut may not be “pathogenic” “pathog enic” in the technical technical sense. We We are still classifying them under “opportunistic pathogens” because they can promote inflammation and contribute to chronic disease when the normal balance is disrupted, when there is a loss of bacterial diversity, and in cases of intestinal permeability.
DYSBIOSIS HAS BEEN ASSOCIATED WITH NUMEROUS DISEASES AND DISORDERS • • • • • • • • •
Autoimmune Autoimmune disorders disor ders (including (including inflammator inflammator y bowel disease) disease) Allergi Aller gicc disease including asthma Irritab Irri table le bowel syndro syndro me Obesity Type II diabetes Colon Colo n cancer Fatty Fatty liver disease Atheroscler Atheroscler osis (heart and vascular vascular disease) disease) Acne Acne (not surprising, surpr ising, acne is an inflammator inflammator y condition) condition)
Dysbiosis—the opportunistic pathogens outnumber beneficial gut bacteria. This leads to an imbalance between between “hippie” Treg cells and “assassin” T-cells. With With mor e assassins assassins around aro und,, we we are mor mo r e prone pro ne to to o ut-of-co ut-of-cont ntro ro l inflammation inflammation and autoimmune disease. There are not enough hippies to balance the assassins.
WHAT CAUSES DYSBIOSIS?
The shift to dysbiosis has been associated with multiple factors, but the primary influence on gut bacteria populations seems to be diet, with environmental exposures such as antibiotic use also contributing. “Diet is the most powerful powerful influence on gut microbial communities in healthy human subjects” —Stig Bengmark (2012)
Evidence is mounting that processed foods containing large amounts of flour, refined oils, and sugar may be a primary culprit in development of dysbiosis. We are used to thinking about food in terms of carbs, fat, and protein—the macronutrients. Diet books are best sellers and each champions a diet strategy promoting one nutrient while damning another, i.e. “low fat/high carb” or “high fat/low car b.” b.” It is interesting that many traditional cultures eat a wide range of diets, including high fat/low carb (the Inuit tribe) and high carb/low fat (the Kitavans). These cultures have extremely low rates of “Western” diseases such as diabetes, obesity, and heart disease, despite the large variability in types and ratios of macronutrients. When people from these cultures begin eating processed Western diets, high in refined grains, sugar, and refined oils, they quickly lose their tribal health and vitality. Obesity, formerly unheard of, becomes epidemic. The tribal members eating “Western” succumb to “Western diseases”.
An intriguing hypothesis was put forward recently in the scientific literature by Dr. Ian Spreadbury. He suggests that processed grain-based carbohydrate foods affect gut bacteria very differently than natural, non-processed “whole food” carbohydrate sources, such as root tubers (sweet potatoes,) stem tubers (potatoes) and fruit. Dr. Spreadbury suggests that the carbohydrate density of a food is importa impor tant nt to to how ho w our populat po pulation ion of o f gut bacteria bacteria r espond. If you are ar e having a har d time conceptualizing density, think of how many people are in o ne square square mile mil e in rural r ural Montana Montana ver ver sus a square square mile mil e in New Yor k City. City. As far as carbohydr car bohydrate ate density density, tubers and fr uit are mo morr e like Montana, while processed grain foods are like New York City. Dr. Spreadbury suggests that high-density carbohydrate foods promote dysbiosis, the overgrowth of specific inflammation-promoting gut bacteria. He further suggests that once this type of dysbiosis has been cultivated and takes root, high dietary fat intake (especially refined oils, corn oil, vegetable oil) promotes further
inflammation. This suggests that the fat intake in the diet may only become harmful if processed grain foods are eaten. For promoting dysbiosis, the worst dietary sin would be combining combining lo ts of pro cessed gr ain-based ain-based foods with lots of refined r efined dieta dietary ry fat. fat. This combination combination describes the composition of most fast food. Do not worry about eating tubers, vegetables, and fruit. These foods contain high amounts of “fermentable fiber.” They are excellent food choices, containing the type type of fiber our beneficial beneficial gut bacteria bacteria use for fo r fuel. These foods will not lead to dysbiosis because the “waste” product of fiber fermentation is short-chain fatty acids (SCFA). Butyrate, propionate, and acetate are all SCFAs that are anti-inflammatory and have numerous health benefits, including
promoting the growth of beneficial gut bacteria.
FERMENT FERMEN TABLE FIBER FIBE R AND GUT HEAL HE ALTH: TH: FIRST PRINCIPLES PRINCIPLES Current scientific thought—eating foods high in fermentable fiber encourages the gr owth of beneficial beneficial bacterial bacterial species in our guts, helping helping maintain the balance. “Western” processed food, largely devoid of fermentable fermentable fiber, encourages encourag es the growt gr owth h of oppor tunist tunistic ic pathog pathogens ens leading to dysbiosis. This hypothesis hypothesis of processed pro cessed food leading to dysbiosis dysbiosis makes sense sense for many reasons:
• There are ar e several several examples of traditional cultu culturr es eatin eating g no processed pr ocessed foo d, but otherwise other wise a relatively rel atively high fat diet without without apparent health consequences. • Pro cessed, gr ain-based high-density high-densi ty carbo hydrates coupled with with r efined oils and fats fats is t he definition definition of o f t he healt healt h-kill h-killin ingg “West “Western ern Diet Diet.” .” • Several traditional traditio nal cultures cultures eat a diet high in unpr unprocessed ocessed carbohydrates carbo hydrates from tubers such as sweet potatoes without succumbing to metabolic
diseases such as obesity or diabetes.
Here again we see the trend of “food quality,” not ratios of carbs or fat, fat , being being crucial for healt healt h. Real Real food foo d trum t rumps ps processed fo od every time.
STRONG MEDICINE TACTICS: To pr event dysbiosi dysbiosis-r s-related elated diseases such as type II II diabetes, diabetes, fatty fatty liver disease, and obesity, cut out processed, grain-based high-density carbohydrates, and replace them with low-density carbohydrates like vegetables, tubers and fruit.
DIGGING DEEPER: The Link Between Obesity, es ity, Diabetes, Diabetes, Atherosclerosis Atheros clerosis,, and Fatty Liver Disease? One of the ways ways microbiolo micro biologists gists gr oup some bacteria bacteria is by how well well they absorb a special type of dye—a Gram stain—in their cell walls when viewed under a microscope. Gram-positive bacteria take up the stain well and look purple in color co lor under under the the micro scope. Gram-negat Gr am-negative ive bacteria bacteria do not no t take take up the the stain, and and have a light lig ht pink color. colo r. Gram-negative Gram-neg ative bacteria bacteria have an outer outer membrane surr ounding their cell wall, wall, which prevents prevents the stain stain from fr om color co lor ing the cell wall. Gram-negative bacteria have something called lipopolysaccharide (LPS) in their outer membrane. LPS is also known as a bacterial “endotoxin”. When LPS LPS gets gets through throug h our intest intestinal inal barr ier and into into the blood bloo d stream, our immune syste system m goes go es crazy and produce pro ducess a large larg e inflammator inflammator y response. This is called endotoxemia. Also the epithelial cells lining our
gut have a system to to r ecognize ecog nize LPS. When LPS LPS is recog r ecognized nized either in the blood stream by immune cells or in the gut wall, inflammation is the result. People with type II II diabetes, diabetes, fatty liver disease, and obesity o besity have been shown to have a gr eater eater pr opor tion of Gr am-negative am-negative bacte bacterr ia in their their g ut (dysbiosis), (dysbiosi s), and thus mor e LPS than than healthy individuals. It is pr obably no coincidence coi ncidence that that many type type II II diabetics diabetics ar e over weight or obese, have fatty liver, and acceler acceler ated ated athero athero sclerosis. sclero sis. In fact, there is a hypothesis that is strongly supported by recent research that that links chro chro nic low levels of LPS LPS in the bloo bloo dstream dstream (chronic (chr onic endotoxemia) with with Type II II diabetes, diabetes, obesity, athero athero sclerosi scler osiss and fatty liver disease. Scientists Scientists suggest sugges t that that constant low lo w levels of o f LPS are getting into i nto the the bloodstream blo odstream fr om chronic intestin intestinal al permeabilit per meability y. “After millions of years of co-evolution, have societal advances paradoxically and adversely affected human health by reducing our exposure to healthromoting bacteria?”
The quote above is from a study published in 2009 and brings to light another possibility for a dietary source of dysbiosis. Many people in modern society have been “sheltered” from exposure to bacteria in our food starting early in childhood. Our modern foods have been largely sterilized compared to traditional cultures. There are a variety of potentially beneficial bacteria present in naturally grown fruits and vegetables. Traditionally these vegetables are an early source of beneficial bacteria in our diets. We have become obsessed with food hygiene as we have modernized, and for good reason. Our modern large-scale farming and distribution methods have led to frequent contamination of our food supply by pathogenic bacteria. News stories about salmonella contaminat contamination ion of produc pro ducee or o r E. coli in meat are common. co mmon. A r ecent ecent study study showed showed significant differences in gut bacteria bacteria found in r ural African children versus those in a group of city-dwelling European children. The African children had a large and diverse population of beneficial gut bacteria able to ferment fiber, while the European kids showed decreased diversity and small amounts of beneficial gut bacteria. A sanitized food supply in Europe was thought to be one of factor factor s accounting accounting fo r this this difference.
ANTIBIOTIC USE: A DOUBLE EDGED SWORD Another potential potenti al contributor contribut or to dysbiosis dysbios is is the use of antibiotics. antibiot ics. The discovery and widespread medical use of antibiotics in the 20th century has saved countless lives. Use of these wonder drugs has become incredibly common in recent years. Some argue that though they are clearly effective and beneficial, in many circumstance cir cumstances, s, antibiotics may m ay have unintended unintended health consequences.
Antibiotic use significantly alters the balance of your gut bacteria, and in some cases leads to dysbiosis. The main job of antibiotics is to kill bacteria that are causing infections; unfortunately beneficial bacteria are mowed down in the process —like innocent inno cent bystanders bystander s killed kil led in a gang ga ng drive-by dr ive-by shooto sho otout. ut. Killing Kill ing beneficial benefi cial bacteria leads to imbalance and dysbiosis. It is often the opportunistic opportunis tic pathogens that are resistant to antibiotics. antibiot ics. Left to fester, dysbiosis spins out of control, and left unchecked leads to chronic inflammation. Pseudomembranous colitis occurs when antibiotics kill beneficial bacteria, bacteria, leading to overgr over gr owth owth of an opportu oppor tunist nistic ic pathogen pathogen known as Clostridium CD overgr overg r owth owth leads to to inflammation inflammation o f the colon and diarr hea. difficile (CD ( CD)) . CD
Pseudomembranous colitis is an extreme example of dysbiosis caused by antibiotics. Recent science has shown that antibiotic use generally results in significant changes in bacterial balance; the clinical significance of this change is unclear. We We know that antibio antibiotic tic use changes the composition compo sition of gut bacteria, but we we have not studied it long enough to determine how or if it affects your health. Disrupting gut bacteria bacteri a equilibrium equili brium with frequent antibiotic antibi otic doses is likely likel y to have unintended consequences.
RESEARCH UPDATE: A new article in the jour nal, Pediatrics, ill ustrate these Pediatri cs, has started to illustrate unintended consequences. The study found that while following a group of 464 children children fo r 15 years, years, the children who who received courses o f antibiotics antibiotics early in childhood had a significantly significantly higher r isk for developing developing inflammatory bowel disease (IBD) as they got older. The authors correctly state that other factors are involved in developing IBD, but early antibiotic use clearly seems to be a significant factor.
The following is clear from current research: • A single sing le cour se of broad-spectrum bro ad-spectrum antibiotics (those that kill a wide variety vari ety of types of bacteria) causes changes in gut bacteria populations lasting from three months to two full years. • Combination antibiotic therapy, therapy, as used to treat Helicobacter pylor i infections (a cause of stomach ulcers), has been shown to alter gut bacteria populations for up to four years after treatment in extreme cases. • Widespread idespr ead antibiotic use is creating cr eating strains of bacteria r esistant to curr ent antibiotic tr eatment. eatment.
Antibiotic source? Many people go to their doctor’s office demanding antibiotics for relatively minor maladies such as upper respiratory infections. A significant number of these patients are successful in getting their doctor to prescribe antibiotics, even though the majority of upper respiratory infections are due to viruses unaffected by antibiotics. Frequent and inappropriate use of antibiotics may end up contributing to longterm health problems from the impact on beneficial gut bacteria. Not to mention, it creates problems fo r the the rest r est of us by developing developing r esistant esistant strains of bacteria. bacteria. We also unintent unintentionally ionally g et low levels of antibiotics antibiotics from fr om environmental environmental sources so urces such as meat and dairy from feedlot animals. Eighty percent of all antibiotics sold in the U.S. are currently used for chickens, cows, and pigs to prevent infection in the crowded cr owded enviro nments in which which they are r aised. Many Many of these antibio antibiotics tics eventually eventually find their way to your dinner table, and most are not destroyed in the cooking
process. Some studies have even found antibiotics in produce such as lettuce, carrots, and potatoes grown in fields treated with manure-fertilizer from antibiotic-treated animals. It is currently unclear how these sources of antibiotics affect gut bacteria and human health, but it seems logical to do your best to avoid them if possible. Knowing where your food comes from is the best way to start. Choose locally grown organic produce and choose meat from pastured animals, free from antibiotics.
STRONG MEDICINE TACTICS: To prevent dysbiosis and antibiotic resistance, avoid frequent treatment with wit h antibiotics antibiotics for minor condit conditions. ions. Also choose meat and produce that is free from antibiotics by demanding or ganic, pastu pastured, red, and locally grown gr own food. “Let food be thy medicine and medicine be thy food” —Hippocrates —Hippocr ates
The best way to restore bacterial balance is through diet. First and foremost— avoid processed food. For people with dysbiosis (and gut inflammation) consumption of probiotics in fermented foods has been found to be extremely beneficial. The treatment of disease with probiotics is a hot topic in current medical research resear ch and deserves deserves furth fur ther er discussion. discussion.
PROBIOTIC PROBIOTICS S AND AN D FERMENTED FOODS FOODS The World Health Organization defines probiotics as, “Live microorganisms which, when administered in adequate amounts, confer a health benefit on the host.” Fermented foods containing live microorganisms (such as yeast and bacteria) have been part of traditional diets for thousands of years. It has been known for 150 years that the bacteria and yeast in fermented foods are responsible for chemical changes that result in health benefits.
Fermentation is defined as a biochemical change in carbohydrates— microorganisms such as yeast, bacteria or mold use the carbohydrate for food. The microorganisms metabolize carbs and create “waste products.” Beneficial gut bacteria transforms fiber into short-chain fatty acids and these short-chain fat “waste products” (from bacterial fermentation of vegetable and fruit fiber) are crucial for the overall health of our intestinal tract. The product of microorganism fermentation most us are most familiar with is alcohol. Alcohol is the waste product from yeast fermenting sugars. Alcohol is not considered a probiotic because the yeast is filtered out of alcoholic beverages before consuming. For thousands of years, traditional tribal cultures have made fermented foods from vegetables, fruit and dairy products. These primal tribesmen were not concerned one wit about health benefits—fermentation allowed foods to be stored for later consumption in the hard winter months. Fermented foods can be stored for years: Korean kimchi is aged like wine. Fermented foods are always widespread when refrigeration is not common or available. Fermented foods are still regularly part of millions millio ns of people’s people’s daily diets diets worldw wor ldwide. ide. The medicinal and health benefits of fermented foods were recognized by ancient cultures and used as medicine. With the advent of industrial food processing, modern society has relegated fermented foods to the trash heap. Recently there has been a resurgence resurg ence in interest interest in fermented foods, driven lar gely by research r esearch into the the health benefits of probiotics. The supplement industry has discovered probiotics and is attempting to commercialize and popularize their usage. This is yet another example of inappropriate reductionism. The supplement industry grows bacteria species thought to be beneficial, isolates and processes them, puts the anemic concoction into a capsule, then makes exaggerated claims for the product. Traditional cultures obtained these beneficial bacteria in their diets—not from a pill—in the form of fermented foods. The most common beneficial bacteria species found in traditional fermented foods produce lactic acid as a waste product during the fermentation process. Using this type of bacteria for fermentation is thus called lacto-fermentation, or lactic acid fermentation. Lacto-fermentation is used on a wide variety of fruits, vegetables, and dairy product pr oductss to pro duce fer fer mented mented foods.
LACTO-FERMENTATION
There are vast amounts of bacteria that naturally make their homes on vegetables and fruit. Even with a thorough washing, bacteria clings to produce in large numbers. We all have seen fruits and vegetables “go bad” quickly or spoil if left out in the air at room temperature for a period of time. The produce will stay fresh longer in the refrigerator, but decomposition and rot are inevitable. Fruits and vegetables decompose because of bacteria. Surface bacteria begin to quickly break down the host when left exposed to oxygen at room temperature. Lacto-Fermented Escabeche (jalapeño, sweet peppers, carrots, onions, garlic). www.thenourishinggourmet.com Lacto-fermentation works because the lactic-acid-producing bacteria on the fruits and vegetables thrive in the following conditions: • In an acidic environment envir onment • In the presence pres ence of r elatively high hig h salt concentrations concentratio ns • Without the presence of oxygen oxyg en
DO IT YOURSELF!
To start the fermentat fermentation ion process, pro cess, vegetables vegetables and/or and/or fruit fr uit are placed in a container and filled with water to ensure no air is present. Salt is added and the container is i s left in a dark place with the the temperature between 68 and 72 degrees. This environment encourages the growth of the lacticacid-producing acid-pr oducing beneficial bacteria. bacter ia. As As these bacter bacteria ia multiply, they they start to use the vegetables and fruit as a fuel source and give off lactic acid as a waste product (this is the fermentation process). The lactic acid reduces the the pH of the surrounding surr ounding fluid, making it mor e acidic. The other bacteria present (the ones involved in the rotting process) die because they are not able to survive sur vive the high salt and acidic environment. envir onment. This leaves l eaves the lacticlacticacid-producing bacteria alone to continue the fermentation process until the lactic acid builds up enough to slow their growth. The resulting fermented vegetab vegetables les and fruit now can can be stor stor ed for long periods perio ds of time because the high acid and salt content prevent the decomposing (rotting) bacte bacteria ria fr om g rowi ro wing. ng. Health benefits of lacto-fermented fruits and vegetables: • Incr Incr eased vitamin content—lacto-fer content—lacto-fer menting bacter bacter ia concentrate large lar ge amounts of vitamins (especially B vitamins) during the fermentation process. • Better Better digestibility: digestibil ity: fermentat fer mentatio ion n breaks br eaks down the indigestible indig estible parts of plants, plants, allowing humans to utilize them. Many traditional cultures use fermented foods to wean wean young children fr om breast-feeding. breast-feeding. • Removal of natur natur al plant plant toxins and anti-nutr anti-nutr ients: many plants have their own defense mechanisms to prevent them from being eaten. The process of fermentat fer mentatio ion n breaks down do wn many of these defensive toxins toxins and anti-nutrients, leaving the plants plants safe to eat.
QUICK DEFINITION: ar e compounds compo unds found in many plants that that bind to to nutrients nutr ients Anti-nutrients Anti-nutri ents are such as vitamins and minerals. This binding process prevents us from absor bing these beneficial nutrients nutri ents when when we eat the the plant. Fermentation
destroys many of these anti-nutrient compounds allowing us to better
absorb the vitamins and minerals found in the plant.
LACTO-FERMENTING BACTERIA AND OUR HEALTH Recent science has shown that lacto-fermenting bacteria are extremely beneficial to our health. These bacteria shore up our immune system. • Lactic Lactic acid fermenting fer menting bacteria (Lactobacil (Lactobacillus) lus) have been shown to directly dir ectly induce induce for mation mation o f Treg cells in the gut. gut. Tr Tr eg cells (the “hippies”) “hippies”) control the the “assassins” and reduce inflammation. • Lactic Lactic acid fermenting fer menting bacteria increase incr ease tight junction for fo r mation in the intestinal epithelial cells and reduce intestinal permeability. They also were found to pro tect tect the the tight junct junctions ions fro m furth fur ther er disruption. It is now thought that the lactic acid fermenting bacterial species from fermented foods do not stay in the gut as long as previously thought. We used to think that these probiotics “repopulated” the gut bacteria directly. Current science seems to show that most of them just “pass through” but still exert considerable beneficial effects on our immune system and health. This is why regular consumption of fermented foods is necessary. This may partially explain the fact that most cultures still eating fermented foods as a regular part of their traditional diets are free from chronic inflammatory diseases such as heart disease and diabetes. The best way to restore the “balance” in your gut bacteria is primarily through eating foods with plenty of fiber such as fruits and vegetables. These types of foods provide a fuel source, and encourage the growth and reproduction of beneficial bacteria living in your gut. Lacto-fermented fruits and vegetables not only provide an anti-inflammatory effect from the probiotic lactic acid fermenting bacteria in the food, but the food itself helps the beneficial bacteria that are already in your gut multiply. Thus, taking probiotics in a pill only gives you half of the solution to
dysbiosisrelated dysbiosisrelat ed inflam inflamm mation. at ion.
Specific preparation methods for fermented foods are beyond the scope of this book. There are several excellent resources in books and on the internet. A comprehensive book on the subject is The Art of Fermentation by Sandor Katz and for beginners, Cultured: Making Health Fermented Foods at Home by Kevin Gianni. Both Both are highly recommende r ecommended. d. Go try some kimchi!
STRONG MEDICINE TACTICS: Eat fermented food 2-3 times per week to control intestinal permeability, inflammation of the gut, balance the immune system, and improve digestion.
THE GUT-BRAIN-BACTERIA TRIUMVIRATE: WHO’S IN CHARGE? Recent research indicates that bacteria may influence our mood and behavior. The T he idea that mute bacteria living within us can affect our behavior is, well, strange. In the the last sever sever al years, some so me intriguing intrig uing r esearch (in animals) has shown that that specific specific bacteria can measurably change levels of anxiety and alter responses to stress. Scientists have shown that anxiety-related behaviors were increased in mice when they were given small doses of “opportunistic” pathogen-type bacteria. They also showed that when given certain probiotic strains of beneficial bacteria, the mice’s anxiety levels plummeted. Researchers have shown that alterations in the normal gut bacteria in young mice left them with exaggerated responses to stressful events later in life as adults.
Our brain and “second-brain” (enteri (entericc nervous nervo us system) system) communicate thro through ugh the vagus nerve—our internal communication “super highway”. We also know that our gut bacteria can directly affect and change the function of our enteric nervous system via intestinal permeability and dysbiosis. Our enteric nervous system communicates communicates these these changes changes to our brain (primari (pr imarily) ly) through the the vagus nerve. Somehow this complex organic communication system is able to differentiate “goo d” from fr om “bad” “bad” bacteria bacteria and sends sends signals to decrease or increase anxiety anxiety states states in the brain.
FIRST PRINCIPLES PRINCIPLES PERSPECTIVE PERSPECTIV E An overgr overg r owth owth of o f o pportunistic pportunistic pathog pathogen-t en-type ype bacteria bacteria could be considered a “threat” to the body. No matter the source, our brain responds to “threats” (any potentially dangerous situations) by stimulating our “flight or fight” sympath sympathet etic ic nervous nervo us system. system. Increasing o ur “flight “fli ght or fight” system can certainly increase anxiety. Think about narrowly avoiding a car accident accident or being confro nted nted by a dangero dangero us wild wild animal. These two two examples examples are external thr thr eats eats and produce larg e flight or fight responses compar ed to comparatively minor “threats” “threats” such such as increased bacterial pathog ens in our gut. But a minor mino r threat to the body that that happens happens chronically every day can constantly keep the brain in a low state of flight or fight. Over time, this constant low-level “threat” response can lead to negative effects in the brain br ain and body. We know that chro nic stress can lead to anxiety and depress depressio ion, n, so given g iven our discussion above, it is not far fetched to consider that imbalances in gut bacteria (a low level chronic stress) may contribute contr ibute to to mental m ental health health problems. Interestingly, an alternative (FDA-approved) treatment for intractable depression is vagus nerve stimulation. As gut bacteria can stimulate the vagus nerve pathway, it is plausible that there could be a connection between gut bacteria composition and mood disorders like depression.
RESEARCH UPDATE: A recent study from 2011 provided early evidence that probiotics improved anxiety and mood within 30 days of use. More research needs to be performed, but these results are very interesting. In addition to communicating with the brain through the vagus nerve, intestinal bacteria may also affect several hormones that act directly on the brain to regulate appetite, the sleep/wake cycle, memory retention and metabolism. These hormones include include leptin, leptin, ghr elin, gastrin, or exin, and and many others. Recent work by a French research team has shown that our immune system produces “auto-antibodies” that actively work against some of these hormones.
QUICK DEFINITION: Auto-antibodies Auto-antibodi es are antibodies produced by our adaptive immune system (assassins) against our own tissues. See our discussion on auto-immunity for more mor e on this. this.
The team of researchers hypothesized that these auto-antibodies are produced by our immune system in response to “signals” sent by specific gut bacteria. The signaling mechanism is thought to be “molecular mimicry.” Molecular mimicry is when when a certain pro tein tein sequence sequence found in bacteria is chemically chemically similar to a pr otein sequence found in our own tissues. The immune system recognizes the bacterial protein sequence and produces antibodies for defense against the bacteria. The problem is that these antibodies will also bind to tissues in our body (in this case the hormones) that have a similar protein sequence as the bacteria. By binding to the hormones inappropriately, these antibodies (now called auto-antibodies) can affect the way the hormones deliver their messages to the brain. Depending on the hormone hor mone affected, affected, signals for functions functions like li ke hunger, hunger, sleep, and mood can be alter alter ed by these auto-antibodies. The resulting hormonal chaos contributes to inappropriate eating behavior, sleep disturbances, and depression. The composition of gut bacteria influences what type of auto-antibodies are
pro duced by the the immune system and what what hormones horm ones ar e affected. These ideas are relatively new and more investigation is needed before jumping to any conclusions, but they were included here to illustrate another way bacteria may profoundly influence our health and behaviors. Basic physiologic processes like sleep, hunger and mood are regulated by chemical-signaling hormones in the brain. Anything that can alter these processes (such as gut bacteria) will affect how the brain functions. Based on recent science, the idea that our gut bacteria can affect our outward behavior may not be as far-fetched as it once seemed. One more reason to hedge your bets and follow the Strong Medicine Defensive Tactics in this chapter to prevent dysbiosis.
GUARDIAN AT THE GATE PART III
CONCLUSION
Chronic inflammation is a central cause of diseases such as heart disease, high blood pressure, diabetes, and cancer. We have shown chronic intestinal permeability and gut inflammation from a variety of sources is not only a potential source of chronic inflammation, but perhaps a necessary component for developing and perpetuating autoimmune diseases dis eases (such as type I diabetes). diabetes).
Using the basic dietary and lifestyle interventions given in this chapter’s Strong chr onic inflammation in the gut Medicine Defensive Tactics can “break the link” to chronic and the diseases and conditions resulting from it.
TYPE TYPE I DIAB D IABETES ETES CASE STUDY STUDY REVISITED Let us resume r esume our initial case study of the 6-year-ol 6-year- old d with with type type I diabetes diabetes from fr om the beginning o f this chapter. chapter. Althoug Although h speculative, a rational way to explain his fantastic results with a gluten free diet is as follows: • Gluten was likely tr tr igger ig ger ing intestinal intestinal permeability permeabili ty.. • Chronic Chro nic intestinal intestinal permeability permeabili ty was setting setting off o ff his adaptive adaptive immune response by exposing the the immune system system to “foreig “fo reig n” molecules daily. daily. • His individual genetics left him predisposed predis posed to an “agi “agitat tated” ed” adaptive adaptive
immune system accidently accidently targ eting his o wn cells—in this case the the insulin producing cells in the pancreas—and started to destroy them. Again we speculate, but but it is plausible that he had dysbiosis, leaving l eaving him with fewer Treg cell “hippies” to to tame tame the out-of-co out-of-cont ntro ro l immune response r esponse from fro m the “assassins.” • We know that that pro per gut g ut bacter bacter ia balance is especially impor impo r tant to the development of the immune system in infants and children. childr en. • Removing Removing the gluten trigg er before befor e all of his insulin-pro insulin-producin ducing g cells were destroyed by the out-of-control immune attack allowed him to recover. Without the gluten trigger, the vicious cycle of chronic intestinal permeability and the resulting immune response stopped. • His condition was caught and treated early enough enoug h to to save sufficient insulin-pro insulin-pro ducing ducing cells in his pancreas. He no longer long er needs needs insulin injections. Early intervention with a gluten free diet eliminated the problem before it was too late. Most type I diabetics are not that lucky, and the damage is already alr eady done by the time time gluten g luten sensitivity sensitivity is caught. In my opinion, opinio n, ther theree are no benefits in including gluten in a child’s diet—and everything to gain by adhering to a gluten free diet at an early age. Most children are not genetically pr edisposed to develop type I diabetes, but but is it wor wor th the the risk r isk with your child?
COACH’S CORNER: Gut Health and Body Composition If you are focused on fat loss and muscle gain, take heed. High cortisol levels from the HPA-axis threat response promote fat gain and muscle loss. Inflammation and oxidative stress in the gut are interpreted as a threat by the brain, leading to activation of the cortisol producing HPA-axis. Stopping the threat response by controlling inflammation in your intestinal tract will impr i mprove ove your health, as well as accelerate your fat loss and muscle building efforts.
Now that you have adequate training on the devastating health effects of chronic gut inflammation, prepare yourself to learn about one of the most powerful members member s of the “Pentav “Pentaver erate,” ate,” obesity.
“MILITARY INTELLIGENCE” INT ELLIGENCE” (REFERENCES): Nutrients 3(1) (2011): 104. Ahrne S, Hagslatt ML. Effect of Lactobacilli on Paracellular Permeability in the Gut. Nutrients Clin Invest 40(5) (2010): 401. Al -Lahham -Lahham SH, et al. R egul ation of Adipok ine Production in HumanAdipose Ti ssue By Propionic Propionic Aci d. Eur d. Eur J Clin Nature 504 (2013): 451-455. Arpaia Arpaia N, et al . M etaboli tes produc produced ed by commensal commensal bacteria promote promote peripheral peripheral reg ulatory T-cell generation. Nature Arrie Arrie ta MC, et al. Al terations terations in Intestinal Intestinal Permeabili Permeabili ty. ty. Gut 55(10) (2006): 1512. Assimakopoulos Assimakopoulos SF, et al. Enterocytes’ Enterocytes’ Tight Junctions Junctions:: From M ole cule cule s to D iseases. World J Gastrointest Pathophysiol 2(6) (2011): 123. Mutagen 51(4) (2010): 304. Attene-Ramos M S, et al. DNA Damage Damage and and Toxicogenomic Toxicogenomic Analyse Analyse s of Hydrogen Hydrogen Sulf Sulf ide i n Human Human Intestinal testinal Epithel Epithel ial Fhs 74 I nt Cell s. Environ Mol Mutagen Immunol (2012): 932072. Azad MB, Kozy rskyj AL. Perinatal Perinatal Programming of Asthma: Asthma: The R ole of Gut M icrobiota. icrobiota. Clin Dev Immunol (2012): Nutr Metab 58 Suppl 2 (201 1): 44. Backhed F. F. Programming Programming of Ho st Me tabol tabol ism By the Gut Mi crobio ta. Ann ta. Ann Nutr Res (2012). Bengmark S. Gut Mi crobio ta, Immune Immune D eve lo pment and andFunctio Functio n. Pharmacol n. Pharmacol Res (2012). Bernard Bernardo o D, et al. Is Gl iadin Real ly Safe f or Non-Coel iac Indiv Indiv iduals? iduals? Produc Productio tio n of Interle uki n 15 in Biopsy Culture Culture From Non-Coe li ac Indivi duals Chall Chall enged Wi th Gl iadin Peptides. Peptides. Gut 56(6) (2007): 889. Blaut M, K laus S. Intestinal M icrobiota andObesi Obesi ty. Handb ty. Handb Exp Pharmacol (209) (2012): 251. Bowe W P, Logan AC. Acne Vulgaris, Probioti cs and the Gut-Brain-Sk in Axi s - Back to the F uture? Gut Pathog 3(1) (2011): 1. Pharmacol (2012). Bravo JA, e t al. Communication Betwee n Gastroi ntestinal Bacteria and and the Ne rvous System. System. Curr Opin Pharmacol (2012). Rev 7(8) (2008): 644. Briani C, et al. Celiac Disease: From Gluten to Autoimmunity. Autoimmun Rev Brown CT, et al. Gut Mi crobio crobio me M etagenomi cs Analysi Analysi s Sugge sts a Functio Functio nal nal M odel f or the De vel opment of Autoi mmunity f or Type Type 1 Diabetes. PLoS One 6(10) (2011): e25792. Clark e SF, et al. The Gut Mi crobio crobio ta and and Its R el ationship to Di et andObesi Obesi ty: New I nsights. Gut Microbes 3(3) (2012): 186. Clemente M G, e t al. Early Eff ects of Gli adin adin on Enterocyte Enterocyte Intrac Intracel el lular Signall Signall ing Involve d in Intestinal Intestinal Barrier Barrier F unction. Gut 52(2) (2003): 218. Coll ins SM, Bercik P. The Re lati onship onship Betwe en Intestinal M icrobiota and and the the Central Central Ne rvous System System i n Normal Normal G astrointestinal Functio Functio n and andDi sease. Gastroenterology 136(6) (2009): 2003. Nat Rev Rev Neurosci 13 (2012): 701-712. CryanJ F, & Di nan nan TG. M ind-alte ring mi croorganisms: croorganisms: the i mpact mpact of the g ut microbiota on brain and and behaviour. behaviour. Nat De F il ippo C, et al. Impact of Di et i n Sha Shaping ping Gut Microbiota R eve ale d By a Comparative Comparative Study Study i n Chil dren dren From Europe Europe and Rural Afri ca. Proc ca. Proc Natl Acad Sci U S A 107(33) (2010): 14691. de Vos Vos WM , de Vos EA. Ro le of the Intestinal M icrobiome i n Heal th and and Di sease: From Correlati on to Causation. Causation. Nutr Rev 70 Suppl Suppl 1 (2012): S45. Microbiol 33(1) (2013): 1. Di Cagno R, et al. Exploitation of Vegetables and Fruits Through Lactic Acid Fermentation. Food Microbiol Di amant M, e t al. Do N utrie utrie nt-Gut-Mi crobio ta Interactions Interactions Play a Rol e i n Human Human Obesi ty, Insuli Insuli n Resi stance stance and and Type 2 Di abete abete s? Obes Rev 12(4) (2011): 272. Drago S, et al. Gl iadin, Zo nuli n and and Gut Gut Permeabil Permeabil ity : Eff ects on Cel Cel iac and and Non-Cel iac Intestinal M ucosa ucosa and Intesti nal nal Ce ll Li nes. Scand J Gastroenterol 41(4) (2006): 408. Fasano, A. Physi Physi ol ogi cal, Pathologi Pathologi cal, and and Therapeutic Impli cations of Zonuli n-Me diated Intesti Intesti nal nal Barrier Modulation: Liv ing Li fe on the the Edge of the Wall Wall . Am J Pathol 173(5) (2008): 1243. Fasano, A. Zo nuli n and and Its R egulati on of Intesti nal nal Barrier F unction: The Biol ogi cal Door to Infl ammation, Autoimmunity, andCancer. Cancer. Physiol Rev 91(1) (2011): 151. Fasano, A. Leak y Gut and Autoi Autoi mmune Di seases. Clin Rev Allergy Immunol 42(1) (2012): 71. Nutrients 4(4) (2012): 243. Ferretti G, et al. Celiac Disease, Inflammation and Oxidative Damage: A Nutrigenetic Approach. Nutrients Fe tisso v SO, SO, Dechel otte, P. The Ne w Li nk Betwe en Gut-Brain Gut-Brain Axi s and and Neuropsychiatric Di sorders. Curr Opin Clin Nutr Metab Care 14(5) (2011): 477. Nutrition 24(4) (2008): 348. Fetissov SO, et al. Autoantibodies Against Appetite-Regulating Peptide Hormones and Neuropeptides: Putative Modulation By Gut Microflora. Nutrition Ford RP, The Gluten Syndrome: A Neurological Disease. Med Hypotheses 73(3) (2009): 438. Sci (2012). Forsythe P, Kunze Kunze WA. Voi ces From W ithin: Gut Mi crobes and the Cns. Cell Mol Life Sci (2012). Forsythe P, et al . On Communication Betwe en Gut M icrobes andthe Brain. Curr Opin Gastroenterol 28(6) (2012): 557. Forsythe P, et al . On Communication Betwe en Gut M icrobes andthe Brain. Curr Opin Gastroenterol 28(6) (2012): 557. Nature 504 (2013): 446-450. Furusawa Y, et al. Commensal mi crobecrobe- derive d butyrate utyrate i nduces uces the diff erentiati on of colo nic regulatory T cell s. Nature Genuis SJ, BouchardTP. TP. Cel iac Di sease Prese nting as Autism. Autism. J Child Neurol 25(1) (2010): 114. Lett (2014). Gerber GK. The dynamic dynamic mi crobio me. FEBS Lett (2014). Physiol 2 (2011): 94. Grenham Grenham S, et al. Brain-G ut-Mi crobe Communication in He alth and Dise ase. Front Physiol Grootj ans ans J, e t al. Non-I nvasive A ssessment of Barrier Integri ty and and Function of the Human Gut. World J Gastrointest Surg 2(3) (2010): 61. ients 3(6) (2011): 637. Hak ansson ansson A, Mol in G. Gut Mi crobio crobio ta and and Infl ammation. Nutr ammation. Nutrients Pharmacol Ther 27(2) (2008): 104. Hamer HM, et al. R evi ew Article : The Rol e of Butyrate Butyrate on Colonic Function Function.. Aliment Pharmacol Obes (2012): 879151. Harris Harris K , et al. I s the Gut Microbiota a New F actor Contributing Contributing to Obesity Obesity and Its M etaboli c Diso rders? rders? J Obes (2012): Hold GL, et al. Role of the gut microbiota in inflammatory bowel disease pathogenesis: What have we learnt in the past 10 years? World J Gastroenterol 20(5) (2014): 1192-1210. FEMS Microbiol Lett 244(1) (2005): 1. Hope M E, e t al. Spora Sporadic dic Colorectal Colorectal Cancer--Rol e o f the Commensal Commensal Mi crobiota. crobiota. FEMS Hvii d A, et al. Antibioti Antibioti c U se andInflammatory Inflammatory Bowel Diseases i n Chil dhood. Gut 60(1) (2011): 49. Ivanov II , & Honda K. Intestinal comme nsal nsal microbes as immune modulators. modulators. Cell Host Microbe 12 (2012): 496-508. Je rnberg rnberg C, et al. Lo ng-Term Impacts Impacts of Antibioti c Exposure Exposure on the Human Intesti nal nal M icrobiota. Microbiology 156(Pt 11) (2010): 3216. Gastrointest Liver Liver Phy siol 298(6) (2010): Karczewsk i J , et al. Re gulatio n of Human Epithel ial Ti ght Junction Protei Protei ns By Lactobacill Lactobacill us Plantaru Plantarum m in Vivo and Protective E ff ects on the Epithel Epithel ial Barrie r. Am J Physiol Gastrointest G851. Nutr Rev 70 Suppl 1 (2012): S18. Kel ly D, M ulder ulder IE, Mi crobiome crobiome and Immun Immunologi cal cal Interac Interactions. tions. Nutr Spring Harb Perspect Med 2(7) (2012): a007690. Knip M, Sime ll O. Environmen Environmental tal Trigge rs of Type Type 1 Diabetes. Cold Spring Koboziev I, Reinoso, Webb C, Furr KL. & Grisham MB. Role of the enteric microbiota in intestinal homeostasis and inflammation. Free Radic Biol Med 68C (2014): 122-133. Gastrointest Liver Liver Physiol 294(1) (2008): G208. Kong J, et al . Novel Rol e of the the Vi tamin tamin D R eceptor in Mai ntaining ntaining the I ntegrity ntegrity of the the I ntestinal ntestinal M ucosal Barrier. Barrier. Am J Physiol Gastrointest
Konturek Konturek PC, et al. Stress andthe Gut: Pathophysi ophysi ol ogy, Cl ini cal Consequences, Consequences, D iagnosti c Approach Approachand and Treatment Optio ns. J Physiol Pharmacol 62(6) (2011): 591. Kronman Kronman MP, et al . Anti bioti c Exposure Exposure and and Ibd Devel opment Among Chil dren: dren: A Populati on-Based Cohort Cohort Study. Pediatrics y. Pediatrics 130(4) (2012): e794. Kwon HK, et al. Generation of Regulatory Dendritic Cells and Cd4+Foxp3+ T Cells By Probiotics Administration Suppresses Immune Disorders. Proc Natl Acad Sci USA 107(5) (2010): 2159. Lakhan SE, SE, Ki rchgessner A. G ut Mi crobio ta and Sirtuins Sirtuins in Obesi Obesi ty-R el ated Inflammation andBowe l D ysfunctio ysfunctio n. J Transl Med 9 (2011): 202. Lammers KM, e t al. Gl iadin Induces uces an Increase in Intestinal Permeabil ity and Z onuli onuli n Re le ase By Binding to the Chemok ine R eceptor Cxcr3. Cxcr3. Gastroenterology 135(1) (2008): 194. 5(2) (2010): e9085. Larsen N, et al. Gut Microbiota in Human Adults With Type 2 Diabetes Differs From Non-Diabetic Adults. PLoS One 5(2) Li F, et al. Human Gut Bacterial Communities Are Altered By Addition of Cruciferous Vegetables to a Controlled Fruit- and Vegetable-Free Diet.
J Nutr 139(9) (2009): 1685.
Looft T, All en HK, Coll ateral ateral Eff ects of Antibiotics on Mammali Mammali an Gut Microbiomes. Microbiomes. Gut Microbes 3(5) (2012): 463. Luckey D , Gome z A, M urray urray J, W hite B, & Tanej a V. V. Bugs & us: the the rol e of the gut in autoi autoi mmunity. Indian J Med Res 138 (2013): 732-743. MacFarlane MacFarlane AJ , e t al. A Type 1 Di abetes-R abetes-R el ated Protein Protein From Wheat (Triticum (Triticum Aesti vum). vum). Cdna Cdna Clone Clone of a Wheat Storage Storage Gl obuli n, Glb1, Link ed to Isl et Damage. J Biol Chem 278(1) (2003): 54. Thromb Vasc Biol (2012). Biol (2012). Mai tra U , Li L. M ol ecular Mechanisms R esponsible f or the R educed educed Expressi Expressi on of Chol este rol Transporters From Macrophages hages By Low- Dose Endotoxin. Arterioscler Thromb Me ssaoudi M , et al. A ssessme nt of Psychotropic-Li k e Properties of a Probioti Probioti c Formulation (Lactoba (Lactobacil cil lus Hel veti cus cus R00 52 and Bif idobacterium idobacterium Longum R0175) i n Rats and Human Human Subjects. Subjects. Br J Nutr 105(5) (2011): 755. Me ssaoudi M , et al. Benefi cial Psychologi cal Eff ects of a Probioti Probioti c Formulati Formulati on (Lactobacil Lactobacil lus Hel veti cus cus R005 2 and Bif idobacterium idobacterium Longum R0 175) in Healthy HumanVolunteers. Gut Microbes 2(4) (2011): 256. Probiotics Antimicrob Proteins 3(1) (2011): Michail S, Kenche H. Gut Microbiota is Not Modified By Randomized, Double-Blind, Placebo-Controlled Trial of Vsl#3 in Diarrhea-Predominant Irritable Bowel Syndrome. Probiotics 1. Mo lo ney RD , Desbonnet Desbonnet L, Cl arke G, D inan TG, & Cryan JF. The mi crobio crobio me: stress, health and and disease. Mamm Genome 25 (2014): 49-74. Mul der IE, et al . Environmentally -Acquire -Acquire d Bacteria Bacteria Infl uence M icrobial D iv ersity and and Natural Innate Innate Immune Re sponses At G ut Sur Surfaces. faces. BMC Biol 7 (2009): 79. Nagano Nagano Y, et al . The Induction of Treg Cel ls By G ut-Indig ut-Indig enous Clostridium. Curr Opin Immunol 24(4) (2012): 392. NutschKM , Hsi eh CS. T Cel l Tol erance erance andImmunity to Commensal Bacteria. Curr Opin Immunol 24(4) (2012): 385. Ochoa-Re Ochoa-Re paraz paraz J, e t al. Central Nervous System De myel inating Di sease Protecti on By the the Human Commensal Bacteroides F ragil is D epends epends on Polysaccharide a Expressi Expressi on. J Immunol 185(7) (2010): 4101. Disord 20(3) (2010): 188. Olsen NJ, et al. Autoant Autoantibod ibody y Profil es i n Two Two Patients Wi th Non-Autoimmu Non-Autoimmune ne Muscle Dise ase Implicate a R ole for Gl iadin Autoreac Autoreactivi tivi ty. ty. Neuromuscul Disord Overman EL, et al. Crf Induces Intestinal Epithelial Barrier Injury Via the Release of Mast Cell Proteases and Tnf-Alpha. PLoS One 7(6) (2012): e39935. Penders Penders J, et al. F actors actors Infl uencing uencing the Compositi on of the Intestinal M icrobiota i n Early Early I nfancy nfancy.. Pediatrics 118(2) (2006): 511. Prak Prak ash S, et al . Gut Mi crobio crobio ta: Next F rontie rontie r in U nderstanding erstanding Human Human Health and and Deve lo pment of Bio therapeutics. therapeutics. Biologics 5 (2011): 71. Gastrointest Liver Liver Physiol 286(6) (2004): G881. Rao RK, et al. Recent Advances in Alcoholic Liver Disease I. Role of Intestinal Permeability and Endotoxemia in Alcoholic Liver Disease. Am J Physiol Gastrointest Ridlon JM, et al. Bile Salt Biotransformations By Human Intestinal Bacteria. J Lipid Res 47(2) (2006): 241. Public Health 1 (2013): 69. Ri le y LW, Raphael E, & Faerstein E. Obesity i n the the U nited States States - dysbiosis dysbiosis f rom exposure to l ow-dose antibiotics? antibiotics? Front Public Ro und JL, M azmanian SK, The Gut M icrobiota Shapes Shapes Intesti nal nal I mmune R esponses During Heal th and andDi sease. Nat Rev Immunol 9(5) (2009): 313. Russell SL, Finlay BB, The Impact Impact of Gut Microbes Microbes i n Alle rgic Dise ases. Curr Opin Gastroenterol 28(6) (2012): 563. Russo I, et al . Butyrate Butyrate A ttenuates ttenuates Li popol popol ysaccha ysaccharide-I ride-I nduced uced Infl ammation in Intestinal Ce ll s and and Crohn Crohn’s ’s M ucosa ucosa Through Modulation of Antioxi dant dant Defe nse Machinery. Machinery. PLoS One 7(3) (2012): e32841. Sakaguchi S, et al. F oxp3+ Cd25+ Cd4+ Natural Natural R egul atory T Cell s in Dominant Sel f-Tol erance erance and and Autoimmune Dise ase. Immunol Rev 212 (2006): 8. Sapone A, et al . Spectru Spectrum m of Gl uten-Re lated Di sorders: sorders: Consensus on New No menclature and Classi fi cation. BMC Med 10 (2012): 13. Sapone A, et al. Divergence of Gut Permeability and Mucosal Immune Gene Expression in Two Gluten-Associated Conditions: Celiac Disease and Gluten Sensitivity.
BMC Med 9 (2011): 23.
Seki rov I, et al. Gut Microbiota Microbiota in Health and and Disease. Physiol Rev 90(3) (2010): 859. Shea-D Shea-D onohue onohue T, et al . Enteric Pathogens and Gut Function: R ol e o f Cyto k ines and and Stats. Stats. Gut Microbes 1(5) (2010): 316. Sigthorsson G, et al. Intesti nal nal Pe rmeabili ty andInfl ammation in Patie Patie nts onNsaids. Gut 43(4) (1998): 506. Simren M. I BS with intesti nal nal mi crobial dysbio dysbio sis: a new andcli nicall y rel evant subgrou subgroup? Gut (2014). (2014). Spread Spreadbu bury, ry, I. Comparison Comparison Wi th Ancestral Ancestral D ie ts Suggests De nse Acel lular Carbohyd Carbohydrates rates Promote an Inflammatory M icrobiota, and May be the Primary Di etary Cause Cause o f L eptin R esi stance stance and Obesi ty. Diabetes Metab Sy ndr Obes 5 (2012): 175. Stengel A, Tache Y. Neuroendocrine Control of the Gut During During Stress: Corticotropin-R el easi ng Factor Sig Sig nali nali ng Pathways Pathways in the the Spotli ght. Annu Rev Physiol 71 (2009): 219. Stil li ng RM , Di nan nan TG, & Cryan JF. M icrobial ge nes, brain & behaviour - epige netic regulati on of the the gut-brain gut-brain axis. Genes Brain Behav 13 (2014): 69-86. Sun Sun CM, et al. Small Intestine Intestine Lamina Propria opria De ndriti driti c Cell s Promote Promote De Novo Ge neration neration of Foxp3 T Re g Cel ls Vi a Reti noic Acid. Acid. J Exp Med 204(8) (2007): 1775. Tilg H, Kaser A. Gut Microbiome, Obesity, and Metabolic Dysfunction. J Clin Invest 121(6) (2011): 2126. Vael C, Desager K. The Importance of the Development of the Intestinal Microbiota in Infancy. Curr Opin Pediatr 21(6) (2009): 794. Verdu EF, et al. Between Celiac Disease and Irritable Bowel Syndrome: The “No Man’s Land” of Gluten Sensitivity. Am J Gastroenterol 104(6) (2009): 1587. Vi sser J, e t al. Ti ght Junctions, Intestinal Permeabil ity, and and Autoimmunity: Autoimmunity: Cel iac Di sease and Type Type 1 Di abete abete s Paradig adig ms. Ann N Y Acad Sci 1165 (2009): 195. Res (2012). Walk Walk er AW, Lawley TD. T herapeutic Modulation Modulation of Intestinal Intestinal D ysbiosi ysbiosi s. Pharmacol Res (2012). Well s J M. Immunomodulatory Me chan chanisms isms of Lactob Lactobac acil il li . M icrob Cell Fact 10 Suppl 1 (2011): S17. Wu S, et al. V itamin D R eceptor Negativel y R egulates Bacterial-Stimulated Bacterial-Stimulated Nf-Kappa Nf-Kappab b Activi Activi ty in Intestine. Am J Pathol 177(2) (2010): 686. Yamaguch amaguchii T, et al. Two M odes of Immune Immune Suppr Suppressi essi on By Foxp3(+) R egulatory T Ce ll s U nder Infl ammatory ammatory or NonInfl ammatory ammatory Conditi Conditi ons. Semin Immunol 23(6) (2011): 424. Yoon SS, Sun Sun J. Probio Probio tics, Nuclear R eceptor Signali ng, and and Anti-I nflammatory Pathways. Pathways. Gastroenterol Res Pract (2011): (2011): 971938. Z hang hang F, et al . Should Should We Standard Standardiz e the 1 ,700- Year-Old Fe cal M icrobiota Transplantation? Am lantation? Am J Gastroenterol 107(11) (2012): 1755.
KNOWING KNOW ING YOUR ENEMY II II
OBESITY: OBESITY: THE TH E ENEMY EN EMY WITHIN WITH IN
A nuclear explosion is an uncontrolled chain reaction leading to a devastating outcome. The obesity epidemic is an out of control chain reaction that is devastating to both our health and healthcare system. By contributing to creating a legion of people with with chronic chro nic diseases, obesity obesity is also killing us economically. Obesity and its resulting health consequences, may represent the single biggest threat to 21st century public health. Obesity transfor transfo r ms our o ur fat cells into an “enemy within.” within.” We We will show sho w you how to reverse this transformation and stop the metabolic corruption that ultimately results in a devastating assault on your body and brain. The Strong Medicine Defensive Tactics learned in this section will repel this assault and restore the flesh machine to state of optimum function. We will over throw thro w the the enemy within. within.
KNOWING KNOW ING YOUR ENEMY II II
INTRODUCTION: A BIG FAT PROBLEM...
THE NEWEST N EWEST MINORITY MINORITY A couple of years ago, I was preparing for job interviews after my time in the military and needed to buy a new suit. For the previous 13 years, I wore military uniforms for formal occasions and had not bought a business suit in years. I went to a well-known men’s clothing store, thinking it would be relatively easy to purchase a decent suit, without spending a fortune on custom tailoring. I was wrong. The salesman worked with me for more than 2 hours, trying on suit after suit, before he said with a look of dismay, “Even with extensive tailoring, I don’t have anything here that I can make fit you. There is just too much extra material around the waist.” I was somewhat taken aback by his statement. At the time, I had a 44-inch chest and a 32-inch waist—hardly freakish proportions. He said there was too much of a difference between my chest and waist size, making off-the-rack suit purchases “impossible.” He directed me to a competitor who carried a brand that was “athletic cut” and which could probably be tailored to fit me. After spending an entire day looking for a suit, I eventually found something to fit my apparently “rare” proportions. I had
no idea that my body type had become a rarity, as I had been around military men and women—who were far fitter than the general population—for more than a decade. I did not truly grasp the extent of the obesity problem until my sheltered bubble was burst while shopping for a suit. The actual statistics for the proportion of U.S. adults that are overweight or obese —almo st 3/4ths o f our populatio popul ation—ar n—aree sober so bering ing.. The r emaining emai ning 1/4th of us who are not no t overweight or obese are the the newest newest minority. minority.
Data Data compiled com piled by the American Heart Hear t Associ Association, ation, 2013.
COSTS COS TS:: HEAL HE ALTH TH AND AN D THE TH E ECONOMY E CONOMY Excess body fat ranges from overweight to obese to morbidly obese. The health consequence consequencess mir r or the the individual’s individual’s degree o f obesit o besity y. These These chro nic diseases and poor health health outcomes are inexorably i nexorably linked to to obesity: obesity: • • • •
Type II diabetes High High blood pressure Heart disease Cancer
The current economic cost of obesity-related disease is estimated at over $250 billion each year. By 2030, it is predicted that the health care costs from obesity could rise to over $950 billion. Obesity and chronic disease are linked very strongly since obesity is a source of chronic inflammation and oxidative stress. We will present what you can do to fight your own battle battle with obesity—and win.
QUICK FACT:
Health care costs related to obesity could reach as high as $950 billion per year by 2030.
TECHNICAL NOTE: Someone is defined as overwe over weight ight or obese by an indictor indictor called the the body mass index (BMI). BMI is calculated using a person’s per son’s height heig ht and weig weight: ht: (BMI). BMI Metric versio n BMI BMI = mass(kg) mass(k g) / height(m)) height(m) ) Metric 2
BMI BMI = mass(lbs) / height(1n)) X703 English version 2
There are several online BMI calculators on the internet, which will automatically calculate the BM BMI from fro m your height and weight measurements.
A BMI from 25.0 to 29.9 indicates being overweight. A BMI of 30 or over indicates obesity.
Many will cor r ectly point out that lean, muscular people may have a BMI BMI in the overweight range when they are not actually overweight. For example, I am 5’9’ tall tall and weigh weig h 175 lbs. I am fair ly lean—about 8-9% body fat. My My BMI BMI is calculated as 25.8, which which is considered consi dered over weight even though I have litt li ttle le body bo dy fat.
Lean individuals who carr car r y mor e muscle mass may find f ind that the BM BMI is not the most accurate assessment. For the general gener al population, populatio n, it is a decent measurement for being overweight o verweight or obese. We will discuss some new body measur ements that that have shown to to be superior superi or to BMI BMI in the Analytics Analytics Section.
OBESITY: OBESITY: THE ENEMY E NEMY WITHIN W ITHIN I
THE FAT CELL: CELL : DR. JEKYL JEK YLL L BECOMES MR. HYDE
The fat cells, or adipocytes are the major storage sites for fat in the body. We all have fat in our body, and and we all need fat to survive.
QUICK DEFINITION: The wor wor d adipocyte comes from: “adipo”= fat and “cyte”= cell. Adipocyte literally literall y means “fat cell.” Adipocytes do much more than just store fat. They provide crucial signals to the brain r egarding egar ding energ y storage. stor age. These fat cells cells r egulate appet appetite, ite, adjust adjust metabolism metabolism and lower inflammation when they are functioning properly. When fat cells are stuffed to capacity from overeating, the adipocytes undergo a metamorphosis from being benefactors of good health into aggressive, bloated
monsters spewing inflammation and oxidative stress.
How does a fat cell transform? Why does an excessive intake of industrial, processed food and drink transform mild-mannered Dr. Jekyll into evildoer Mr. Hyde? The following diagram (from the Central Concepts chapter) shows chronic inflammation inflammation and oxidative oxidative stress cont co ntri ribut buting ing to chronic chr onic diseases.
The over-stuffed adipocytes in an obese person are one source of chronic inflammation and oxidative stress that “links” obesity to cancer, heart disease, diabetes, and high blood pressure as well as accelerated aging and neurodegeneration.
The “link” between obesity/insulin resistance and chronic disease.
THE METAMORPHOSIS OF A FAT CELL The normal nor mal fat cell cell seeks to to stor e excess excess energy in the form for m of triglycer tr iglycerides—t ides—the he storage form of fat. The adipocyte, functioning correctly (as found in lean individuals) secretes an important hormone, adiponectin. This little-known hormone performs several health-promoting functions:
• Decreases Decrea ses inflam inflamm mation at ion - adiponectin controls inflammation caused by the immune system. It decreases the number of inflammator inflammato r y cytokines, the the messenger messengerss of inflammation. adiponectin decreases levels of inflammator inflammator y • Increases insuli insulin n sensitivi sensit ivitt y - adiponectin cytokines. This allows insulin to do its intended job: pulling glucose into the cells to prevent a toxic buildup of glucose in the blood stream. adipo nectin stimulates stimulates the machinery that • Increases Increases fat burnin burningg for fo r energy energy - adiponectin breaks down fat for energy. The healthy adipocyte stores just the right amount of fat, and because it is not overworked, it functions properly. When we eat food during the day, we stockpile nutrients and have a good supply to use for energy while we sleep. The healthy adipocyte adipocyte pro duces duces high amounts amounts of o f the beneficial beneficial hor mone adiponectin adiponectin regularl r egularly y.
When we take in more calories than we can use for energy, the adipocyte starts to grow in size. It swells to capacity as it tries to store excess triglycerides. When excess dietary fat and triglycerides made from extra glucose combine, they overwhelm the storage and processing capacity of the fat cells. Now, the bloated adipocyte starts to attract the attention of the immune system. The immune imm une system exists to to defend us fr f r om “threats” and the the bloated blo ated adipocyte has appeared on the immune radar as a potential health threat. A very interesting process involving an immune cell called a macrophage begins in our fat cells as they get am-packed with fat.
QUICK DEFINITION: Macro o = “big” “big ” Macrophage literally means “big “big t hing hing t hat devours”. Macr and phage = “thing that devours” (from Greek phagos). The macrophage is an “innate guardian” cell that “eats debris” when a cell dies. Macrophages also fight invading bacteria and other foreign material. A type of macrophage called an M2 macrophage “stands guard” inside an adipocyte in case something bad happens. happens. When the adipocyte starts to swell with triglycerides (fat), the M2 macrophage senses a threat and goes on “alert,” then starts to arm itself with weapons. Like prison guards who get assault rifles and tear gas ready when they sense a riot may start, the M2 macrophage “arms” itself by transforming into a deadly M1 macrophage. The M1 macrophage prepares for battle by secreting inflammatory messengers called cytokines.
The swelling adipocyte, adipocyte, stuffed stuffed with with tri triglyceri glycerides des trigg ers the the transfor mation mation of the the M2 macro phage to the inflammation-pr inflammation-producing oducing M1 version. versio n.
The adipocyte starts secreting inflammatory cytokines as a “911 call” summoning immune reinforcements reinfo rcements.. If more food is eaten—despite the fact that enough fat to fuel the body for weeks may be available available for energy—the energy—the normal nor mal cellular pr ocesses break down.
Inside the swelling adipocyte fat cell, the mitochondria work overtime and produce large amounts of oxidative stress in the form of free radicals. More of the M2 macrophages are converted into the M1 variety, as the immune system registers a “prison riot” in full swing inside the swollen fat cell. Higher amounts of inflammatory cytokines are sent into the bloodstream as the fat cell tries to protect itself itself fr om the the excess energy and r esulting esulting oxidative oxidative stress. The immune system responds by sending in more soldiers, triggering and increasing intense, prolonged and devastating inflammation. Stressed and bloated adipocytes create obesity-related inflammation. Intense inflammation causes the fat cells to reduce secretion of the beneficial hormone, adiponectin. Without the anti-inflammatory effects of adiponectin, the inflammatory momentum picks up even more steam. The body considers fat deposited next to vital organs—the liver, intestines, and blood vessels—as especially threatening. This is called “visceral obesity,” as viscera means internal organs. People with visceral obesity have the classic “apple shape” with the majority of the fat stored in the abdominal cavity around the organs. This type of visceral obesity is seen with the classic beer belly. People proudly sporting a beer belly often brag that it is “hard as a rock” and not squishy like superficial fat. This is the absolute worst type of fat and nothing to be proud of, as it is highly inflammatory.
QUICK QUICK MEDICAL MEDICA L NOTE: Visceral obesity (also called abdominal obesit o besity y or centr centr al obesit o besity) y) is highly associated with a variety of diseases related to inflammation: • • • • • •
Type II diabetes Heart disease Fatty Fatty liver disease Cancer Alzheimer ’s dementia Accelerated physical aging agi ng
Given what you now know about fat cell transformation and inflammation, inflammation, these associations associations should sho uld not be surpr ising.
The swollen adipocytes surrounding the vital organs in visceral obesity are no longer recognizable as the innocent fat cells found in lean individuals. These monsters truly have become Mr. Hyde. They spew forth massive amounts of inflammatory cytokines into the rest of the body like an oil rig fire. These beasts often end up dying in their attempt to protect themselves, leaving the M1 macrophages to clear their bodies away. This dying and clearing process is also highly inflammator inflammator y. Recent research has shown that swollen fat cells can be a substantial source of chronic inflammation and oxidative stress. As we mentioned at the beginning of this section, the inflammation and oxidative stress produced daily by these bloated fat cells is likely the link between obesity and the chronic diseases of cancer, heart disease, diabetes, and high blood pressure.
QUICK QUICK MEDICAL MEDICA L NOTE: It was once thought that by adulthood, adulthood, you yo u had all o f the fat cells (adipocytes) you would ever have, and people got fatter only by overstuffing their existing fat cells in a process called hypertrophy. Hypertrophy simply means “growing bigger”. It turns out that an overweight or obese person can actually grow gro w new fat cells. This pro cess is called hyperplasia . People can increase their fat mass by storing fat in existing fat cells (hypertrophy) AND by producing new fat cells (hyperplasia). Drawing o n the ideas from fr om the Central Central Concept Co nceptss chapter, obesity can be viewed as a process of allostasis —trying —try ing to achieve stability stabili ty in a changing chang ing envir onment. onm ent. In this case, your body attempts attempts to to adapt to the enviro nmental stimulus stimulus o f overeating o vereating.. It increases your fat storage as a protective mechanism to keep high levels of damaging glucose and certain fats (palmitate) out of your bloodstream. Over time, this protective mechanism becomes problematic, causing excessive inflammation and contributing to disease. The diseases caused by this process can be viewed as part of allostatic overload , or the body’s failure to adapt (long-term) to an envir environment onmental al stress such as overeat over eating. ing. The following sections will cover obesity’s contribution to chronic diseases, including an appropriately detailed discussion of diabetes, given its current impact on public health.
OBESITY: OBESITY: THE ENEMY E NEMY WITHIN W ITHIN II
THE PLAGUE LA GUE OF “DIABESITY” “DIABESITY”
Obesity and type 2 diabetes (T2D) have a powerfully negative relationship. Obesity and T2D occur together so often, that amongst medical professionals the combined affliction is often referred to as “Diabesity.” Diabetes + Obesity = Diabesity. Massive public health campaigns, an increased focus on diabetes prevention, and diabetes management in clinical settings have not been able to turn the tide. The evil combo of diabesity is a health Armageddon—a literal tsunami leaving death and destruction strewn str ewn in its wake. wake. The statistics statistics for fo r T2D are disturbing di sturbing evidence that that we we are losing this fight. According to the latest update from the American Diabetes Association (2013), 26 million people in the US have diabetes, and an additional 79 million millio n people are pr e-diabet e-diabetic. ic. • The economic econo mic cost of diabetes diabetes has r isen to $245 billion billi on per year in the US alone. • If curr ent trends continue, it is estimated that one in three adults will have diabetes by the year 2050. Although we know a genetic component contributes to a person’s risk for developing diabetes, genetics do not account for the dramatic increase in diabetes over the past half-century.
The massive increase in T2D is parallel to a radical change in our daily environment—degradation of food quality, lack of physical activity, increased stress, and detrimental habits. Recent science reveals epigenetic changes—the way environmental signals turn our genes on and off—are at the center of the T2D epidemic. epidemic. Borr owing from fr om our o ur earlier ear lier analogy in Basic Basic Tr Tr aining (Cent (Central ral Themes), T hemes), we are are “bookmarking” “bo okmarking” r ecipes that that wreck our metabolism metabolism lo ng-term.
RESEARCH UPDATE: Recent research has shown that exposure to high amounts of glucose in utero (in the womb)—as in gestational diabetes—will produce epigenetic changes making the fetus much more likely to develop T2D as an adult. Even our earliest environment (the womb) affects our epigenetics and lifelong health. health. Epigenetic changes produced by the modern environment predispose us to disaster. Left unchecked, the metabolism “breaks”—the smooth efficiency of a normal metabolism is shattered. When a healthy adipocyte turns into a bloated monster of a fat cell, massive amounts of inflammation and oxidative stress are produced. These two culprits are largely responsible for the loss of insulin sensitivity that that leads to T2D over time. Inflammation and oxidative oxidati ve stress cause a loss of insulin insuli n sensitivi sensi tivity ty in two main ways:
1. Inflammatory cytokines (in this case from adipocytes) “break” the signaling mechanism o f t he insulin insulin recept rece ptoo r. The door bell ringer ring er on o n the the “doo “door” r” to the cell is an insulin receptor, a protein on the surface of the cell to which insulin can “dock.” When insulin docks to the insulin receptor, it “rings a doorbell” on the cell. Usually, a special kind of door called a glucose transporter opens and allows glucose into the cell from the bloodstream. The inflammatory cytokines “shortcircuit” the insulin receptor. Once the insulin receptor is short-circuited, insulin can still still normally no rmally bind to to the the recep r eceptor, tor, but the the signal to open the the glucose door does not get thro through. ugh. Mor e and more insulin is required requir ed by the the malfunctioning malfunctioning r eceptor eceptor over
time. These “broken” receptors will eventually require the pancreas to produce a tidal tidal wave wave of insulin i nsulin to to clear glucose fr om the bloodstream.
KEY POINT: Inflammatory cytokines “short-circuit” the insulin receptor. This is one of the primary ways inflammation causes loss of insulin sensitivity and leads to T2D. Your body doesn’t know how to fix the receptor, it just responds to the problem by producing more insulin to “ring the doorbell harder.” Fixing the problem requires stopping the chronic inflammation from the bloated adipocyte-monster,
not puttin putt ingg more more insulin insulin into into t he bloo bloodst dstream ream.. The analogy is a doorbell with a short-circuit that someone keeps hitting harder to ring—inst r ing—instead ead of just fixing it! Swollen adipocytes reduce beneficial secretions of adiponectin, the inflammation-reducing hormone. Reduced adiponectin production leads to
increased numbers of inflammatory cytokines.
INSULIN INSULIN SENSITIV SENSITIVE E The healthy adipocyte helps ensure insulin sensitivity by keeping inflammation (inflammatory cytokines) low. The insulin receptor is sensitive to the signal generated when insulin “docks” to the receptor. This signal o pens the the “door” “door ” of the glucose transporte transpor ter, r, allowing glucose gl ucose into into the cells from the bloodstream. Glucose will not build up in the bloodstream, and proper pro per blood blo od sugar levels will will be maintained. maintained.
INSULIN RESIST RESISTAN ANT T The bloated adipocyte “monster” spews forth inflammatory cytokines, which “short-circuit” the insulin receptor. The insulin receptor is now resistant to sending a signal to the glucose transporter when insulin docks to the receptor. The signal does not get thro through ugh and the the glucose transporter “doo r” r emains closed. Glucose can no longer enter the cell and builds up in the bloodstream. As you become mor e insulin r esistant esistant,, diabetes begins to develop. Chronic inflammation drives dri ves diabetes. In this this case, the bloated adipocyte is the source o f the inflammation.
2. Increased oxidative stress in the mitochondria. The second major way obesity causes insulin resistance is through elevated stress levels in cell energy factor factor ies. This cause of insulin resistance resistance is similar simi lar to a smoke smo ke detect detector or sounding an alarm if your house catches fire. The overheated, over-stressed mitochondria are simply overwhelmed overwhelmed by a floo d of food/fuel. fo od/fuel.
Mitochondrial energy factories produce ATP, the vital “energy currency” generated from the fuel obtained from food. During normal circumstances, we eat enough food to fuel our body’s requirements for energy—but not so much that we overwhelm the capacity of our mitochondria energy factories. We need to eat enough but not too much to operate within mitochondrial limits and capacities. How do we determine such a minute and finite thing as cellular fuel capacities? Sounds mor e like a biophysics equat equation! ion! In In mor e earthy terms, terms, it is similar to runn r unning ing your car’s engine at low to moderate RPMs.
DIGGING DEEPER: What Exactly Exactly is a Cytokine? Cy tokine? We have refer ref errr ed to cytokines extensively in this this section sectio n and in “Immunology 101.” Cytokines are signaling molecules, carrying messages from cell to cell throughout the body. Cytokines are best known as messengers of the immune system. A very simplified way of looking at cytokines is to classify cl assify them by the the messages they car car r y. As you might have guessed, inflammatory cytokines carry the message of inflammation. inflammation. Inflammat Inflammator or y cytokines cytokines ar e generate g enerated d during infections infections or injury injur y, and signal sig nal the immune system to attack attack an invader such as a for eign bacteria bacteria or o r vir us, or to start start the the healing healing process pr ocess in response to to an injury injur y. As we have have just seen in chr onic oni c diseases like l ike diabetes, inflammator inflammator y cytokines cytokines can also disrupt normal metabolic metabolic “machinery” such as the insulin r eceptor. Oxidative stress can also trigger
inflammatory cytokines. There are also anti-inflammator anti-inflammator y cytokines cytokines pro duced duced to keep the the immune system “in check” and to stop the inflammation response. The Treg cells we discussed in Immunol Immunolog ogy y 101 and the the Gut Chapt Chapter er are ar e examples of of cells that produce anti-inflammatory cytokines. The M2 macrophage also produces this type of cytokine. Cytokines Cytokines communicate comm unicate the the curr ent “str “str ess state” of the body between between cells and organs. In this way, the liver “knows” if there is an infection or injury in the right leg because it is communicated by inflammatory cytokine
messengers. It is important for the various organs to “know” what is happening in other parts of the body so they can respond appropriately. Cytokines Cytokines allow allo w this this to happen.
Even running at safe and moderate RPMs, the mitochondria will naturally—like a engine’s exhaust—produce free-radicals (oxidative stress). As long as the free radical production is relatively low, our body’s antioxidant systems can take care of this “green level” of oxidative stress. Eat Eat ing just just enough food foo d to fuel your energy energy
requirements will keep your “Mito-RPM” in the green.
If you consistently take in more fuel than your body needs by overeating, the mitochondria factories go into overdrive trying to process the extra fuel. The energy-producing machinery in the mitochondria will start to heat up and produce high quantities of free radicals. Oxidative stress reaches “red” danger levels. The increased oxidative stress starts to overwhelm the antioxidant systems and triggers
a stress response within the cell, similar to a 911 “call for help.” High oxidative stress triggers alarm systems within the cell when “smoke” (free radicals) is detected from the over-heating mitochondria. The alarm system carries the message that something bad is happening in the mitochondria, alerting the cell to damage from large amounts of free radicals.
The absolute best way to stop a fire is to remove the fuel source, and that is exactly what the cell tries to do. When we eat starches and other glucose-containing carbohydrates, insulin is produced and docks to the insulin receptor (ringing the doorbell). This signal would usually open the glucose transporter (door), allowing glucose into the cell to be utilized for energy production by the mitochondria. The cell tries to shut this this door-o doo r-o pening pening signal down to protect pr otect itself. itself.
INSULIN RESISTANCE FROM THE INSIDE When the “Mito-RPM” is in the red from processing too much fuel, the overload of free radicals (oxidative stress) “turns off” the insulin receptor signaling mechanism, which stops the glucose transporter from opening. This removes the fuel source by stopping glucose from entering the cell. The cell is trying to protect itself itself from fr om too much fuel. fuel.
TECHNICAL NOTE: The “nuts and bolts” of how ho w insulin resistance r esistance actually actually happens on the molecular level is an active area of research. We have just presented simplified versions versio ns of two two mechanisms mechanisms suppor suppor ted ted by current curr ent r esearch.
TAKE HOME MESSAGE: A malfunctioning insulin receptor, broken by inflammatory cytokines or oxidative oxidative stress in the mitochondri mitochondria, a, is called insulin resistance resistance (or loss o f insulin sensitivity). Insulin resistance will slow the entry of glucose into the the cells, allowing g lucose to build up in the bloo bloo d stream. Any environmental stimulus that provokes long-term increases in oxidative stress and inflammation will result in insulin resistance. This
also includes sleep deprivation and psychological stress. As chronic inflammation and oxidative stress get worse, insulin resistance gets worse, and blood sugar levels get higher, resulting in type 2 diabetes.
CONSEQUENCES OF OBESI OBE SITY TY AN AND D CHRONIC INSULIN RESISTANCE Insulin is a storage stor age hor mone. Insulin’ Insulin’ss job jo b is to stor e glucose and fat when when food foo d is plentiful. When the insulin signal is not transmitted to the cell due to insulin resistance (the doorbell is broken) several things start to happen simultaneously: nor mal 1. Stored Sto red fat in fat cells cells (adipocyt (adipocytes) es) starts start s t o break down. In nor circumstances, insulin signals the storage of excess energy as fat in the adipocyte. Insulin usually signals the storage of fat and stops it from breaking down. Since the insulin signal is interrupted because of chronic inflammation and oxidative stress, the brakes are taken off. Fat is released from the adipocyte into the bloodstream. This release r elease of fat is not a goo d thing, thing, considering that that there there is no place for this this fat to to g o. The body alr eady has a fuel excess at this this point poi nt and and there is no where to “burn” the the fat. The liver gr abs the the fat from fro m the bloodstream and transfor transfor ms it into into trig lycerides before placing it on a lipoprotein carr ier cir culating culating in the the bloodstream looking lo oking for fo r a place to to dr op the fat. It is like an ever-gr owing gr oup of people riding a bus with no destination and no one ever gets off the bus. Instead of the fat getting stored in adipocytes as triglycerides, it is aimlessly
circulated in the bloodstream on lipoproteins. This inevitably causes real problems. pro blems. The trapped, trapped, endlessly endlessly circulating trig lycerides are the the reason r eason
diabetics almost always have high triglycerides when their doctor checks their blood-work.
COMING ATTRACTIONS >>> See the cholesterol section in the Analytics Chapter to Chapter to learn how high triglycerides in diabetes and metabolic syndrome can lead to heart and vascular disease.
Adding fuel to the fir e.. e...
2. T he liver liver “banker” start st artss making glucose. gluco se. When the insulin signal is not getting through, the liver starts to do something unthinkable—it starts making new glucose glucose (glu (g luconeo coneogenesis) genesis) and releasi releasing ng it int int o t he bloo bloodstream dstream.. The liver is i s pouring pour ing fuel on o n the the fire fir e by making making and releasing r eleasing glucose when the the bloodstream is already highly saturated with with glucose. As far as the liver is concerned, the body is in a state of stress, and the liver needs to ensure that the the brain brai n has adequate adequate supplies of o f glucose—especial g lucose—especially ly when stressed. Insulin resistance “fools” the liver into thinking that the body is starving and needs needs more g lucose.
QUICK QUICK MEDICAL MEDICA L NOTE: The anti-diabetic drug Metformin works by stopping stopping gluconeogenesis gl uconeogenesis in the liver. Metformin helps stop this source of extra glucose in the blood, and decreases decreases blood sugar levels.
3. Insulin Insulin resistance resist ance puts put s t he pancreas in overdrive. ove rdrive. When the insulin signaling system is broken and glucose builds up in the blood, the pancreas responds to its programming by producing more or e insulin. insulin. Chronic inflammation and oxidative stress short-circuit the insulin receptor “door bell button” button” mechanism. mechanism. The pancreas r esponds by making making mor e insulin (mor e door doo r men to hit the the button). button). Because the person will not change his or her lifestyle and eating habits to decrease inflammation and oxidative stress, the body has no choice but to produc pro ducee mor e insulin. Unfor Unfor tunat tunately ely,, producin pro ducing g larg e amounts of insulin to cope with with insulin r esistance burns o ut the the pancreas o ver time. Eventually, Eventually, the the pancreas will fail fai l and lose lo se the ability to pr oduce insulin insul in at all. A type II II diabetic diabetic r eaching this stage will have major health problems. They need to take insulin at higher and higher higher doses as their their disease prog resses.
DIGGING DEEPER: Beta-Cell Failure in i n the Pancreas Pancreas The cells which produce insulin in the pancreas are called beta-cells. They detect glucose and respond by producing insulin. As insulin resistance develops from chronic inflammation and oxidative stress, the beta-cells compensate compensate by producin pro ducing g mor e insulin. They can only compensate compensate for so long, l ong, and the stress stress o f constantly constantly producing high amounts of insulin will wear out the beta-cells. They
eventually break down and die, leaving fewer beta-cells to carry the workload of insulin secretion. When many beta-cells fail, the remaining ones can no longer effectively compensate to keep blood sugar in check. Then, blood sugar rises into diabetic levels, and things just get worse as the process pro cess continues. continues.
4. Muscle Muscle wast wasting ing occurs when o ur lean muscle mass start st artss to disappear. disappear. Insulin Insulin r esistance causes muscle wasting. wasting. Recent Recent resear ch on muscle wasting—as it relates to obesity and diabetes—has focused on a protein, myostatin. Myostatin’s Myostat in’s function is to reduce muscle mass by stopping muscle growth (myo= muscle; statin= stop or inhibit). Myostatin is secreted secr eted by by muscle, and is thought to be the centr centr al player in muscle loss associated associated with with aging (sarcopenia). A r ecent study study has shown myostatin myostatin production pr oduction is i s elevated in obese and insulin resistant people. The hor r ific combination of chronic chro nic inflammation inflammation and insulin resistance was found to increase myostatin production levels. The elevation of myostatin myostatin is thought to to be a major contributor contributor to the loss of muscle mass often seen in severe cases of obesity and diabetes.
Obesity, Obesity, insuli insulin n resistance, and diabet diabetes es act as “age-accelerators” “age-accelerato rs” for fo r loss of o f muscle mass. All humans lose muscle mass as we age, but obese people and diabetic people experience muscle loss at an accelerated rate. The body will break down do wn its its own muscle tissue to strip str ip it of amino acid content. The cannibalized amino acids will be used to feed the now-deranged “liver-banker,” in its mad quest to to make m ake mor e glucose gl ucose when none is needed. In addition addition to muscle-wasting myostatin secretion, the chronic inflammation associated with obesity and diabetes directly dir ectly contributes contri butes to to muscle wasting. Insulin Insulin stimulates building new protein, but the “building” signal is not getting through. As insulin resistance incr incr eases, muscle muscle building gri g rinds nds to a halt.
KEY POINT: Obesity, insulin resistance, and diabetes create a perfect storm for muscle wasting.
FIRST PRINCIPLES-BASED PRINCIPLES-BA SED SPECULATION: MYOSTAT MYOSTATIN IN
It makes sense that myostatin increases in cases of insulin resistance from chronic inflammation. inflammation. The body is r eacting eacting to the “threat” “threat” of chronic inflammation and insulin resistance much like it reacts to the threat of starvation. Myostatin is also elevated in times of starvation to decrease muscle mass. From a survival perspective, maintaining muscle mass has a very “expensive” energy energ y cost. If the the body can decrease muscle m uscle mass, it will have more energy to keep the brain going. We can survive with reduced muscle mass, but we don’t do well without without brain br ain function. Insulin Insulin r esistance and diabetes diabetes are ar e interpr eted by the body as a state state of starvation and/or stress—even though plenty of fuel is available—and it will decrease muscle muscle mass to conserve energy energ y for the the brain.
5. Fat wit wit hout a home... home... When the adipocytes (fat cells) are too full and unable to store excess energy as fat, the liver and muscle will start to retain some of it, simply because it has nowhere else to go. Excess fat contributes to development of fatty liver disease. The fat will also start to replace the muscle mass lost to myostatin. Large amount amo untss of fat circulating circulating in i n the the bloodst bloo dstream ream amplify the inflammator inflammator y response and insulin resistance. Fat cells store a significant amount of fat in the for m of palmitate. In the the Nutr Nutr ition 101 section, we learned lear ned palmitate is a 16 carbon car bon saturated satur ated fat that that gives saturated fat a bad name.
Palmitat Palmitatee is the primar y fat liver cells make fr om excess glucose. When palmitate is released into the bloodstream by malfunctioning malfunctioning fat cells or when when the the liver produce pro ducess it from fro m larg e amounts amounts of excess glucose, it activates alarm systems normally r eserved for detect detecting ing foreig fo reig n invaders invaders such as as bacteria. bacteria. The alar m system activated activated by palmitate palmitate ramps r amps up the immune system system promo pr omo ting increased inflammation, inflammation, oxidat o xidative ive stress, and further increasing insulin resist r esistance. ance. The fact that this this specific specif ic saturated satur ated fat activates activates this alar m system shows sho ws that large amounts of palmitate are a threat to the body. High amounts of palmitate occur your body is is tryi t rying ng to t o prot ect itself! with obesity and insulin r esistance— your
The middle picture is an MRI cross section of a 74 year old sedentary man’s thigh thigh muscle. m uscle. The view in the pictures pictures is the same as if i f the thigh was cut in half, and we lo oked down do wn at the the stump. You can see the fat (adipose) tissue surrounding the shrinking muscle, as compared to the large muscle mass in both of the pictures above and below. If you are insulin resistant or diabetic, this process is happening to you right now. If you are not exercising, this process will happen even faster. Unfortunately, many young diabetics are exhibiting the dramatically decreased muscle mass associated with much older people.
PA LMITATE—GIV LMITATE—GIVIN ING G SATURAT SATURATED ED FAT A BAD BA D NAM N AME: E: Without fail, almo st every scientific study examining the effects of saturated fat uses uses palmitate for testing testing—as —as if it were the only saturated satur ated fat in existence. It is perplexing how very smart scientists continually overlook this fact and in their research, generalize palmitate’s effects to represent all saturated fat. As previously previo usly stated, stated, palmitate palmitate indeed has some bad effects on o n metabolism and contributes to chronic disease. Of importance to this chapter, please in the t he liver liver from fro m excess note that a significant sig nificant amount of fat produced in
glucose and fructose fructo se in the t he obese o bese and diabetic diabetic person perso n is specificall specificallyy palmitate. In hig high h amounts, palmitate can wreak metabolic metaboli c havoc: • Palmitate causes inflammatio n, oxidative str str ess, and increases incr eases insulin resistance. • Palmitate decreases adiponectin secretion by fat cells, increasing increasi ng insulin resistance. • Palmitate has been shown to to incr ease inflammation in the hypothalamus, which disrupts appetite regulation (causes hunger when the body already has enough energy.) Look Loo k back at the satur satur ated fat sectio section n in Nutritio n 101. Most satur satur ated fats have very beneficial effects, don’t judge them all by the actio actions ns of palmitate. Remember Remember that it i t is normal nor mal for low levels level s of palmitate palmitat e to be stored in healthy fat cells, and it does not cause any of the above problems. problems.
6. Obesit Obesit y and chronic chro nic insulin insulin resistance resist ance increase increase the t he risk risk of cancer. cancer. Cancer is not a single disease, like diabetes or heart disease. Each type of cancer is very different, depen depending ding on o n the the or iginal cell type. type. The trigger trig ger s for cancer cancer development are just as diverse. For instance, liver cancers can be caused by infections, exposure to chemicals, and chronic alcohol use. Since cancers come in many different varieties, varieties, there there is no o ne “cur “cur e for cancer. cancer.””
However, there are several characteristics that some—and in some cases all— cancers have in common that are important to obesity, insulin resistance, and diabetes: • Cancerous Cancerous cells show uncontro uncontro lled, aggressive agg ressive cell gr owth owth and have transformed from previously normal cells. • Many cancer cancer cells become depende dependent nt on glucose as their their only source sour ce of ener ener gy (called the “War “Warburg burg Effect”). • Some cancers such as breast br east and endometrial endometr ial cancer are ar e sensitive to estrogen. estro gen. • A common tr tr igger igg er for many cancers cancers is chronic inflammat inflammation ion and oxidative oxidative stress. We’ll tackle these characteristics individually to show you why cancer loves obesity, insulin r esistance, and diabetes. diabetes. “Cancerous cells show uncontrolled and aggressive cell growth, and have transformed from previously normal cells.”
Uncontrolled cell growth is the hallmark of all cancers. These cells no longer respond to normal, healthy “check and balance” signals that control growth and reproduction. Insulin resistance creates a “growth favorable” environment. During insulin resistance, the pancreas responds by producing more insulin. People with insulin resistance have relatively high insulin levels all the time. Because insulin is a “growth, building, and storage” hormone, the presence of high insulin levels helps cancer cancer gro g ro w out of contro contro l. “Many cancer cells become dependent on glucose as their only source o energy.”
Nobel prize winner Otto Warbur Warburg g first fir st descri described bed the the phenomenon phenomenon of o f cancer cells switching their metabolism to only use glucose without the need for energy production from mitochondria. At first glance, this does not make sense, because much more energy can be generated if the mitochondria finish burning glucose. (See Metabolism Basics.) Most cancer cells only break glucose down to lactate, generating a paltry 2 ATP, compared to the 38 AT P they could get from glucose if they used the mitochondria.
The area ar ea shaded in pink is the energy energ y pathway pathway that that cancer cancer cells use, showing sho wing the “Warburg “Warburg Effect.” Effect .” Only 2 ATP ATP is gener ated because because the mitochondria mitochondr ia are ar e not used. Scientific speculation holds that because cancer cells are fast growing, they need rapid energy energ y product pro duction, ion, and the the mitochondria take take too long. The cancer cancer cells don’t care if they are wasting energy, they want fuel immediately and don’t care about sloppy inefficiencies. Cancer cells become the ultimate glucose hogs; a raging cancer cell will burn thr thr ough g lucose 200 times times faster than a normal cell. They are like l ike 500-hor 500-hor sepower sepower muscle cars that get 7 miles per gallon. They do not care about fuel efficiency, they ust go very ver y fast. fast. Normal cells are like l ike Smart Cars Cars by comparison, they use use glucose for fuel in a reasonable and highly efficient way.
The fact that cancer cells become dependent on glucose is important for those with with insulin r esistance and diabetes: diabetes: • A diabetic’ diabetic’ss high high blood sugar levels levels give cancer cancer cells a huge supply supply of glucose to survive and thrive. • Most cancer cancer cells use glucose transpor transpor ter ter s (door s) that that do not not need to be opened by insulin. insulin. The cells can scarf up lar ge amount amo untss of glucose fr om the bloodstream without without relying on insulin.
QUICK QUICK MEDICAL MEDICA L NOTE: If some cancer cells are dependent on glucose through the Warburg Effect, it would would make sense that a low carbohydr car bohydrate ate diet would would be a valuable part of o f treatment. Most cells in the body can use fat as an ener ener gy source, so a low carbohydrate diet could potentially “starve” and weaken the cancer cells that need glucose to survive, allowing traditional treatments to to be mo r e effective. This could co uld be a “one-two punch,” weaken weaken the cancer cancer cells by starvation, starvatio n, then then kill them with the drugs. For some r eason, low carbohyd carbo hydrr ate ate diets have have not seen widespread widespread use in the treatment of cancer. Recent research has shown some promise using low carbohydrate (ketogenic) diets in conjunction with traditional cancer treatment. Widespread use of both therapies together could potentially help save many lives. If the specific cancer is dependent on glucose for energy, low carbohydrate diets really have no potential negative side effects for cancer patients. patients. If you are ar e newly diagnosed with cancer, discuss starting a low l ow carbohydrate diet with with your doctor to see if it is appropr iate for your type type of cancer. cancer.
STRONG MEDICINE TACTICS: If you have cancer, discuss the use of a low carbohydrate or ketogenic diet with wit h your doctor as part of your treat treatment ment plan. plan. “Some cancers such as breast and endometrial cancer are sensitive to estrogen.”
The point applies to obesity in general. Adipocytes (fat cells) produce an enzyme called aro matase. matase. Aromatase converts hormones hor mones such as testostero testosterone ne into estrog en. The mor e fat you have, have, the the mor e aro matase matase present, present, and the the mor e estrogen estrog en you are producin pro ducing g (this (this also applies to to men).
Cancers such as endometrial cancer, and some breast cancers are “estrogen sensitive.” This means estrogen can trigger them to grow. Losing fat mass will reduce the amount of estrogen in your body, which may help reduce the growth of breast and endometrial cancers. If you attempt a fat-loss plan when you have one of these cancers, make sure to discuss discuss it with with your doctor first. fir st.
STRONG MEDICINE TACTICS: Losing fat mass through a well-constructed weight loss plan may help reduce the the tr tr igg igger er fo r breast cancer cancer and endometrial endometrial cancer cancer gr owt owth. h. Discuss this approach with your doctor as a potential part of your treatment plan. “One of the triggers for many cancers is chronic inflammation and oxidative stress.” stres s.”
As we have covered extensively, obesity is a disease which produces chronic inflammation and oxidative stress. The inflammatory cytokines produced by the bloated “monster” adipocytes are the same ones known to trigger the development of several types of cancer. The constant barrage of inflammatory cytokines from deranged fat cells encourages the survival, gr owth, owth, and spread spread of o f cancer cells. The high levels of free radicals that accompany oxidative stress damage DNA in normal cells. Under some circumstances, free radicals can transform normal cells into cancer cells. This DNA damage caused by free radicals, will mutate the normal cell into cancer. Obesity, insulin resistance and diabetes are all inflammatory diseases linked to an increased risk of cancer. Being highly inflamed is the ideal cancer hothouse.
7. Obesit Obesit y and chronic chro nic insulin insulin resistance resist ance increase increase the risk of heart and vascular disease. Obesity and diabetes greatly increase your chances of heart and vascular disease. The statist statistics ics for this this association ar e frightenin fr ightening: g:
• A diabetic is t wice attack or stroke stro ke than than a non-diabetic. wice as likely likely to have a heart attack • 66% of diabetics diabetics end end up dying from fro m a heart attack attack or stroke. str oke. Only 1/3 of diabetics diabetics die fro m oth o ther er causes. causes. • A r ecent study showed that obese men had a 60% gr eater chance chance of dying from fro m a heart hear t attack attack than than non-obese non-o bese men. • Diabetics Diabetics are ar e up to four times as likely to to have vascular disease in the lower lo wer extremities (legs, feet) than non-diabetics. • Diabetes Diabetes also causes a type of heart failure called diabetic cardiomyopathy. • Diabetes Diabetes leads to small blood bloo d vessel damage which which causes nerve damage damage and can lead to amputation. These statistics are not surprising if you know that the main trigger for heart and vascular disease is chronic inflammation and oxidative stress. Obesity and diabete diabetess are ar e sour ces of chronic chr onic inflammation and oxidative oxidative stress.
KEY POINT: Heart Heart and vascular vascular disease are are trigg tri ggered ered primarily pri marily by chronic chro nic inflammation and oxidative stress.
COMING ATTRACTIONS >>> The cholesterol section section in the Analytics Chapter contains contains a thor thor ough discussion discussion on o n why why the the cholester cholester ol car r iers (lipoproteins) (lipopr oteins) directly cause cause problems pro blems in heart and vascular vascular disease, disease, instead instead of cholestero cholestero l itself.
8. Obesit Obesit y and chronic chro nic insulin insulin resistance resist ance can lead t o accelerated accelerat ed aging. aging . Chronic oxidative stress from obesity and insulin resistance/diabetes can cause premature aging (accelerate the rate at which you age). Dysfunctional mitochondria in the fat cells of obese and diabetic people can produce large quantities of free radicals. These free radicals can damage specific parts of DNA called telomeres. Telomeres are ar e the the “caps” “caps” on the ends ends of chromo chr omosomes. somes.
TECHNICAL NOTE: We have represented the telomeres as multi-colored “caps” on the tips of the chromosome for clarity. In reality, the telomeres look exactly like the regular genetic DNA that contains your genes. The telomer telom eree DNA DNA “caps” function to pr otect the the genetic DNA from fr om damage. Bad things things happen when when your genetic DNA is damag ed, namely cancer cancer and accelerated accelerated aging. Telomeres are made from DNA and protein. They function to protect DNA that
contains contains your genes—your genes—your genetic genetic material. When most cells divide to make new cells, some of the telomere structure is lost. After a certain number of cell divisions, the telomere no longer exists. The cell is unable to divide any further and often dies. Most of the cells in the body do not divide often enough for this to be a problem. The issue for people who who are obese and/or diabetic diabetic is that that the constant onslaught
of free radicals from chronic oxidative stress has been shown to shorten telomeres by damaging the telomere DNA. The telomere DNA is more susceptible to free radical damage than genecontaining DNA. Telomeres are much like a “sacrificial lamb” when high amounts of oxidative stress are present as in diabetes and obesity.
BIOLOGICAL BIOLOGICA L VERSUS VE RSUS CHRONOLOGICAL AGE:
Chro Chro nic oxidative str str ess and inflammation inflammation r esult in accelerated accelerated telomere loss and more rapid aging. Most of us have seen obese and diabetic people who who look loo k older than than their their actual actual age. Biological Biolog ical age is how old the cells cells in your bo dy are based on telomere length, length, while while chronolo chro nological gical age ag e is based on the the year year you were bor n. This is how a 50-year-old diabetic can have the body of a 70-year-old (similar to a r usty usty car) based on telomer telomer e length.
This gr aphic shows shows a single “arm” o f a chro mosome moso me with with the the telomer telomer e cap in place. place. Chronic oxidative stress from the mitochondria in diseases such as obesity and diabete diabetes, s, shorte shor ten n the telomer telomeres es over time. time. Chro Chromoso mosome me A shows shows a nor mal telomere telomer e length before any damage takes place. The telomere shortening is shown in the picture as the chro mosome mos ome passes through thro ugh the stages shown in B, C, C, D, and E. Chromosome E is unprotected by the telomere and the DNA containing your genes can now be damaged. (Notice the free-radical “drunk guys” wreaking havoc.)
dividee to t o produce new Cells that have have DNA DNA like chr omo some som e E can no longer divid wor n-out cells cells are ar e not replaced. This is r eally the the definition definition of o f aging— aging — cells. Old worn-out when your cells can no longer divide to replace the worn-out cells. Eventually the “worn-out” cells in your organs such as the liver, pancreas, heart, kidneys, brain, begin to die and are not replaced because they no longer have functioning telomeres. Shortened telomeres are seen in people with many diseases associated with oxidative stress such as heart disease, diabetes, Alzheimer’s dementia, and obesity, as well as environment enviro nmental al exposures such as smoking, smo king, air pollution, and str str ess.
Researchers are now using telomere length to analyze the rate of aging and even predict lifespans.
MITOHORMESIS: EXTENDING LIFESPAN LIFESPAN WITH OXIDATIVE OXIDATIVE STRESS?
Recent research has shown that when mitochondria are not overloaded with fuel, they increase their efficiency in producing energy. Free radials are pr oduced dur dur ing this efficient energ energy y product pro duction, ion, and result in oxidative stress. Periodic reduction reduction o f glucose g lucose in the diet, diet, physical physical exercise, and calorie restriction all create short-term stress to the metabolism. Specifically, these conditions increase oxidative stress in the mitochondria. The result r esult of these str str essors essor s and the increase in oxidative stress is an increase in our cells’ antioxidant defense systems capacity for dealing with free radicals. These increases can protect us from aging specifically they they can stop telomer telomeres es fro m shorten shor tening ing fr om fr ee radical — specifically damage. Mitohormesis is the stimulation of mitochondria by oxidative stress. It is ver y impor impo r tant to point po int out that taking antioxidant supplements has not been shown to improve health or slow aging. They may even be detrimental because antioxidant supplements supplements stop the beneficial beneficial do se of oxidative stress in the mitochondria and prevent the increased capacity in our natural natural free r adical defense defense system. system. In fact, most of the beneficial “antioxidants” (such as polyphenols) found in plant products do not act directly as antioxidants. They only stimulate our free fr ee radical defense syst system. em. In keeping keeping with the the concept of ho r mesis, periodic stresses that increase short-t short -term erm oxidative stress st ress are beneficial, beneficial, while chr chr onic increases in
oxidative stress from obesity and diabetes overwhelm the mitochondria and the free r adical defense system. Keep Keep your “Mito-RPM “Mito-RPM”” in the green to stimulate stimulate mitohor mesis with regular exercise, and the the nutritional strategies we will cover soon. Your telomeres will thank you!
RESEARCH UPDATE: ALL IS NOT LOST Learning how obesity and especially diabetes can accelerate aging can be pretty discouraging. Before you update your life insurance policy, let us discuss discuss some findings in r ecent ecent research showing that that loss of telomer telomer e length can be slowed dramatically. A study on diabetics showed that total loss of telomere length was prevented in diabetics who maintained good bloo blood d sugar control. cont rol. In the upcoming sections, we will give you the tools and knowled knowledge ge to maintain good goo d blood sugar sug ar co ntr ntr ol, slow slo w down down prematur prematur e aging, aging , and perhaps even reverse the disease. disease.
STRONG MEDICINE TACTICS: Maint aintain ain good go od bloo d sugar control to prevent accelerate accelerated d aging.
9. Obesit Obesit y and chronic chro nic insulin insulin resistance resist ance can lead t o “brain wasting.” wast ing.” Paralleling the increase in obesity and diabetes, neurodegenerative diseases such as Alzheimer’s disease (AD) are reaching epic proportions. AD is the most common cause of dementia dementia in our aging population. population. We all have have heard horr ho rr or stories about friends, relatives and parents parents succumbing succumbing to AD or other neurodegenerative diseases. The financial and emotional burden it places on families is catastrophic. Family members—non-professionals—provide 80% of home care for AD patients. AD has become more and more common in recent years and strikes people at an age when they should be enjoying life the most. Spending the last decades of life in a tortuous existence, marked by a slow fall into
mental and physical decay is occurring with increasing regularity. Why?
“TYPE “TYP E 3 DIABE DIA BETES” TES” In 2005 a research group from Brown University Medical School described Alzheimer’s disease as type 3 diabetes. Their research showed AD to have characteristics of both type 1 (decreased insulin production) and type II diabetes (insulin resistance). Proper insulin regulation is highly important for brain cell neurons—they die very quickly when insulin is not properly regulated. Ketogenic diets and supplementation of ketone-producing substances (such as medium chain triglycerides) are showing very promising results in early clinical studies on nutritional therapies for AD. Short-term ketogenic diets and low carb diets can also be very effective in reversing type II diabetes—a result which supports the metabolic similarities between T2D and AD. Additionally, chronic inflammation, oxidative stress, and formation of advanced glycation end-products (AGE) are common to the development of both Alzheimer’s disease and type 2 diabetes. Obesity and the resulting insulin resistance greatly increase your chances of succumbing to neurodegenerative diseases such as Alzheimer’s disease.
STRONG MEDICINE TACTICS: Prevent Alzheimer’s disease by reversing rever sing o besit besity y and insulin resistance resistance using strategies in the upcoming intervention section.
CENTRAL CENT RAL THEMES THEMES CONNECT CONNECTION: ION: Most of us who have a parent or close relative with AD often wonder if we will be likely likel y candidates candidates for fo r AD and dementia. dementia. There is i s no gr eater eater nightmare than than for a functioning, functioning, able, independen independentt
and intelligent adult to—without warning—begin a slow and inexorable descent into into a state of mental m ental infancy. infancy. While there is a lot of talk about the “genetic risk factors” associated with Alzheimer ’s disease, we we need to look lo ok at AD and genetics through thro ugh the lens of epigenetics. Recent research has shown a strong connection between development of AD and diseases such as type II diabetes (T2D), cardio vascular disease and high bloo d pressure. T2D was was found to double the risk for fo r dementia. dementia. Individu Individuals als requiring r equiring insulin i nsulin therapy therapy are four fo ur times mor e likely to to acquire AD. AD. These diseases are associated with metabolic syndrome and can (often) be prevented by altering lifestyle factors. Altering our habits and environment can dramatically reduce the chances of acquiring brain atro atro phy—no phy—no matter matter how strong our genetic predisposition. Alzheimer Alzheimer ’s and other causes o f dementia follow foll ow the same pattern: pattern: they they have a strong genetic genetic componen compo nent, t, but but need need the right rig ht enviro enviro nmental nmental trigg ers to ger minate minate and take root.
STRONG MEDICINE TACTICS: Cook with with coconut oil for fo r a “dose” of medium chain tr tr iglycer iglycerides ides to to help keep your brain cells healthy, especially if you have a family history or early signs sig ns of Alzheimer’s disease.
HOW DO I KNOW KN OW IF I HAVE HAVE DIA DIABE BETES? TES? Do you have diabetes? Are you starting to show signs of developing diabetes or insulin resistance? A person just does not wake up one morning with type II diabetes. T2D and the broken metabolism m etabolism that accompanies it i t takes takes years to develop. develo p. But, there are early signals of which to be aware. Insulin resistance and diabetes involve increases in blood sugar from malfunctioning insulin receptors. The laboratory tests for diabetes and
“prediabetes” analyze blood sugar levels and how well you “handle” a glucose load in the diet. 1. The fir st test used to diagno se diabetes (and prediabetes) pr ediabetes) is the hemoglobin A1c (HbA1c) test. test. Hemogl Hemoglobin obin is a pro tein tein inside red blo od cells that carr carr ies oxygen. Depending on how much glucose is in the blood, a certain amount of glucose will stick to the hemogl hemoglobin. obin. Higher Higher concentr concentr ations ations o f glucose g lucose in the blood (as seen in diabetics) diabetics) result r esultss in mor e of the hemoglobin hemoglo bin getting getting glucose g lucose percentage of o f hemog hemogllobin that has glucose stuck to t o it gives “stuck” to it. T he percentage
t he HbA1c value. value. The average r ed blood cell has a lifespan of 120 days, days, so the hemoglo bin in the the cell is exposed to bloo d glucose fo r the the same length of time. This allo ws the the HbA1 HbA1cc measurement to to g ive an average level o f bloo d sugar for the the past 3 months. The percentage amounts of HbA1c is used to classify someone as normal, prediabetic, or diabetic:
The values in this table were taken fro m the Amer American ican Diabetes Diabetes Association Associatio n (ADA). (ADA). Notice that there is a “no-man’s “no-m an’s land” for values between between 5.1 5.1 and 5.6. 5.6. Our personal per sonal bias is that although this area is not officially prediabetes, the numbers in this range may indicate a developing problem with insulin resistance. My personal bias is the closer to 5.0 5.0 (or lower), the better. better. 2. The next commonly comm only used labor atory ator y test for fo r pr pr ediabetes and diabetes is fastin fast ingg blood bloo d sugar. sugar. This is our least favorite test because is it only represents a brief snapshot in time—your blood sugar at the time of the blood draw. Other factors, such as a night of poor sleep can elevate this number even if you do not have diabetes. Nevertheless, the official values for this laboratory test, again taken from the ADA guidelines, are as follows:
3. The third test is called the Oral Or al Glucose Gluco se Toler ance Test (OGTT). (OGT T). The OGTT OGT T is perfor perfo r med by fastin fasting g fo r 8 hours, then dri drinking nking a glucose and water water mixture mixture containing containing 75 grams g rams of g lucose. After After drinking the liquid and waitin waiting g 2 hours, your blood glucose is measured. The diagnosis is based on the ADA guidelines below:
The idea behind the OGTT is to test your tolerance for glucose. Remember, when people have insulin resistance (diabetes or prediabetes), the insulin signal does not get through to allow glucose into the cells. Then the glucose builds up in the bloodstream. Depending on how severe your insulin resistance is, and how well your pancr pancr eas is secreting insulin, the the more mor e of the 75 gram g lucose solution will stay stay in your bloodst bloo dstream. ream. As we will discuss later, when figuring out how much carbohydrate a prediabetic or diabetic diabetic can can toler toler ate, ate, perfo perfo r ming a home versio n of the OGTT using real r eal food foo d can help you track improvement of insulin sensitivity, and figure out what kinds and quantities of foods cause trouble for you in terms of blood sugar. We will talk much more about this in the Intervention section. For convenience, convenience, her her e is a chart char t compiling all three three tests: tests:
All of these charts show very definite divisions with ranges of numbers indicated as “normal”, “prediabetic”, or “diabetic”. Insulin resistance leading to diabetes is a
long process that takes years before most people are officially classified as diabetic by a blood blo od test. test.”
A - This point represents good insulin sensitivity. Oxidative stress and inflammation are in the green zone. But, you start to eat processed food and stop exercising due to a hectic work schedule. l ifestyle is beginning to catch up with with you. Your B - 2 years later yo ur lifestyle blood tests tests are still in the “normal” r ange, but but you are gaining g aining weight around aro und your midsection. midsection. Your Your blood bloo d tests tests are ar e nor mal because because your pancr pancr eas has started started to to g o int i nto o o verdrive verdr ive to to pr oduce more mor e insulin to to deal with with the star startt of insulin insuli n resistance. r esistance. Inflammation and oxidative stress ar e increased and your your telomer telomer es are likely shorte shor tening. ning. Age Age acceleration has begun.
C - 3 years later you are upset after your annual checkup because your doctor said your blood tests show you have prediabetes. The insulin secreting cells in your pancr pancr eas are starting to fail, result r esulting ing in incr eased blood sugar. You have gained 20 more pounds over the last 3 years. Oxidative stress has further increased and your telomeres continue to shorte shor ten, n, accelerating accelerating aging. ag ing. when your your doctor tells you are D - 2 years later you ar e shocked when “bor derline der line diabetic.” diabetic.” You You have not gained g ained any mor e weight but your blood pr essure has gott go tten en wor wor se, and and your telomer telomer es are quickly shrinking.
E - Your doctor says your HbA1c is 6.8 and that you have diabetes. You now make a resolution to change your lifestyle because you “have diabetes”, but wonder how it happened so fast. Do not be the person at point E, and wait too late to do something about your disintegrating health. By the time a person has attained pre-diabetes status, a significant amount of damage to the insulin-secreting beta-cells has likely already occurr ed. This perso n will likely never r egain full function function o f these these cells—but they they
always have the the power to halt the damage. The time for action is at point A and B, before much damage takes place. Use the pr escriptions in the inter inter vention vention section section to preven pr eventt chronic insulin i nsulin Strong Medicine prescriptions r esistance and diabetes. diabetes. If you have no symptoms and normal blood tests (points A and B) how do you know if you are at risk? The following groups of people should be focused on prevention, prevention, as they are at higher r isk for developing developing diabete diabetes: s: • A family famil y histor y of diabetes—your diabetes—your par parents, ents, bro thers, or sisters have have diabetes • Recent Recent diagnosis of high blood bloo d pressure • High trig lycerides lycer ides and low lo w HDL HDL on bloo d tests tests • Histor Histor y of polycystic polycystic ovarian ovar ian syndr syndr ome (PCOS) (PCOS) • Histor y of gestational diabetes • Sedentar Sedentary y lifestyle • Ethnic Ethnic gr oups including African Afri can Americans, Hispanics, Native Native Americans, or Pacific Islanders • Overweight or obese, obese, especially especially abdominal abdominal obesity
CENTRAL CENT RAL THEMES THEMES CONNECT CONNECTION: ION: Revisiting the “stress cup” from Central Themes V (Allostasis), the gr aphic aphic below is a “stress “stress cup” overflowing fr om a poor diet of processed food filled with sugar, flour, and vegetable oils. The obesity and diabetes resulting from this type of daily diet has overfilled the individual’s “stress cup,” and caused allostatic overload. For the obese and diabetic, the the “stress cup” does no t have the the capacity to to handle poor po or sleep and job stress. Those Those additional stresses will will o nly cause cause mor e overflow over flow.. This chro nic allostatic allostatic over load—an overflo wing wing “str “str ess cup”—plus cup”—plus the the inflammation and oxidative stress that goes with it, will lead to accelerated aging, heart disease, high blood pressure, neuro degenerative degenerative diseases (such as Alzheimer’s), and cancer.
STRONG MEDICINE TACTICS: Find out if you have risk factors for developing diabetes. If so, start a program prog ram o f early prevent prevention.
DRIVEN TO EXCESS We have talked extensively about the health risks of obesity, and especially diabetes. The $64,000 question is why are so many of us getting overweight and obese? After all, all , the majority of Americans are overweight or o bese. Why are we consistently eating so many of the wrong calories? Have we all become gluttons and hedonists in the last 50 years? That is what social critics would have us believe! Dietitians would urge us to count our calories, and limit the amount we eat, in the attempt to gain some control of our growing waistlines. Counting calories is not natural or sustainable, and it does not get to the root of the underlying problem. It turns out there are some very real problems in the modern brain—problems that drive us to eat beyond our physiologic need for calories. Some of these problems are coming from within our bodies and others are from our environment. Appetite is controlled in the brain. Ergo, the brain can become our worst enemy or best friend in our efforts to shed body fat and add lean muscle mass. We will decrypt the hunger communication system’s “black box” and understand how the brain controls our drive to t o consume food. Without Without understanding this system sys tem we are doomed to fight a losing battle against hunger. Counting calories and other neurotic practices are all destined to fail in the long term. Obesity, the “enemy within,” will will never be vanquished without an understanding understanding of the drive to eat.
OBESITY: OBESITY: THE ENEMY WITHIN W ITHIN III:
HOW WE W E GET FA FAT: THE TH E BRAIN, BRA IN, HORMONES, AND A ND APPETITE APPETITE
THE DRIVE TO EAT EAT Humans are hard-wired to find high-energy foods to fuel our body. This primordial survival mechanism is built into our brains and resides just below conscious thought. “Hunger” is an urge created by a sophisticated communications system in the primitive parts of our brain. Once the hunger message is received, humans use their superior problem-solving abilities—that other animals do not possess—to find creative ways to acquire and make decisions about food. The hunger drive is indeed a primal one. It is based on a complex communications system of hormones and chemical messengers within the brain— neurotransmitters. These hormones and neurotransmitters interact with the primitive structures in the brain responsible for the “reward system.” The reward system in the brain produces feel-good neurotransmitters to create a pleasurable response to eating eating fo od. This pleasur pleasur e response r esponse helps us survive as a species.
For ancient hunter-gatherers, there was a caloric cost associated with the acquisition of food. They would expend thousands of calories bringing down and butchering an elk—and even more calories transporting the carcass back to camp on foot. We no longer have to expend energy to hunt, gather, or cultivate our food. We purchase our artificial, industrial foods without burning a single additional calorie. We need to readjust our thinking and our actions; we need reexamine our relationship with food. Let us stop being slaves to the subconscious primordial impulses and and urg es from fr om a bro ken metabolism metabolism and shor t-circuited t-circuited reward system. If we let it, hunger can turn us into a ravenous saber-tooth tiger on the hunt. We have to understand understand our dr ive to eat before befor e we can can exert exert some cont co ntro ro l.
THE HUNGER COMMUNICATION SYSTEM “The regulation of appetite” is exceedingly complex. To faithfully describe all the players in the system and their interrelations would quickly lead to confusion. We want to explain new ideas and scientific breakthroughs in a simplified way so we can gain control of our nutri nutritional tional destiny destiny..
1. FAT IS TALKING—SO LISTEN UP! Fat is not just a storage site for excess energy, it is an active participant in metabolism. In the past, fat was thought to be inert material. Then scientists discovered that normal, healthy fat cells (adipocytes) secrete a substance called adiponectin. As discussed previously, this fat-hormone keeps inflammation down and insulin sensitivity high throughout the body. Recent research supports that fat tissue is highly active. Healthy fat secretes several different compounds that have effects on the body and brain. A major player in the hunger communication system is a hormone called leptin. Leptin Leptin is secreted secr eted by fat cells. The more fat mass you have, the more leptin is pumped
into the bloodstream.
KEY POINT: The mor e fat you you have (and the the larg er your fat cells), cells), the the mor e leptin leptin is produced.
The mor e fat you have have (and the the larger larg er your fat cells), cells), the the mor e leptin leptin is produced. pr oduced. Leptin travels from the fat cells and communicates with the brain by docking on leptin receptors located on certain brain cells. This is similar to how insulin docks to insulin receptors. Leptin communicates with specific cells located on the hypothalamus (part of the Stress/Threat system we discussed earlier). The hypothalamus is the central receiving and command center in the human brain which responds to environmental signals. The hypothalamus is at the center
of the brain’s hunger communication system. The brain is normally protected from the rest of the body by the “blood-brain barrier” (BBB). Part of the hypothalamus is located at a “crack in the wall” of the BBB and has direct access to the bloodstream. Leptin crosses into the brain through a specialized transport system after being released by fat cells. When leptin “docks” with the leptin receptor on the hypothalamus, the hunger communication system generates a signal signal to st op eating. The brain knows how much energy is available from fat because of the leptin
system. As fat stores decrease (from fasting or starvation), less leptin is available to signal the hypothalamus. This results in the feeling of intense hunger. As body fat increases, leptin increases and the signal to stop eating will be stronger.
TAKE HOME MESSAGE: Leptin Leptin functions as a signal sig nal to keep body bo dy fat at optimum levels. When it is working correctly cor rectly,, the the leptin leptin signal fr om fat cells to the hunger hunger communication system—controlled by the hypothalamus—will keep a person’s body fat amount in an ideal range.
Low body body fat = low leptin l eptin = signal to eat (hunger) Higher body body fat = high leptin = signal to stop s top eating (satiety) (s atiety)
Leptin Leptin is secr eted into into the bloodstr blo odstream eam by adipocytes (fat cells). Leptin Leptin tr tr avels through the bloodstream to the brain and docks with leptin receptors on the hypothalamu hypothalamuss through the the break in the blood-br ain barr ier. The hypothalamus r eceives the signal that the body has plenty of ener gy, and the the hunger communication communicatio n system tells tells the body to “stop eating.” When the leptin system is working correctly, you should be less hungry as you collect more body fat. More body fat = more leptin. More leptin = a stronger signal
to stop hunger. Based on what we now know about leptin and the the hunger signal, sig nal, how does anyone get fat? The overweight and obese have higher leptin levels than lean people. If the communications system was working properly, people with more fat should get a str str ong signal to stop eating. eating. The reason overweight and obese people are still hungry even with high leptin levels is leptin resistance. As with insulin resistance, the signal that leptin is supposed to carry (stop eating) is not getting through to the hypothalamus.
KEY POINT: Despite Despite high leptin l eptin levels, the the obese and overweig o verweight ht do not get the “stop “stop eating” signal because of leptin resistance.
DIGGING DEEPER: Leptin and Having Babies Babies...... Although we are discussing leptin’s role as a signal to stop eating when body fat is high, this this is only a piece of its great gr eater er ro le, that that ensures ensures survival sur vival of o f not no t just the the individual, but the the human species. One of leptin’s primary functions is to signal the brain when energy levels are high enough to sustain a pregnancy. When there is an appropriate level of body fat, the leptin signal from fat cells to the hypothalamus is r elatively stro ng. The hypothalamus “knows” body fat is adequate adequate and sends a signal to the pituitary gland which secretes the sex hormones controlling ovulation, menstrual cycles, and fertility. It is impor impo r tant that women have an adequate adequate supply supply of o f energy ener gy stor sto r ed as
body fat to successfully car r y a fetus to to term. ter m. If If a woman’s body fat levels fall, the leptin signal to the hypothalamus decreases, and fertility hormones hor mones from fr om the the pituitary pituitary gland also decrease. This is why some young women with ver very y low lo w body fat (endur (endur ance athletes, athletes, women women with anor exia nervosa) stop having their menstrual cycles and certainly have fertility problems. There is an ideal level of body fat for the optimum leptin levels needed to maintain fertility. Infertility is not just a problem for women with very low body fat. Overweight Over weight and obese women with hig high h levels of o f leptin also have fertility problems. But, should not high levels of leptin from the extra fat mass give a strong signal for fertility based on what we just said above? The overweight and obese develop leptin resistance, and the signal doesn’t get through despite high levels of leptin. This concept should sound familiar to insulin resistance in the previous section. No leptin
signal = no fertility signal.
KEY POINT: It is important to understand that overweight and obese people (especially diabetics) t ruly ruly feel hungry most of the time, despite the large amounts of body fat they carr car r y. Because leptin is not functioning correctly, their brain behaves as if they have low body fat and sends the the signal sig nal to eat. This cr eates a vicious cycle of eating, eating, mor mo r e weight gain and inflammation, inflammation, and mor e leptin resistance, resistance, leading to to mor mo r e eating. eating. Knowing about this pro cess can help an obese person per son understand under stand why why they they are always hungry, which can give them some control. It is very helpful for fo r friends fri ends,, family members, and medical medical providers pr oviders to also understand this this process pro cess to suppor suppor t the the obese or diabetic diabetic per per son in your life without without dismissing their their eating eating habits as gluttony gluttony or o r lack of will power.
LEPTIN RESISTANCE The bloated adipocyte “monster” is secreting high amounts of leptin and inflammation. The inflammation breaks the transport system and short-circuits the r eceptor. Now, Now, ver very y little leptin reaches r eaches the receptor, and the small amount am ount that gets thr thr ough cannot transmit a signal thro thro ugh the broken recep r eceptor. tor.
Wit Wit hout t he “stop “sto p eating” signal from lept lept in, in, t he hypot hypot halam halamus us sends the message to eat more! You can see from the graphic that despite high body fat and high leptin levels, the brain “thinks” that body fat is low because the leptin signal is not received. Why? The bloated adipocyte (fat cell) “monster” is producing large amounts of inflammation and oxidative stress which interrupts the leptin signal.
2. THE THE GUT TALKS TO THE BRA BRAIN IN Having just read through the gut chapter, you know that the digestive tract communicates to the brain through the gut-brain gut-brai n axis. Communication hormones and messenger molecules are produced by our digestive system in response to the food we eat. Trying to describe their myriad functions and how they interrelate is beyond the scope of this book. The complexity of how the gut-brain axis works is truly mind-blowing; even the scientists researching these amazingly complex biological biolo gical functions functions ar e mystified as they they nibble nibble around ar ound the edges edges o f understanding. understanding. What are the practical considerations? How does the digestive system signal the hunger communication system? How does the brain’s response to food vary depending on the food in question?
Most of the digestive tract signaling messengers send a message of satiety to the brain. Satiety is defined a feeling of fullness and satisfaction after being fed. Once the digestive tract (stomach, intestines, gall bladder, liver, and pancreas) senses a meal has just been eaten, it sends multiple signals—all designed to promote a feeling of satiety—to the brain. The satiety signal stops intake of more food—the goal is to allow time for digestion, and to prevent overeating. Most of the satiety signaling in the digestive tract is designed to control short-term eating behavior. This is an important distinction, leptin is not a short-term satiation solution, it is mor e effective effective at exerting long-term co ntro ntro l over eating eating behavior. behavior.
The feeling of being full after a big dinner, but still being hungry the next mor ning is a shor t-term t-term eating signal. Digestive Digestive tr tr act signals are ar e mostly concerned with stopping continued eating in the short-term to allow for digestion. But, the digestive tract will signal for more food when digestion fro m t he previous meal. is nearing complet co mpletion ion from Long-term eating signals (leptin) control the quantity of what you eat over multiple meals. Routinely eating large amounts of food at every meal— gr eater eater than than the the fuel requ r equir irement ementss of o f your body—is an example example of disrupted disrupted long-term eating eating signals. sig nals. An examp example le of proper pro per lo ng-term eating eating behavior behavior from fr om cor rectly funct functioning ioning lo ng-term eating eating signals is ro utinely utinely eating eating the rig ht amount amount of foo d to supply supply your body’s body’s energy energ y needs without much excess.
TECHNICAL NOTE:
There are many specific digestive tract messengers that send a “stop eating” (satiety) signal. sig nal. They include: Peptide Peptide Tyrosine Tyros ine (PYY), (PYY), Pancreatic Polypeptide (PP), Glucagon-Like Glucago n-Like Peptide Peptide (GLP-1), and Chol Cholecystokinin ecystokinin (CCK). One of the the only messengers messenger s from fr om the the digestive tr tr act that that tr tr iggers igg ers the the hunger response is ghrelin ghreli n. Ghrelin is produced in the stomach and is active between between meals. When When the stomach is empty, empty, ghrel g hrelin in is secreted secr eted to to stimulate hunger.
PROTEIN PRODUCES THE LARGEST AND LONGEST SATIETY SIGNAL TO THE BRAIN. Amino acids from protein digestion are sensed in the intestine. A signal is sent to the the brain thro ugh a variety var iety of messengers, and produce pro ducess a strong stro ng signal sig nal of satiety satiety.. The satiety signal from protein is the strongest of all the food satiety signals. Many studies have shown that high protein diets result in lower intake of total calories throughout the day. This is because protein triggers the best short-term signal to stop eating. People that eat a good quantity of protein with each meal are less hungry and naturally eat less throughout the day—without discipline. Their
protein-satiated brain tells them that they do not need food. Eating Eating 20-30 grams gr ams of pr otein as part of your breakfast will keep you you fr om being hungry later in the morning and resorting to “snacking.” Many people succumb to sweet, sugary snacks because they did not provide the right satiety signal to the brain fir st thing thing in the mor ning with with a high pr otein meal.
KEY POINT: Remember this for the rest of your dietary life: protein produces satiety. It generates the largest and longest satiety signal to the brain of any and all nutrients. Want to kill an appetite? Eat protein!
STRONG MEDICINE TACTICS: Eat 20-3 20-30 0 gr ams of pro prote tein in as part of o f breakfa br eakfast st to to pro provide vide a str str ong sat satiety iety signal to the brain first thing in the morning. This will help decrease the calories you eat for the rest of the day without feeling hungry. Protein is the only macronutrient that consistently produces satiety signals in the brain. Carbohydrates and fat can produce satiety as well, but the specific types of carbohydrates and fat are important. In some forms, carbohydrates and fat can produce a hunger and food craving response. That leads us to our next point...
3. “PALATABLE” FOODS CAN STIMULATE THE REW RE WARD CENTERS CE NTERS OF THE BRAIN BRAIN,, INCREASI INCREA SING NG APPETITE. “Palatability” of food can be a confusing topic, and should not always be equated with with go od tasting tasting fo od. Palat Palatability ability refers to the feeling feeling of satisfact satisfaction ion o r “reward” coming from eating a particular food at a particular time. A good way to explain this is the immediate satisfaction and “comforting” feelings you may get by eating ice cream after a stressful day. Although ice cream generally tastes good to most people, it may not always be satisfying to eat depending on the circumstances. For instance, if you have not had ice cream with chocolate syrup for a month, it may be extremely palatable because you have not had it for so long. It generates the “feelgood” response and satisfaction. If you have ice cream nightly, it may still taste good but you may not have the intense “feel-good” satisfaction response you experienced after being deprived of it for a month. Having ice cream every night has made it less palatable.
Palatability of food is very individual, but in general, calorie-dense foods that contain sugar and fat are generally palatable to most of us. Fast-food and other processed pro cessed foods are ver y palatable palatable to to many people for this this reason. r eason.
Palatable foods? Palatable foods that stimulate our reward system can override our normal “stop eating” signals. A good way to tell if a food falls into this category (for you) is if you feel driven to eat the food even when you are full—and will go out of your way to acquire this specific food. The normal “stop eating” signal that emanates from the digestive tract’s communication system will often be silenced or overruled by the food reward system. There is a chemical reason you continue eating certain foods even when full. The reward system in the brain is the same area activated by drugs such as cocaine.
When the reward system is stimulated, “feel good” chemicals like dopamine and endorphins are produced. Stimulating the reward pathway makes us feel good and can encourage us to stimulate it over and over.
THE REWARD SYSTEM HAS CHANGED IN OBESE PEOPLE. Two main parts of the reward system are in the brain, and recent research has shown that that the the reward r eward system functio functions ns differ ently in an obese person pers on than it does in a lean person. The two parts of the reward system are interconnected and influence one another. • The first fir st part of the the reward syste system m is controlled controll ed by the the parts of the the brain involved in the actual experience of pleasure. Palatable food signals this part of the brain to produce a chemical called dopamine. Other chemicals that increase dopamine include include opiat o piates es such as mor phine, phine, heroin, hero in, and prescription painkillers, as well as drugs like l ike cocaine. • The second main part of the the r eward system is the the part of the the brain brai n involved invol ved in
or ganizing and planning planning actions to o btain btain a r eward. eward. Once something something like palatable food stimulates dopamine release (in the first part of the reward system) the second part of the system system plans how to obtain o btain the the palatable food foo d again. This part of the reward system is involved when you leave your house, get in your car, and travel to the store to pick up your favorite ice cream when a craving hits. It is also the system that helps you imagine how good the ice cream is going to taste before you eat it. it. One current theory holds that the overeating seen in overweight and obese people is due to the two parts of the reward system changing in a very similar way to what is seen in drug addiction. addiction. In an obese person, the first part of the reward system involved with experiencing pleasure from dopamine release is suppressed. This means that just like developing tolerance to a drug, a higher amount of the palatable food is needed to get the same “feel-good” pleasure response. While the “pleasure-part” of the reward system is suppressed in the obese person, the second part of the system involved with planning to obtain palatable food, and predicting how much pleasure will be involved with eating it, is overactive. This broken br oken rew r eward ard system may explain explain why some people are ar e compelled to seek out palatable food more often and in larger amounts. It is a subconscious attempt to stimulate the pleasure part of the reward system. People will literally fantasize about how good favorite foods will taste—only to feel unsatisfied when they actually eat the food. This creates a vicious cycle of fantasy, fulfillment, and continuing to forage and eat because nothing satisfies. Many people continually seek out highly palatable foods in a futile attempt to feel pleasure and satisfaction.
FIRST PRINCIPLES PERSPECTIVE: PERSPECTIVE : WHY WH Y THE REWARD REWARD SYSTEM SYSTEM?? The brain’s food reward system makes sense as a system to ensure survival when food is scarce. Ancient humans did not have grocery stores and fast food foo d chains available when they they wer wer e hungry hungr y. Access to to lar l arge ge quantit quantities ies of calorieden calor iedense se foo d was was not a commo n occurr ence in a hunte hunterrgather gather er so ciety ciety. When these these gro ups obtained obtained a large so urce of o f calor ie
dense food, the ability to override the “stop eating” signal may have had some advantages. Periodic overeating to stor e excess energ energ y as body fat would would be a valuable stored energy energ y source sour ce to draw fr om when food became scarce again. In In this this way, the ability to override the “stop eating” signal could be a survival advantage. The same food fo od r eward eward system system that helped helped ensure survival sur vival of primitive humans humans is ir onically contributing to the poor health health of modern humans. humans. The fat cells and the gut communicate with the brain (especially the hypothalamus) to signal when we have eaten enough or, conversely, if we need to eat more to derive additional energy from food. The energy system that drives us to eat can be overridden by the reward reward system. sys tem. An obese person may continually have the the urge urg e to eat—eve eat—even n though though there is no need for mor e energy fr om fo od—because od—because the the rew r eward ard system is in contro l.
TAKE HOME MESSAGE: An obese or overweight person has two strikes against them in their battles battles to co ntrol ntro l how ho w much they they eat: 1. The “energy” hunger communication system involving leptin is not working. They are not get g etting ting the the “stop eating eating sig nal” fro m leptin and and are hungry. 2. The “reward” hunger communication system is broken, which will cause over eating in the attempt attempt to to feel f eel satisfied. If you you are ar e overwe over weight ight or obese, hopefully hopefully this information can help you you r ealize that you are no t “weak-willed,” “weak-willed,” but have a real drive dri ve to eat—even eat—even when your body does not need the energy. This may help you gain some control over these urges when they hit.
“...knowing is half the battle.” battle.” —G.I. Joe (1985 )
KEY POINT: The reward system system can overr ide the the “energ “energy” y” system system for control of the drive to eat.
DIGGING DEEPER: Process Processed ed Food, Palatability, Palatability, and Reward Fast food and processed food tastes good to most of us. That is why multibillion dollar food foo d industries industries are a major contributor contributor to the the obesity obesity epidemic. Why does this type of food maximally stimulate our food reward centers in the brain?
Food processing pr ocessing r emoves much of the the natural natural flavors fl avors present in whole whole food ingredients. Most of the ingredients—that most of us cannot pronounce— pro nounce—seen seen on pro cessed food labels are ar e preservat preser vatives ives to keep the the food foo d from fro m spoiling o r flavor fl avor and color additives. additives. Color additive additivess make the the pro cessed food mo re visually appealing, appealing, and flavor flavor additives additives are engineered to make the food palatable. There is a whole whole pr ofession ofessio n of “flavor ists,” ists,” chemists chemists who specialize specialize in creating flavor s to add to to pr ocessed food, and which which maximally maximally trigg er the reward centers in the brain. Flavorists are highly trained individuals
with with the the primary pri mary g oal o f making processed pr ocessed food foo d extremely extremely palatable. palatable. Many of us are ver y loyal to product pr oductss like specific soft drinks (fro m particular manufacturers) because of the unique and reward-stimulating flavors flavor s created in laborator ies. These flavors are manipulating manipulating your behavior through your reward system. If they can “hook” you with a flavor, they have a loyal customer for life. Unfortunately, the reward system system “hooked” “hoo ked” on artificial, ar tificial, laborator y-concocted y-concocted flavors flavor s contributes to to the rampant overeating that underlies the current obesity epidemic.
COUNTING COUNTIN G CALORIES: ISSUES ISSUES WITH CONTROL
Daily, I overhear dieters’ conversations about the latest strategies, gadgets, and resources resour ces for determining determining the calorie calori e count of every meal. They They are counting counting calori calo ries es in an atte attempt mpt to to g ain some contro l over a broken bro ken hunger hunger communication communication system. system. They They are ar e not addressing the the underlying problem. pro blem. The healthcare community (especially dietitians) has promoted counting calories in a big way. This practice has done a disservice to the public and their their health. health. Sure, counting counting and restricting calor ies will work fo r shortshor tterm weight loss, but it is not sustainable for the long-term. It is not sustainable sustainable because because we we are trying to exert contr contr ol over a primal pri mal hunger system that is hardwired in our brain to ensure survival. We cannot restrain it for for prolonged prolo nged periods periods of o f time. time. A properly pro perly wor king hunger communication communication system will will not no t let you you overeat. We have to restore proper operation of the hunger system with
the right food, sleep, stress-reduction and exercise. It will take some time to fix the hunger system but it can be done following the Strong Medicine approach. Restricting Restricting calor ies while while still eating the the wrong wro ng type of food fo od (processed (pr ocessed foods, etc.) will not restore the hunger communication system. The brain thinks you are starving the body and will will activate activate the str str ess-threat system produc pro ducing ing cor tisol, interr interr upting upting the the actions of leptin. leptin. The r esult is constant constant hunger hunger and a losing battle battle to to maintain maintain calorie calor ie r estr estr iction. Calor Calor ie counting often becomes a neurotic and self-defeating practice in the long term. Have Have some patience patience when when working to rest r estor or e your hunger hunger communication communication system. The rest will take care of itself. This has been a very simplified overview of what drives us to eat, and what can go wrong when the hunger communication system breaks down with obesity and diabetes. Now that you understand what is going on “under the hood” with obesity, diabetes, and the drive to eat, the interventions we will discuss to fix and prevent these problems should make a lot more sense. We are going to put obesity “on the ropes” and prepare to deliver the knock-out punch.
OBESITY: THE ENEMY WITHIN IV:
INTERVEN INTERVENTION: TION: THE 8-STEP PROGRAM FOR OBESITY AND DIABETES
How do we reduce the chronic inflammation and oxidative stress that promotes obesity and diabetes? Both obesity and type II diabetes can be treated and reversed with nutritional and lifestyle interventions. Our approach is geared towards the systemat systematic ic reduc r eduction tion of body fat and pr pr oven methods methods for controlling controll ing blood blo od sugar.
QUICK QUICK MEDICAL MEDICA L NOTE: Please work with your health care provider when implementing the recommendations that follow in this section—especially if you are taking medications to treat diabetes. Your medications will likely have to be adjusted as you change your diet and lifestyle, so it is important that your healthcare provider is in the loop. You are encouraged to take this book
with with you to your yo ur appointment to to help hel p with with the conversation. conversatio n. If your clinician is unwilling unwilling to support these intervent interventions ions as part of o f your treatment treatment plan, plan, consider finding fi nding another another healthcare healthcare provider pr ovider to work wor k with. with. There ar e plenty plenty of us out there there who who are willing and able able to help a motivated patient. Let’s dive right in to our stepwise approach to losing fat and controlling blood sugar...
STEP 1 DE TERMINE YOUR TOLERANCE DETERMINE TOLERANCE FOR F OR STARCH AND SUGAR. Reducing starch and sugar to “tolerance levels” is fundamental. If you are obese, but without a diabetes diagnosis, it is a safe bet that you are on your way to insulin resistance, so this step will also apply to you. Insulin resistance—malfunctioning insulin receptors—caused by chronic inflammation inflammation and oxidat o xidative ive stress leads to poo r entr entr y of glucose int i nto o muscle and fat cells. As insulin resistance gets worse, the amount of glucose in your bloodstream increases, damaging your blood vessels and accelerating aging. Someone with insulin resistance resistance cannot toler toler ate ate the same amount of glucose gl ucose from fr om starch starch and sugar that a healthy per per son with good go od insulin i nsulin sensitivity can tol toler erate. ate. After a meal, a healthy person with good insulin sensitivity will rarely experience blood sugar exceeding 140 mg/dL, even directly after a starchy meal. For the the insulin r esistant esistant obese per per son or o r diabetic, diabetic, small small amount amo untss of o f starch and sugar may increase their blood sugar well above 140 because they cannot “dispose” of the glucose. They cannot get it into muscle or fat cells because of malfunctioning insulin receptors. A long-term diabetic likely has twice the problem–broken insulin receptors and a burned out pancreas. A damaged pancreas cannot produce enough insulin to help handle handle significant sig nificant amounts amounts of o f dietary starch or sugar.
KEY POINT: Someone with insulin resistance cannot tolerate the same amount of glucose fr om dietary dietary starch and sugar that that a health healthy y person perso n with with good go od insulin sensitivity can tolerate. Depen Depending ding o n the severity severity of o f your insulin resistance, resistance, your tolerance for glucose will vary. To achieve optimal results, you will have to consistently measure your blood sugar after meals to assess your tolerance for the amounts and types of specific specific foo ds. Even Even regular reg ular people can benefit benefit fro m identifying identifying how certa cer tain in foods fo ods (and amounts of those foods) react within their bodies. I recommend purchasing a glucose meter from your local pharmacy. Meter technology has improved considerably over the last several years and most glucose devices are inexpensive and require very little blood. Remember that starches are just thousands upon thousands of glucose molecules “linked” together. Digestion rapidly turns starch into glucose, and insulin is then needed needed to clear the the glucose g lucose fr om the the bloo dstream dstream so it doesn’t stay stay at high levels.
Many people do not know which foods are large sources of starch and glucose. You can favorably manipulate blood glucose and insulin by making expert use of food. We need to understand some basic biochemistry to intelligently discern which foods foo ds are beneficial beneficial or detr detr imental. imental.
KEY POINT:
STARCH = GLUCOSE An important point to make is that not all of the foods listed are necessarily “bad” for you. Tubers, root vegetables, and fruit are nutrient dense and can have high nutritional value. The whole point of the list is to identify sources of starch and glucose in your diet so you know what to eliminate or reduce if your blood sugar readings are ar e too too high after after a meal. Ideally, you should eat the amount of starch/glucose that your insulin system is able to effectively clear from the bloodstream with relative immediacy after a meal. Using the blood sugar monitor, you can perform your own glucose tolerance test. We will test your individual ability to clear glucose from many different types of meals instead of just testing with a glucose solution at your doctor’s office. You have the power to experiment with many different food combinations to find out what foods (and in what amounts) are beneficial or detrimental. An oral glucose tolerance test is used to diagnose diabetes and prediabetes. You can use this as a food foo d tolerance test test to to help you plan your meals and keep keep blood sugar under under control.
COMMON SOURCES OF STARCH AND AN D GLUCOSE: GLUCOSE:
• Rice is basically starch and not much else. • Flour includes favorites such as bread, pasta, pastries, bagels, and tortillas. ANYTHING made with flour is a large source of starch.
• Cereals ar e a g rain-based processed pro cessed breakfast breakfast food foo d packed packed with with starch. tatoes and sweet potatoes, potatoes, etc. • Tubers Tubers and root roo t vegetabl veget ables es include po tatoes
amounts of o f glucose g lucose and fructose • Soda and and “fruit “fruit beverages” have high amounts —especiall —especi ally y in the for fo r m of o f hig h fructose fr uctose cor c or n syrup. syr up.
• Fruit juice is really the concentrated sugar from fruit and water. A glass of or ange juice contains contains the juice of several o ranges without without much much of the the beneficial fiber.
• High High sugar sugar fruit fruit s include bananas, mangos, apples, pears, grapes, etc. Dried fruit is even higher in i n glucose! enough said! • Candy Candy,, sweet sweets, s, pastries— enough Self-testing is simple, take two readings after each meal. Use the blood glucose meter one hour after a meal, then two hours after a meal. This will take the guesswork out of the process—no more guessing how that lunchtime sandwich affects affects your blood blo od sugar. A healthy person with normal insulin sensitivity will rarely have their blood sugar elevate above 140 after a meal, so we will use 140 as a “normalcy benchmark.” We offer these goals for appropriate (normal) amounts of starch/g starch/glucose lucose in the the bloodstream after after consumin co nsuming g a food fo od or a meal or a beverag beverage. e.
QUICK QUICK MEDICAL MEDICA L NOTE: Why are these goals stricter than the Oral Oral Glucose Glucose Tolerance Test? The first fir st reason is that we ar ar e using real r eal food foo d instead instead of a glucose gl ucose solution. Most importantly, the “normal” ranges in the OGTT (and diabetic testing in general) are not adequate for achieving optimal health in my opinion. The traditional tests set the bar too low and categorize too many people with early insulin resistance as “normal.”
REAL LIFE EXA E XAMPLE MPLE
“Joe” was recently diagnosed with prediabetes. He is using our selfmonitoring program and wants to find out how the baked potato he is having for lunch today will affect his blood sugar. He eats a whole baked potato and measures blood glucose at 180 at the first hour and 142 by the second hour. ho ur. Obviously Obvio usly he cannot tolerate toler ate that that much star starch ch in a meal, as these readings are outside the goal values in the chart above. The next day Joe has 1/3 of a baked potato for lunch. His 1-hour blood glucose gl ucose measur ement is 136, and and his 2-hour measurement measur ement is 118. 118. Now he knows that gener ally, he can toler ate the the amount of starch in 1/3 o f a baked potato. He moves on and does the same experiment with more of his favorite meals so he can make the necessary adjustments. For most overweight, obese, and type II diabetics early in their disease, these goals are achievable. You will need to reduce the amounts of starch/glucose in your meals appropriately. How insulin sensitive (or resistant) you are will determine how much you need to reduce the starch load in your meals. You will also notice which foods are problemat problematic ic for you.
T he amount amount of starch st arch you can handle handle will will also change depending depending on o n what what you eat with the starchy food in the meal. For instance, eating fermentable fiber with the starch will slow the release of glucose in the bloodstream allowing you to
tolerate more starch with the meal. Measure your blood sugar this way for a while to get a sense of which specific foo ds you can handle and which ones you yo u cannot. It can also help you identify which foods to eat with a starchy food help control blood sugar (i.e. fiber from vegetables). There is no guesswork. Things you thought were “healthy” might shoot your blood glucose through the roof. You will never know unless you use this testin testing g protocol. pr otocol. Over time, you will not need to measure as much. You will have assembled enough empirical data to intuitively know what kind of foods you should avoid. All you need is an inexpensive glucose monitor to get started. We will now refer to what you are ar e measuring with with this this method as your indi individ vidual ual glucose t olerance (IGT). (IGT ).
WHOLE WH OLE GRAINS FOR DIABETICS? DIA BETICS? SERIOUSLY? Somewhere, somehow, someone got the bright idea that whole grains were good for diabetics. This has never made any sense to me, and sometimes makes m akes me a little crazy cr azy when when I hear hear that a well-meaning health care provider pr ovider has told told a diabetic diabetic person perso n “to “to eat mor e whole whole gr g r ains” as nutrition advice to help their diabetes. While it is true that the starch in whole grains is converted to glucose a little little slowe slo werr than than processed pro cessed flour, eating eating whole gr g r ains still still r esults esults in a larg e glucose lo ad the the body must clear fr om the bloodstream. If you you don’t believe me, eat a sandwich sandwich made of “healthy whol wholee gr ain” bread br ead and check your one and two two hour blood bloo d sugars. Try Try a plate of “whole gr ain” pasta pasta and do the same same blood bloo d testin testing g protocol pro tocol and see what what it does does to your yo ur blood bloo d sugar. Unpro Unprocessed cessed whole whole g rains such as o ats ats and pseudo-g pseudo-grains rains such as quinoa quinoa can definitely be part of a healthy diet for someone with good insulin sensitivity, sensitivity, but even these these foo ds in lar ge amo unts will will often of ten pr pr esent too too much of a starch load for most diabetics and prediabetics to effectively process.
“Stop “St op recom reco mmending whole whole grai g rains ns for fo r diabetics!!!!” Diabetic educators and other well-meaning clinicians keep parroting the whole grain mantra they learned in their training, but it is not doing their patients patients any favor favo r s, believe me. It It drives me a litt li ttle le nuts when whole whole grains are recommended to diabetics, and everyone wonders why the patient patient’s ’s blood sugar sug ar is not well contro lled. Sometimes I feel like Inspector Dreyfus in the old Pink Panther movies with with the “whole “whole g r ain” issue. The bumbling Inspector Inspector Clouseau’s antics antics torment Dreyfus over the years, and eventually land him in an insane asylum. I am not yet in a mental health institution, but I do get the occasional occasi onal eye twitch. twitch. As you get leaner and healthier, you will be able to tolerate more starch. Along the way it is your duty to experiment and verify the changes. If you have excellent insulin sensitivity, and can tolerate high starch levels, eat it, enjoy it, and clear it with no worries. Do not lie to yourself about having high insulin sensitivity if you do not. The IGT will not lie to you.
QUICK QUICK MEDICAL MEDICA L NOTE: Type II II diabetics diabetics (especially (especial ly those who have had the disease fo r a while) may need need additional additional help fr om pharmaceutica pharmaceuticals ls to cont co ntro ro l their blo od sugar. Drugs like li ke Metformin Metformin cont co ntrr ol the the release r elease of g lucose the “liver “liver banker” banker” pr oduces from fro m gluconeogenesis g luconeogenesis (see item #2 in the Consequen Consequences ces of Obesity and Insulin Resistance from the previous section) and can definitely definitely help some achieve achieve their their blood blo od sugar goals. go als.
Again, if you are currently on diabetes medication, please work with your doctor while implementing the starchy carbohydrate reduction as described descri bed in step one. Your Your medication may need adjustment to keep your blood sugar fr om falling too lo w. Type I diabetes can be mor e complicated com plicated to manage. Type I diabetics definitely need medical supervision if they try dietary changes.
COACH’S CORNER: Recent research strongly supports the contention that restricting starchy carbohydrates and sugars is of substantial benefit for the type II diabetic and the the insulin-r esistant obese. Welcome elco me to the or thodox elite eli te who who showed sho wed up to to the party par ty 30 year yearss late to proclaim pro claim that that starchy starchy carbs, car bs, grains, gr ains, liquor, man-made man-made industri industrial al food fo od and artificial chemically poisoned proteins are BAD for us and contribute to obesity and type II II diabetes. diabetes. Thank you for fo r confir confi r ming what the athletic athletic elite alr eady knew in 1983! 1983! Individuals with a broken insulin system should reduce stress on the system system by decreasing dietar dietar y glucose (cr eated eated fro m starch and sugar) to an amount that their system s ystem can effectively pro cess. It It is so simple! Again, the amount each person can tolerate will differ between individuals. The mor e insulin resistant you are, ar e, the the less starch starch and sugar you will be able to tolerate. Get serious about regaining your health and use the science science and techn technolo ology gy available for identifying identifying your individual individual glucose tolerance.
REAL LIFE EXA E XAMPLE MPLE
Lettuce Lett uce wraps wraps are a great alt alt ernative ernative to reduce the amount amount of starch in your favorite wrap recipe. Maintaining healthy bloo blood d sugar levels levels can stil st illl be tast y. “Sally” has had the diagnosis of type II diabetes for 4 years, and probably had insulin resistance developing for more than a decade. She could not figur e out why why her blood glucose kept reading high after after her lunc l unch. h. She had switched from making her sandwiches with bread to making wraps with with cor n tortillas. Her Her glucose r eadings impro ved but but were were still considerably high after lunch. lunch. During a clinic visit, Sally was reminded that corn tortillas are made with corn cor n flour and are mostly starch. starch. Since Since Sally Sally has had her her condition for a while, she cannot tol toler erate ate much star starch ch with with her meals m eals while keeping her after-meal after-meal glucose g lucose within within the the goal range. Switch Switching ing fr om cor co r n tortilla wraps to lettuce wraps did the trick and now her after-lunch blood glucose readings ar e well well within within the the goal go al range. r ange.
STEP 2 STOP EATIN STOP EATING G FOOD F OODS S THAT CONTAI CONTAIN N GLUTEN! Obesity and diabetes are inflammatory disorders. For many individuals, gluten adds fuel to the inflammation fire by causing gut irritation, intestinal permeability,
and inflammation. Gluten-containing products provide no nutritional advantages. There is no downside to to eliminat elimi nating ing glute g luten n fro m your diet. diet.
“GLUTEN “GLUTEN-FREE” -FREE” DOES NOT NECESSARILY EQUAL HEALTHY!
I have seen plenty of people cut out gluten from their diets only to run to the the gluten-free section section of o f their their gr ocery ocer y stor stor e to buy a bunch bunch of pro cessed glutenfree replacement products. Many of these processed products are far from healthy. Most are just highly dense sources of starch with very little nutritional value. A glutenfree cake is still a cake, cake, and a gluten-fr gluten-free ee cookie is i s still a coo kie—the kie—the only difference is they do not contain a potentially gut-irritating protein (gluten). These gluten-free gluten-free pr ocessed products will will wreak havoc on your blood bloo d sugar and waistline. Do not fool yourself into thinking that these are health foods! Do gluten-free the right way and stay away from these processed products.
STEP 3 ELIMINATE PROC ELIMINATE PROCESS ESSED ED SEED OILS FROM YOUR DIET Processed seed and vegetable oils are some of the largest contributors to inflammation and oxidative stress in modern society. These rancid concoctions are
in 99% of all processed (man-made) foods. Fast food manufacturers find ways to include include seed and vegetable vegetable oils in nearly every ever y foo d pro duct they they make—fro make—fro m milk shakes to burger “meat,” from the hot apple pie crust, to the bacon bits sprinkled over your salad, these bad fats are everywhere. Processed Pro cessed seed seed and vegetable vegetable oils ar e high in omega-6 PUFA and contribute to
chronic inflammation and oxidative stress. • High dietary intake of omega-6 omega- 6 PUF PUFA can disrupt disr upt the omeg a-3/omega-6 a-3/o mega-6 balance leading to a chronic inflammatory state. • Omega-6 Omeg a-6 PUF PUFA, like all polyunsat pol yunsatur urated ated fats are ar e pro ne to free fr ee r adical damage because because of their their multiple multiple double bonds. This leads to to free-radical fr ee-radical chain reactions in the body, which quickly produce large amounts of oxidative stress. This is i s linoleic lino leic acid (LA ( LA)) an omega-6 om ega-6 PUFA. PUFA. High amount amo untss of o f LA are ar e found in many processed foods and in the vegetable/seed oils used to cook fast food.
Free radica radicals ls are attracted att racted t o doubl do ublee bonds! The last thing thing you need if you are o bese or diabetic diabetic is to to “impor t” more o xidative xidative
stress and inflammation from vegetable and seed oils found in processed food and fast food.
KEY POINT: Insulin Insulin resist r esistance ance is trigger trig ger ed by chronic inflammation inflammation and oxidat o xidative ive stress. Do not make it wor wor se by “importing” mo r e inflammation inflammation and oxidative stress by eating high amounts of omega-6 PUFA from fast food and processed foods. Read your labels!!
OMEGA-6 OMEGA -6 CONTENT OF VEGETAB VEGETABLE LE AND SEED OILS OILS
Corn Oil • 24% MUFA MUFA • 60% Omeg a-6 PUFA PUFA • 12% SFA
Sunflower Seed Oil Oil • 19% MUFA MUFA • 65% Omeg a-6 PUFA PUFA • 10% SFA
Safflower Oil Oil • 14% MUFA MUFA
• 75% Omeg a-6 PUFA PUFA • 6% SFA
Soybean Oil Oil • • • •
23% MUFA MUFA 51% Omeg a-6 PUFA PUFA 6% Omeg a-3 PUFA PUFA 14% SFA
You can see s ee the high per centage of omeg a-6 PUFA PUFA in each of o f these oils. oi ls. Check processed food packages and salad dressings for these oils. Many of them are even advertised as being healthy for you! • MUF MUFA = mo monouns nounsatura aturated ted fatty acid • PUFA PUFA = polyunsatur pol yunsaturated ated fatty fatty acid • SFA SFA = satur saturated ated fatty fatty acid
WHAT SHOULD I USE FOR SAUTÉING FOOD OR FOR SALAD DRESSING? Why not use the choice of the world’s elite chefs, olive oil or coconut oil? Do you really think the world’s best chefs use trashy, highly processed vegetable oil for sautéing top quality ingredients? Of course not! They use the finest extra virgin olive oil, or the purest of high MCT coconut oil—these magnificent fats are highly beneficial beneficial and introduce introduce great gr eat flavors flavor s into into your foods. foo ds. If we are going to ask you to stop using something, we will give you substitutes: Use Use extr extr a virg in olive oil to make your own homemade salad dressing dressing instead instead of using store-bought dressings. I challenge you to find a store-bought salad dressing low lo w in omeg a-6 PUFA. PUFA. For cooking, coconut oil is superb. It is high in medium-chain triglyceride saturated fats (including lauric acid) that have amazing health benefits. Because it contains saturated fat, coconut oil will not oxidize and produce free radicals when you cook with it. Medium-chain saturated fats aid in weight loss and provide some benefit to people with Alzheimer’s disease. They are “heart safe” and do not aggr avate avate risk ri sk factor factor s for heart and and vascular vascular disease. Medium-chain triglycerides go to the head of the fuel-burning line as soon as
they are consumed; MCTs are used directly for energy instead of being stored as excess body fat. MCT consumption is especially helpful for insulin resistant individuals cutting back on starchy carbohydrates. The medium chain-fats can provide “replacement energy” for the “lost” starchy carbs. Ironically, this is the identical strategy (replace starch calories with MCT calories) used by competitive bodybuilders leading up to competitions where 5% body fat percentages are common. Overall, the high content of medium chain saturated fats makes coconut oil an excellent excellent alternative alternative to to vegetable vegetable oil oi l for fo r most cooking coo king needs. Also, coconut oil does not impart a strong coconut flavor to food as you might imagine. Tr Tr y it when when making making a vegetable vegetable stir-fry stir-fr y and see for yourself.
STRONG MEDICINE TACTICS: As alternatives to processed seed and vegetable oils, use olive oil for homemade salad salad dressings dressings and coconut oil fo r cooking. co oking.
STEP 4 EAT AT LEAST 20-30 GRAMS OF PROTEIN WITH EVER EV ERY Y MEAL Every time you eat, consume some protein: at least 20 grams if you are smaller and 30 grams if you are a larger person. Protein provides the amino acids critical for maintaining (or increasing) lean muscle mass, and protein is also an appetite suppressor. Protein satiates, nourishes, and quells hunger. Quality protein triggers the br br ain’s satiety satiety (the (the “fullness”) centers, centers , and eating eating pro tein thr throug oughout hout the the day will quench hunger. Determining how much protein you are eating with a meal is relatively easy using the following “rule of thumb” estimates for protein. All you need is a kitchen scale that that measures measures cooked protein pr otein sources sour ces in ounce o unces. s.
PROTEIN ESTIMATOR: THE EASY WAY The following following ar e good go od “rules of thumb thumb”” for figuring out pro pro tein amounts amounts fr om animal sources. For For plant sources, sour ces, we we recommend r ecommend using using the the National Nutrient Database (http://ndb.nal.usda.gov/ndb/search/list (http://ndb.nal.usda.gov/ndb/search/list) since plant sources sour ces are hig hly variable in protein pr otein amounts. amounts. • Cooked Coo ked chicken, turkey, beef, or por k have have about 7 grams of protein o f these these cooked coo ked meats meats for every 1 ounce of meat. Four ounces of any of provide approximately 28 grams of protein, and are well within the 20-30 gram goal.
• Ground Gr ound meats such as hamburger hamburg er are ar e less dense, dense, and and have have about about 7 grams of protein for every 1.5 ounces of cooked meat. You will need 6 ounces of cooked coo ked ground gro und meat meat for the the same 28 gr ams of protein. pr otein. • 1 egg has about 7 grams gr ams of prote pro tein. in. So, 4 scrambled scrambled eggs provide pr ovide 28 gr ams of protein. protein. • Fish and fatty fatty poultry (duck) have about 7 grams of protein for every ounces of fish or o r duck duck contain contain 28 grams of o f prote pro tein. in. 1.5 ounces. Six ounces
Over time you should be able to literally “eye-ball” the amount of food fo od you need to get wit within hin the 20-30 gram g ram protein goal for each meal.
STEP 5 INCREASE PLANT PLANT-BASED -BASED FOODS FOR
FERMENTABLE FIBER FERMENTABLE FIBE R AND ANTIOXIDANT DEFENSE. Fruit and vegetable fiber is fermented (broken down) by our gut bacteria. This process produces beneficial “waste” products including short chain saturated fats like butyrate.
Unlike our digestive machinery, the beneficial bacteria that live in our gut can break the connecting bonds in fiber and they can feed on the released glucose. These bacteria secrete the short chain fats (butyrate) as “waste” products, but these waste product pro ductss have amazing anti-inflammator anti-inflammator y properties. pr operties. Here is a quick r eview on the benefits benefits of butyr butyrate: ate: • Butyr Butyrate ate has potent anti-inflammatory properties. Obesity and diabetes diabetes are ar e inflammatory conditions, therefore substances like butyrate and other short chain fatty fatty acids acids produced pr oduced from fro m the fermentation fermentation of fiber help counteract the chronic
inflammation produced from bloated fat cells. • Butyr Butyrate ate has been shown to have anti-cancer proper pr oper ties, and potential antiespecially with colon cancer. cancer action— especially
KEY POINT:
The main health health benefits benefits from fro m fiber r esult from the the shor t chain chain fat (butyrate) production from fermentation of fiber by the gut bacteria. Fiber fro m many types types of gr ains (especially (especially wheat) wheat) is not as fer mentable. mentable.
WHA WH AT ABOUT AB OUT THE FIBER F IBER IN WHOLE W HOLE WHEAT?
The fiber found in whole wheat is not nearly as fermentable as the fiber in most fruits and vegetables. The beneficial gut bacteria cannot break down the whole wheat fiber as well, so very little butyrate is produced. The main health health benefits benefits from fro m fiber r esult from the the shor t chain chain fat (butyrate) production, so fiber that is not as fermentable (like whole wheat) wheat) is i s not no t the the best choice. choi ce. Whole wheat is also very dense with starchy carbohydrates, making it a poor choice (like many of the whole whole gr ains) for people with with obesity obesity and diabetes.
STRONG MEDICINE TACTICS: To help stop chro nic inflammation, inflammation, choose choo se vegetables vegetables and fruit fr uit over gr ains as your sources so urces of ferment fer mentable able fiber. fiber.
Eating fermentable fiber from a wide variety of fruits and vegetables can help decrease the level of glucose in your bloodstream after meals. This will help you meet the one-hour and two-hours after-meal glucose goals discussed in step one.
Make fibrous vegetables and fruits a cornerstone of your nutrition. Fermentable fibers can slow the rate in which food is moved from the stomach during digestion. This can help create a feeling of satiety (fullness). The follo wing wing list li st is some of the best best sources of fiber fi ber fr om fr uits and and vegetab vegetables, les, but it is not no t nearly a complete co mplete list.
GOOD SOURCES OF FERMENTABLE FIBER
T he Veget Vegetabl ables: es: • Leafy green vegetables char d vegetable s such as kale, spinach, and char • Stem tubers such as potatoes • Root tubers such as sweet potatoes potatoes • Root vegetables vegetabl es such as carrots, turnips, rutabaga, daikon, radish, parsnips, jicama
Fruit: • Berries Berri es such such as strawberr strawberr ies, blueberr blueberr ies, blackberr blackberr ies, raspberr ies • Avocados • Pears, apples, or anges, bananas (be awar awaree of the the sugar conten co ntent) t)
INCREASING INCREASING ANTIOXIDANT ANTIOXIDAN T
DEFENSE WITH PLANT-BASED FOOD
There ar e certain health health-pro -promoting moting compound compo undss found only in plant foods. foo ds. Many of these compo unds stimulate stimulate our body’s antio antioxidant xidant defense systems and counteract the chronic oxidative stress linked to obesity and diabetes. Many fruits and vegetables are “edible pharmacies” containing hundreds of different compounds to combat inflammation and oxidative stress— especially important for diabetics and the obese. For a long lo ng time it was thoug thought ht that that these these plant compounds acted as antioxidant antioxidants, s, scooping scoo ping up fr ee radicals r adicals and preventin preventing g them them fr om damaging the body. Some of these compounds may work in this fashion to a limited limi ted extent, extent, but but current curr ent resear ch shows that many of these chemicals
work primarily by stimulating our natural antioxidant defense and detoxi deto xification fication system syst ems. s. Some of these plant-chemicals also work by stopping stopping inflammation. inflammation. Some gr ains such as oatmeal oatmeal do contain contain a r elatively elatively high amount of fer mentable mentable fiber, but also have a pretty high starch load, so use with caution if you are diabetic. Legumes such as beans, peas, and lentils have high amounts of fiber, but can cause gut inflammation in some people. If you are going to use legumes as a fiber source, sour ce, make make sure you soak so ak them them for 24 hours then cook them them thor thor oughly to r educe educe some of the toxic compounds found in dried legumes. If you tolerate legumes, they can be an excellent source of fiber if prepared correctly. Vegetable and fruit-based
fiber generally causes less irritation than legumes and is generally preferable from a gut health perspective. There are thousands of plant-derived chemicals, and many have positive health benefits. Some are outstanding and deserve to be singled out because they are especially beneficial to the insulin resistant obese or diabetic person.
SULFORAPHAN SULFORAPHANE: E: BROCCOLI’S BROCCOLI’S BOUNTY
Sulforaphane is a chemical chemical found in all cr uciferous vegetables (br (br occoli, cauliflower, cabbage, bok choy, horseradish, mustard seed, wasabi, rutabagas, radishes, turnips and others). Sulforaphane stimulates the central controller of the antioxidant response system, which fights oxidative stress from the free radicals inside your cells. It also directly helps to stop the inflammatory response. Since obesity and diabetes are diseases of chronic inflammation and oxidative stress, sulforaphane can be especially helpful for diabetes in particular. Sulforaphane has also shown potent anti-cancer activity in some types of cancer, and may inhibit the growth of the ulcer-causing bacteria, Helicobacter Heli cobacter pylori. py lori. Additionall Additionally y, sulfor sulfo r aphane can stimulate stimulate the body’s body’s natural detoxification detoxifi cation system, helping to detoxify certain types of toxins and toxicants from the air, water, water, and food. foo d. The best dietary dietary source so urce of sulfo raphane is from fro m broccoli bro ccoli sprouts spr outs (3-5 day
old broccoli bro ccoli plants). plants). Bro Bro ccoli sprout spro utss have 20 times the the sulfor aphane aphane content content as full-grown full-gr own broccoli bro ccoli plants.
TECHNICAL NOTE: Sulforaphane is pr pr oduced from a chemical building building block blo ck in broccoli called glucoraphanin. A special enzyme in the plant is needed to co nvert glucoraphanin to sulforaphane. You must damage the plant through chopping or chewing chewing for fo r the the conversion conversio n to sulfor aphane aphane to to take place place directly from the plant. Glucoraphanin can also be converted to sulforaphane by the gut bacteria.
KEY POINT: Broccoli Broccol i sprouts spr outs must be be damaged by chew chewing ing o r cutting cutting to get sulforapha sulfor aphane ne directly fro m the plant. plant.
RESEARCH UPDATE: A r ecent study study has shown that sulfor sulfo r aphane can alter the epigenetic epig enetic progr pro gr amming of o f certain cancer cancer cells. Researchers Researchers found that that sulfor sulfor aphane aphane “turns “turns off” o ff” a gene responsible r esponsible for gr owth in these these cancer cancer cells. This is importan impor tant, t, since since cancer cancer is uncontrolled cell gr owth. owth. This r esearch suggests that that sulfor sulfor aphane aphane can stop stop uncontrolled uncontroll ed gr owth owth in some cancer cells by “switching “switching off” o ff” gro g ro wth wth genes, thr thr ough an epigenetic epigenetic
process. If you need a review on the epigenetic process, go back to the Central Concepts section on Gene-Environment Interaction.
RESEARCH UPDATE: Of special interest for diabetics—new research has shown that adding foods with high sulforaphane content such as broccoli sprouts to the diets showed substantial substantial benefit for diabetics. All of o f the diabetic patients patients in the study study showed impr ovements in insulin i nsulin resistance, and overall decreased oxidative stress and inflammation after adding adding broccoli bro ccoli spr outs to to the the diet. diet.
DO IT YOURSELF! Broccoli Broccol i sprouts spr outs are easy to g ro w at home. home. An An internet internet search will yield several sites with with instructions instructions o n how to gr g r ow your own sprout spro uts. s. Given Given the the benefits benefits of sulfor aphane, aphane, having having your own indoo indoorr br occoli sprout spro ut garden is well worth the effort, and they will be fresher and more effective than than spr spr outs from the gro cery store.
STRONG MEDICINE TACTICS: Eat crucifer cruciferous ous vegetables such such as broccoli br occoli,, cauliflower, cabbage, cabbage, bok choy, horseradish, mustard seed, wasabi, rutabagas, radishes, and turnips to get the benefits of sulforaphane. Broccoli sprouts are the best source.
POLYPHE POLYPHENOLS: NOLS: DARK D ARK CHOCOLATE ANYONE? Polyphenols Polyphenols are ar e a large lar ge gro g ro up of plant-chemica plant-chemicals ls found in most plant species. Laboratory studies have shown they have strong anti-oxidant effects and inhibit inflammation.
ube (called in vitro) show that polyphenols act as Studies Studies in a test t ube antioxidants, scavenging free radicals. However, recent research has shown that in the body, polyphenols do not have as much direct antioxidant effect themselves, but activate the antioxidant defense system (see the “bouncers in the bar” from the Central Concepts chapter). Polyphenols are found in many plant-based foods, but the highest concentrations are found in cocoa beans, coffee, red wine, green tea, black tea, and olive oil. The bitter taste in many of these foods comes from the polyphenol content. The higher the polyphenol content, the more bitter the flavor. Pure cocoa has one of the highest polyphenol contents of any food, but is inedible because of the bitter bitter taste. 85% dark chocol cho colate ate is an excellent source of polyphenols and tastes pretty good once you are accustomed to
the the flavor (and lack lack of sugar ). Research on polyphenols is still ongoing, but recent studies have shown that that polyphenols polyphenols may be o f some so me benefit for diseases diseases of o f inflammation and oxidative stress such as diabetes, heart disease, cancer, and Alzheimer ’s dementia. Incor Incorpor porat atee a variet vari ety y of polyphenols polyphenols in your diet—t diet—there here ar e plenty plenty of sources to to choose from. fr om.
STRONG MEDICINE TACTICS: Incorpor Incor porat atee polyphenol-r polyphenol-r ich foods foo ds like dark chocolate (80-85% (80-85% cacao), cacao), coffee, red wine, green tea, black tea, and olive oil into your diet.
FIRST PRINCIPLES PERSPECTIVE: PERSPECTIVE : PLANT CHE CHEMICALS MICALS AND HEAL HE ALTH TH There are multiple theories as to why so many plant-based chemicals show health benefits. But, But, the the theory theor y that these these chemicals chemical s act as direct dir ect antioxidant antioxidantss is slowly losing losi ng favor. Plant-based chemicals such as polyphenols are produced inside inside the t he plant in response to t o environm environmental ental stresses st resses on o n the t he indivi individual dual pla plant. nt. Poor soil nutrients, insect predators, and lack of water can all produce a stress response in plants, plants, increasing polyphenols. polyphenols. Recently an intriguing hypothesis was put forward—chemicals such as polyphenols, produced in plants during stressful conditions, are known to activate stress defense mechanisms (antioxidant defense) in our bodies when eaten, and they act as an environmental stress sensor. The author authorss of this hypothesis think that these plant-chemicals plant-chemicals (when eaten) eaten) allo w us to sense stress in the food supply (stress to the plants) and prepare our bodies for an upcoming upcoming threat threat to the the food foo d supply supply such as a dro dro ught or insect
infestation. In the hunter-gather societies of our distant ancestors, the ability for our body to to pr epare for a food foo d shortage by “sensing” “sensing” stress in the the food foo d supply supply would be a survival sur vival advantage. It may be one r eason why so many chemicals in plants have health benefits benefits for humans. This is still just a hypothesis, but it makes sense through the firstprinciples lens.
STEP 6 CUT OUT HIGH FRUCTOSE CORN SYRUP AND SUGAR. Like alcohol, fructose can only be metabolized in the liver. The liver does two things with fructose—converts it to glucose or body fat for storage at one of the many fat-storage depots dotting the bodily landscape. The amount of fructose in the fruit we eat is relatively small and can be easily processed by the liver without causing problems. It is the added sugar and high fructose corn syrup in processed foods causing the health problems in many modern societ so cieties. ies.
When the the liver has stored stor ed as much glucose as possible in the form of g lycogen, it will convert the extra glucose into fat, specifically triglycerides. Usually these triglycerides triglycer ides are transpor ted ted to fat cells cells for fo r storage, storag e, but but if you are somewhat somewhat insulin insulin resistant, the fat cells are not storing triglycerides well. The liver and muscles become the new “storage sites” for fat. This process damages the liver leading to “fatty liver disease”, also known as Non-Alcoholic Fatty Liver Disease (NAFLD). Overloading the liver with glucose and fructose leads to NAFLD.
KEY POINT: The primary causes of NAFLD are: • Insulin Insulin r esistance • Intestinal Intestinal permeability permeabili ty (see Gut chapter chapter)) • Excess sugar in i n the diet Recent research has shown that a combination of insulin resistance, intestinal permeability, and excess dietary sugar (especially fructose) causes NAFLD. High-fructose corn syrup continues to get bad press as a “dietary devil.” Some of this portrayal as a nefarious character is deserved, but further discussion in the following “Digging Deeper” section is warranted to establish its role in health problems in a scientific context.
DIGGING DEEPER: Why the fuss over high-fructose high-fructose corn syrup? syrup? High-fructose corn syrup (HFCS) is almost identical to table sugar (sucrose) (sucr ose) when you compar co mparee them as chemicals. Most HFCS HFCS is 55% fructose and 45% glucose, while sucrose is 50% fructose and 50% glucose. Eating either in large quantities can cause health problems, especially especially if you have insulin resistance resistance or o r outright outrig ht diabet diabetes. es.
The reason behind the bad press on HFCS is because food manufacturers add it to to most pro cessed foods and fast food to impr ove taste taste and palatability. palatability. The primar pr imary y reason r eason they can do this is because the government go vernment subsidize subsidizess farmers far mers gr owing corn, co rn, which makes makes HFCS HFCS very very cheap. Processed food manufacturers can use large amounts of HFCS in their their produc pro ducts ts more mor e cheaply cheaply than than sucro sucrose se harvested harvested from fro m sugar cane or sugar beets. beets. The body can handle small amounts of HFCS or sucrose, but the amount consumed by the average American is causing health problems. The average American eats an estimated 80 to 100 pounds of added sugar in the for ms of o f sucrose sucr ose and HFCS annually. annually. “Added “Added sugar ” simply means sugar not naturally naturally present pr esent in real r eal foods. foo ds. It is a large lar ge part par t of pro cessed and fast food.
This stagg staggering ering amount of added sugar sugar in our diet is certainly contributing to NAFLD, obesity, and diabetes. HFCS is not chemically different fro m sucrose, sucro se, but but the the large larg e amount we we are exposed exposed to in processed pro cessed food foo d is the the real issue.
SUGAR AND “AGE” Sugar, consumed in large amounts over a protracted period of time, inevitably creates serious health problems, especially for diabetics. Table sugar and HFCS are larg e concentrations concentrations of o f glucose g lucose and fructose. Large amount amo untss of o f these these simple sugars sugar s leads to increased formation of Advanced Glycation End-products (AGE). AGEs are formed when glucose and fructose undergo chemical reactions that allow them to “stick” to proteins inside and outside cells. Low amounts of AGEs are normal. They are naturally produced on a constant and ongoing basis as part of a healthy metabolism. Health problems occur when large amounts of AGEs form in part from high amounts of sugar and HFCS in the diet, then trigger inflammation. If the cause is dietary, then we can control it. Just as there is a receptor, or “dock”, for insulin, leptin, and countless other molecules in the body, there is a receptor for AGEs as well. This receptor is the Receptor for Advanced Glycation End-products (RAGE). (RAGE). When AGEs “dock” with RAGE, an inflammatory response is generated. The more AGEs present in the body, the more inflammation is produced when they dock with RAGE. The chronic inflammation from high levels of AGEs, contributes to accelerated aging of the body. AGE makes you age faster, but we can control this with diet.
KEY POINT: As the the amount of AGEs increase incr ease in the body, body, so does do es the level of inflammation. This worsens chronic diseases and contributes to acceler acceler ated ated aging. aging .
Fructose forms AGEs eight times faster than glucose. Some organs in your
body—kidneys, brain and blood vessels—will produce AGEs rapidly when subjected to high levels of glucose and especially fructose. High amounts of glucose and fructose (as found in high fructose corn syrup) damage these organs and turn them into AGE-producing machines. The kidneys and blood vessels prone to AGE-caused inflammation are damaged in diabetes. Kidney failure, vascular, and heart disease are often seen in long-term diabetes.
KEY POINT: When overall sugar is high, the blood vessels and kidneys kidneys are especially prone pro ne to to for ming AGEs. Chr Chr onic inflammation from fr om AGEs AGEs in these organs contributes to the high incidence of heart disease and kidney disease seen with with diabetes.
ADV AD VANCED AN CED GLYCA GLYCATION TION END E ND PRODUCTS IN FOOD
We have just discussed how levels of sugar can lead to AGE formation inside your body, but AGEs can also be preformed in the food you eat, even before it gets into your body. The type type of food foo d and cooking process pro cess gr eatly eatly affects affects how much AGE AGE is present. High temperature cooking, such as deep frying, can elevate AGE for mation mation by up to to 100 times.
Animal-based Animal-based foods ar e pro tein-rich tein-rich and are ar e especially vulnerable vulnerable to AGE for mation mation with cooking methods such as frying. Processed foo ds often contain sugar and proteins subjected to high temperatures during the manufacturing process. They are often loaded with AGEs. Alternate cooking methods can greatly reduce the amount of AGEs in your food. foo d. So-called “moist” cooking methods methods using water water and lower temperatu temperaturr es (slow cookers/cro cooker s/crock ck pots) pots) are excellent for reducing AGE formation. Also, adding acidic liquids such as lemon juice and vinegar will also reduce AGEs formed from cooking. Making stews, stews, soups, and slow cooker meals are all gr eat ways ways to to prepare your food foo d to avoid high levels of AGEs, especially especially if you are diabetic. diabetic.
STRONG MEDICINE TACTICS: Reduce AGEs by decreasing sugar and HFCS in your diet and follow lowAGE cooking methods.
HOW TO ACCELERATE DISEASE AND AGING: THE NUCLEAR OPTION
If you are diabetic or overweight/obese, the best way to accelerate disease and aging is to continue continue to eat fried fast foo d and processed foo d. There is no doubt that that fried fr ied chicken chicken and Fr Fr ench fries from fr om your yo ur favor ite fast food foo d r estaurant taste taste amazing. It It is why the the fast food foo d industry makes billio bill ions ns of dollars dollar s per year fr om consumers. But But,, these these foods are inflammation/o inflammation/oxidat xidative ive stress nuclear weapons weapons in your body: • The processed pro cessed vegetable vegetable oils oil s (PUF (PUFA) used to to fry fr y the the food create cr eate huge
amounts amounts of fr ee radicals. • The breading (starch) and and prote pro tein in cooked at high high temper temper atures atures creat cr eates es AGEs by the bucket-load. • Most of these foo ds have added sugar sugar and HFCS HFCS to make them them mor e palatable, which which potentially incr ease the AGEs AGEs produced pr oduced in your yo ur body. • Most of these foods have larg e amounts of gluten that that can contribute to to inflammation in the gut if you are sensitive. These foods taste taste gr eat and generate generate stro stro ng r eward eward signals sig nals in your brain, br ain, but are deadly to your health. If you are obese or diabetic and continue to eat these foods regularly, you are simply not serious about getting healthy. The following graphic summarizes how preformed AGEs in processed and fried food, as well as AGEs generated in the body from high glucose levels—seen with diabetes and insulin resistance—lead to chronic inflammation and oxidative stress.
SOFT-DRIN SOFT-DRINKS, KS, ENERGY EN ERGY DRINKS, DRIN KS, FRUIT DRINKS: HEAL HE ALTH-KILLING TH-KILLING
SMART BOMBS Soft drinks, energ energ y drinks, and “fruit-flavored” “fruit-flavor ed” drinks are devoid of any nutrition and will slowly wreck your metabolism. If you already have prediabetes, diabetes, or obesity, you need to steer clear of these beverages. They are all filled with sugar and HFCS. They are taste-engineered to stimulate your food reward system. Many of us have “soda addictions” which which are hard to kick. Clever Clever marketing is also involved in fruit-drink labeling such as “made with real fruit”, yet they are all loaded with sugar! Some children are even showing signs of o f fatty fatty liver disease in their their early teenage teenage years lar gely due to soft-drinks, fruit fr uit beverages, beverages, and energy drinks.
Energy drinks are hugely popular with teenagers and young adults. Not only ar e they loaded with with caffeine, but some have almost almo st 3 times times the sugar as a soft drink! Here Here ar e some numbers: • One 12-ounce can of soda can have between between 10-15 teaspoons of o f sugar. A 20-ounce bottle has 16-25 teaspoons of sugar depending of the brand. • Energy Energ y drinks can have as much as 40 teaspoons of sugar sug ar in one can! Most brands have 25 to 30 teaspoons of sugar per can. Fruit drinks marketed to children can have just as much, if not more sugar than soft drinks.
WHA WH AT ABOUT AB OUT FRUIT JUICE?
It is a big shocker for most people, but fruit juices can have just as much sugar (glucose and fr uctose) uctose) as so ft drinks. While juice has some nutritional value in the form of vitamins and minerals, they also have huge sugar lo ads for the body: body: • One glass of or ange juice is equiva equivalent lent to 10 teaspoons teaspoons of sugar. • One glass of apple juice juice has has 10-12 10-12 teasp teaspoo oons ns of sugar. • One glass of gr ape juice juice can have up to to 15 teasp teaspoo oons ns of sugar. Fruit can be a part of a healthy diet diet and and is a g ood oo d source sour ce of fermentable fermentable fiber, vitamins, and minerals. miner als. Remember Remember that it takes takes 4-6 go od-sized od-si zed whole whole oranges o ranges to make one 8-ounce glass of or ange juice.
Eat the t he whole whole fruit rather rat her than the t he jui juice ce to g et the the nutrition nutritio n without without the huge sugar load.
HOW DO I KNOW HOW H OW MUCH MUCH SUGAR IS IN A FOOD OR DRINK? 1. Read the label to to find the amount of sugar in i n gr ams. 2. Divide the number in grams gr ams by 4 (there (there are ar e about about 4 gr ams in 1 teaspoon teaspoon of o f sugar). sugar ). For For example, example, 40 grams gr ams of sugar, divided divided by 4, equals equals 10 teaspoons teaspoons of sugar. 3. Watch “serving “ser ving size.” This is a small deception deception often used used by food fo od and bever bever age market mar keters. ers. The amount of sugar is labeled by serving size. If If a beverage is labeled as having 40 grams of sugar in a 16 oz. bottle, but with a serving size of 2, you ar ar e really consuming 80 grams of sugar if you drink dri nk the the whole bott bo ttle. le.
STRONG MEDICINE TACTICS: Limit the amount of soft drinks, energy drinks, and fruit juice in your diet. If you are ar e obese and/or and/o r diabetic, cut them out completely. completely.
STRONG MEDICINE TACTICS: Read food Read foo d labels to determine determine how much sugar is in the processed foo ds you are ar e eating eating (If you ar e eating eating unpro cessed food without without a label, you generally do not no t have have to to wor ry).
STEP 7 INCREASE INSUL INSULIN IN SENSIT SENSITIVITY IVITY WITH EXERCISE. Step 7 is probably one of the most powerful ways to increase insulin sensitivity and help normalize blood sugar for a type II diabetic or insulin resistant obese person. Even the conservative Centers for Disease Control (CDC) recommends at least 2.5 hours per week of “moderate intensity” aerobic exercise or 75 minutes per week of “vigorous intensity” aerobic exercise. They also recommend 2 or more days of resistance training in addition to aerobic exercise. These recommendations are often lacking when it comes to exercise specifics—but we have them for you. We can show you how to g et fit with with maximal time effici ency. ency. Out-of-shape Out-of-shape people avoid fitness fitness and exer exer cise for a variety of r easons. Some of their reasons are legitimate—mistreatment by fitness professionals and personal trainers, incompetent exercise instruction, or from using exercise modes incapable
of producing results. We will guide you through setting up a proven exercise template used to this day by elite athletes. Every intelligent exercise program needs a cardiovascular training regimen (builds and strengthens heart and lungs, flushes arterial highways), and a resistance training regimen (builds and strengthens the 600 + muscles on the human body.) We will successfully blend these two exercise modes. Exercise is i s one of the best bes t ways to restore res tore insulin ins ulin sensitivi sensi tivity. ty.
You do not have to spend hours in the gym to obtain the insulin-sensitizing benefits of exercise. Recent research shows the possibility of getting these benefits using short exercise protocols—if the protocols are sufficiently intense. Exercise intensity is measured by the percentage of maximal heart rate achieved during the exercise. As a preview to our exercise approach, we will present an abbreviated exercise pro tocol that has been tested tested in a lab with actual actual diabetic patients, and which which showed excellent results. The key to the success of this protocol is the intensity of the exercise. In this case, we are measuring exercise intensity of exercise by the percentage of
maximal aximal heart rate rat e achieved during exercise. Let’s back up a bit to explain more about exercise intensity before we dive into the protocol. The CDC defines “moderate intensity” exercise as anything that gets your heart rate between 50% and 70% of your maximum. “Vigorous intensity” is defined as exercise exer cise that causes heart r ates between between 70% 70% and 85% of maximum.
WHA WH AT IS MAXIMUM MAX IMUM HEA H EAR RT RATE? RATE? The maximum hear t rate (HRmax) (HRmax) is the highest heart hear t rate you can expect to achieve during exercise. HRmax is mostly affected by a person’s age— the older you get, the lower your maximal heart rate. In other words, a younger person per son can generally achieve achieve a higher heart rat r atee during exercise than than an older per son. HRmax HRmax varies co nsiderably among individuals, individuals, but some some general for mulas have have been developed developed to to provide pro vide reasonably go od estimates estimates of your personal maximum heart rate. We used to rely on the simple “220 minus age” ag e” for fo r mula to calculate HRmax, HRmax, but that that was was found fo und to be
relatively inaccurate. Some of the the mor e recen r ecently tly developed developed formulas for mulas will will better better suit our purposes for determining determining your HRmax: HRmax:
For men: 208 - (0.7 X Age) = HRmax For women: 206 - (0.88 X Age) = HRmax Example 1: Chr Chris is is 43 and wants wants to calculate his maximum heart r ate. He will multiply his age (43) by 0.7, which equals 30.1. He will then subtract 30.1 30.1 from fr om 208 to get 177.9 177.9 (we will r ound to 178). So Chris’s Chri s’s HRmax HRmax is about 178 beats per minute. Example 2: Carr ie is 46 year s old. ol d. To calculate her HRmax, HRmax, she would would multiply her age (46) by 0.88 to get 40.5. She would then subtract 40.5 from fr om 206 to to g et 165. 165.5 (we will will r ound up to 166). Carr ie’s HRmax HRmax is 166 beats per minute mi nute.. Following the CDC’s recommendations for “moderate” intensity exercise, Chris needs to keep his heart rate r ate between between 50% 50% and 70% of his maximum m aximum heart hear t rate during duri ng exercise. He will take the HRmax of 178 that he just calculated and multiply that number by 0.5 (50%) and 0.7 (70%): • 178 X 0.5 0.5 = 89 beats per minute • 178 X 0.7 0.7 = 125 beats per minute When Chris Chris is exercising at “moderate” “moderate” intensity intensity for 2 1/2 hours per week as recommended r ecommended by the CDC, CDC, he will will keep his heart hear t rate between between 89 and 125 beats beats per minute. Carrie decides she doesn’t have 2 1/2 hours per week to devote to exercise, so she is going to exercise with a little more intensity. She wants to go into the heart rate zone the CDC CDC classifies as “vigor “vig or ous.” With With this this intensity she only needs to exer cise for 75 minutes (half the time of the moderate exercise goal) per week. Carrie uses the HRmax she just calculated and figures out her “vigorous” target zone of 70% to 85% of her HRmax. She takes her HRmax of 166 beats per minute
and multiplies this number by 0.7 0.7 (70%) and 0.85 (85%): • 166 X 0.7 0.7 = 116 beats per minute • 166 X 0.85 0.85 = 141 beats per minute When Carr Carr ie is exercising exer cising at a “vigor “vigo r ous” intensity intensity for 75 minutes minutes per week as recommended reco mmended by the CDC CDC,, she will keep her heart r ate between between 116 and 141 beats per minute. Exercising Exercising 3 times per week, week, Chris will need to work wor k for 50 minutes minutes per session to get his 2 1/2 hour ho ur total at moderate moder ate intensity intensity.. Car Car rie ri e will schedule schedule 25 minutes minutes per exercise session, 3 times per week for her 75 minute weekly weekly total at a vigor vig or ous inten i ntensity sity..
EXERCISE EXERCISE TIP: T IP: Do not rely on the heart rate monitors built into the handles of exercise machines. They are notoriously inaccurate. Invest in a personal heart rate monitor moni tor with with a chest str str ap and watch watch receiver. This is a wor thwhile thwhile investment investment if you ar e serious seri ous about your fitness. fitness.
HIGH INTENSITY BEATS MODERATE OR VIGOROUS INTENSITY High intensity, short duration exercise protocols have more physiological benefits than the “steady-state” exercise recommended by the CDC. One of these protocols, High Intensity Interval Training (HIIT), is especially beneficial to people who are insulin resistant. As the name implies, HIIT is exercise ramped up to a high intensity for short bursts. For example, a burst or sprint, stop and recover, burst or sprint again, over and over until the session is complete. This method has been shown to reduce high blood sugar as seen in type II diabetes and prediabetes.
HIGH INTENSITY INTE NSITY INTER INTE RVAL TRAINING TRAIN ING PROTOCOL PROTOCOL The HIIT HIIT protocol pro tocol involves pushing your heart rate to approximately 90% 90% of your maximum heart heart rate for short shor t perio perio ds of time with with rest breaks breaks in between. between. Let Let us use Carr Car r ie as an example: Carr ie has alr eady calculated her her HRmax HRmax at 166 beats beats per minute, then then she multiplied her HRmax HRmax by 0.9 0.9 (90%) to g et approximately appro ximately 149 beats beats per minute.
• 166 X 0.9 0.9 = 149 149 beats beats per minute mi nute (her target targ et hear heartt rate). • While wearing wearing her heart rate monitor, monitor, Carr Carr ie will will choose a piece of cardio equipment such as a bike, elliptical, treadmill, stair climber, etc. • She will will start star t at a slow pace for 2-3 minutes minutes to get her her muscles warmed warm ed up. • She starts exercising as har d as possible possi ble to to get g et her heart hear t r ate up to to her target targ et of 149 beats per minute, and continues until until the 60 second interval is complete. • After After the 60-second exercise interval, she will rest for 60 seconds (or pedal/walk very slowly). • After After r esting esting for fo r 60 seconds, seconds, she she will will start another another 60-second exercise exercise interval to achieve her target heart rate of 149 beats per minute. Car Car rie ri e will repea r epeatt this this patte patterr n for a total total of o f 10 60-second 60-second exercise intervals before cooling co oling down for 2-3 minute minutes. s. The HIIT protocol is only 10 total minutes of exercise (10 60-second intervals), and 10 total minutes of rest (10 60-second rest periods). These intervals combine to
only 20 minutes in total—and you are done. “I don’t have time for exercise” is no longer a valid excuse. excuse.
KEY POINT: The most common excuse for not exercising exercising is “I don’t have enough enough time...” If that is the case, then use the HIIT protocol. Short bursts of activity at a high intensity, followed by rest periods has been shown to be just as—and in many cases more—effective as traditional sustained lower intensity exercise. While Chris is plugging away for 50 minutes of “moderate” intensity exercise, Carrie has finished her workout, showered, and is back to the day’s business. Despite the short duration of her workout, she has also gained some advantages that Chris won’t get from “moderate” intensity workout. The benefits benefits of o f shor t dur dur ation ation high hig h intensity intensity training training come fr om the the effect it has
on glu g lucose cose storag st oragee in muscl muscles. es.
FLASHBACK Quickly r eview concept #3 and #10 in the Metabolism Metabolism Basics sectio n, before reading onward. As intensity is increased from “moderate”, “vigorous”, and finally to the 90% HRmax seen in our HIIT protocol, more glucose is used by the muscle for energy. This is because the body cannot supply oxygen to the muscle fast enough to keep up with the demands of high intensity exercise. As a result, the muscle is forced to use glucose without oxygen for energy. This produces lactic acid buildup as a waste product, and starts to empty the muscles of their stored supply of glucose. Fat needs oxygen to be used as fuel, so the low oxygen in the muscles during intense exercise shifts shifts the pr pr imary fuel source so urce to glucose. g lucose.
Wait a minute! I want to burn fat with exercise. You are saying that I will mostly be burning glucose with the HIIT protocol, and I want to get rid ri d of fat! You will burn plenty of fat during the rest periods and after this workout, especially. This type of high intensity workout will keep your metabolis
working working at a higher rate for t he next 24 to t o 36 hours, and wil willl prim primarily arily burn burn fat as fuel. The point of burning up all of this glucose will become evident in the following discussion. The reason we want to use high intensity interval exercise to empty the muscles’ storage supply of glucose is because of what happens after the exercise. As far as your body and brain are concerned, the high intensity exercise may have happened because you ran from a wild animal to escape getting killed. Your body wants to replenish the the supply of glucose in case you need to to escape from fr om an animal again in the near future. Yo u know that you are riding a bicycle, and not running from a predator, but your body responds to the high intensity stimulus as a threat and wants to make sur sur e you are pr epared to to sur vive for another another day. day. In response to the high intensity exercise “threat,” the muscle does a neat trick and bypasses the insulin signaling mechanism we saw in the “Diabesity” section. After intense exercise, muscle cells do not need an insulin signal to open the glucose transporters to let glucose in from the bloodstream. Even if you have substantial insulin resistance, after intense exercise the glucose transporters are “unhooked” fro m the insulin insulin signal. sig nal. Going back to to o ur “electronic do or ” analogy, high intensit intensity y exercise is like installing a manual door-opening mechanism which bypasses the insulin receptor receptor ’s elect electro ro nic door system. system. High intensity interval exercise not only opens the glucose transporters, but it also signals sig nals the the muscle to to make more mo re glucose transp tr anspor or ters. ters. This allows the glucose that has been accumulating in a diabetic’s bloodstream to push its way into the muscle cells, thus thus lowering blood bloo d sugar.
KEY POINT: After intense exercise, muscle cells do not need a signal from insulin to
open the the glucose transpor ter ter s to let glucose in fr om the bloodstream. The great thing about high intensity exercise is that the benefits continue for the next 1-2 days after a single 20-minute session. Glucose transporters stay active well into the next day. When this protocol was tested on diabetics, not only was their fasting blood sugar lower the following day, but their blood sugar levels after meals were were also lower fo r 24-36 24-36 hours after the wor wor kout.
This is i s the normal nor mal state of a type II II diabetic diabetic (let’s call him Jim) Ji m) with bloated fat cells spewing spewing out inflammation inflammation which blocks the insulin insulin signal sig nal from fr om opening the glucose transporter. Glucose is left in the bloodstream and builds up to toxic levels. Jim is not engaging engag ing in any exercise exerci se at this this point poi nt because because he thinks that that he doesn’t have time to spend hours in the gym.
Jim has now no w star started ted a high intensity exer exercise cise protoco pr otoco l. He He likes the fact that that he he only onl y has to spend 20 total minutes a day, day, with only 10 minutes of actual exercise. Jim has calculated his HRmax HRmax and is using the HII HIIT T pr otoco l with a tar target get heart hear t rate of 90% of his HRmax. HRmax. The high intensity intervals are decreasing his muscle glucose storage, and the muscle responds by “unhooking” “unhooking” the glucose transporters fro f ro m the insulin insulin signal, and by by making making more mo re transp tr anspor or ters. ters. The fat cells are still shooting out inflammation which block the insulin signal, but it does not matter since the transporters have “bypassed” the insulin signal. Glucose fro m his bloodstream is now pouring into into his muscles and is decreasing his blood glucose levels.
To grasp the concept, it may be easier to think of your muscles as “containers” that stor stor e glucose (as glycog en) for emergencies emerg encies like like running from fr om a bear. HIIT HIIT
deplete depletess muscle glucose and creates creates an open stor stor age area ar ea for the the glucose fr om the bloo dstream. If If you yo u did not no t deplete deplete the muscle glucose gl ucose with HIIT HIIT,, the extr extr a glucose gl ucose would build build up in the bloodstream causing causing high bloo d sugar, or it would would be converted conver ted and and stored stor ed in the fat cells as fat. f at. For these these reasons, HIIT HIIT is a very ver y powerful pr otocol for diabetes diabetes and pre-diabetes. pre-diabetes. It can substantially help keep your after-meal blood glucose levels within the target ranges discussed in earlier sections. sections. If you consistently apply this protocol with a proper diet, over time the better blood sugar control will result in increased insulin sensitivity. The pancreas will now secrete less insulin because there is less glucose in the bloodstream for it to process.
Also, Also, now that t hat t he extra glucose will will be stored sto red in the muscl muscles, es, t he fat cells cells will will not need to process the excess glucose and turn it into fat for storage. The fat cells will start shrinking, and return to their “happy state” with decreased inflammation. This is how you lose fat with HIIT
As fat cells return to their normal size over time, the decrease in inflammatory cytokines will also increase insulin sensitivity. Chronic inflammation is a major cause of “broken” insulin signaling. You can modify the HIIT protocol to fit any type of exercise. You just need to ensure your heart rate is sustained at 90% of your HRmax for 60 seconds. Find the exercise or equipment that works for you. In the exercise chapter we will discuss other high intensity exercise strategies and resistance training extensively. Resistance training coupled with HIIT will give diabetes and prediabetes a knockout kno ckout punch!
IMPORT IMPORTANT AN T MEDICAL NOTE:
As beneficial as high intensity exercise is for diabetes, it is extremely importan impor tantt that that you you fir st discuss discuss it with with your doctor before befor e starting a protocol pro tocol like li ke HII HIIT. T. This is especially especially true if you yo u have had had prio r heart attacks attacks or chest pain with with physical exer tion. If If you yo u fall into these categor categor ies, you MUS MUST T get g et appro approval val fro m your physician physician first for safety safety reasons. There are plenty of other exercise routines that you can safely do and that that will will still be beneficial. We We will cover co ver some o f these in the the exercise exerci se chapter. HIIT is highly beneficial, but make sure your heart can tolerate high intensit intensity y exercise before befo re you dive in.
STRONG MEDICINE TACTICS: Once cleared by your doctor, high intensity intensity interval interval training is a g reat method if you are short on time. Incorporate three sessions a week of HIIT in your exercise exercise program. prog ram.
STEP 8 FIX YOUR SLEE SLEEP P AN AND D USE STRESS REDUCTION TECHNIQUES. If you ar e not getting getting at least 7-9 hour hourss of restful sleep per night, your fat loss and blood sugar control g oals will come to a scr scr eeching eeching halt. We are going to extensively discuss sleep and stress reduction in following chapter chapters, s, but will get g et started with with the main points. po ints. Studies have shown that more than a third of adults in the U.S. are getting inadequate sleep—and the health consequences are more than just being tired the next day. Sleep deprivation is a large stressor and turns on the body’s “threat response.” Part of the threat response due to poor sleep is increased oxidative stress and
inflammation.
KEY POINT: Poor sleep tri trigg ggers ers your body’s body’s threat threat response. Just 1-2 nights of poor sleep have been shown to put healthy people into a nearly diabetic state of insulin resistance! Imagine what this would do to someone who is already obese or has prediabetes or diabetes. Poor sleep also promotes weight gain as a likely effect of chronic insulin resistance. resistance. Although the amount of sleep one needs can be substantially different among individuals, The National Sleep Foundation recommends between 7-9 hours of sleep per night for adults. adults.
KEY POINT: Inadequat Inadequatee sleep leads to inflammatio i nflammation n and oxidative stress, making insulin resistance resistance and other chr onic diseases worse. wor se.
STRONG MEDICINE TACTICS: To stop making insulin resist r esistance ance and and weight weight gain wor se, ensure ensure you yo u are getting between 7-9 hours of sleep per night. We are not going to delve any deeper into sleep here, since there is a whole chapter devoted to it later in this book. Just be sure to make sleep a priority; you
will not achieve your weight loss goals or healthy blood sugar levels without consistent, adequate adequate sleep. s leep. Chronic psychological or “life stresses” also activate the threat response in the brain, leading to chronic inflammation and oxidative stress. Stress reduction techniq techniques ues are crucial fo r the the chro nically stressed stressed and will be covered in i n detail detail in a for thcoming thcoming chapte chapterr devoted devoted to chronic chro nic stress.
COMING ATTRACTIONS >>> Make sure you read the Chronic Stress and Sleep chapters to fully understand the concepts, then incorporate the recommendations from those chapters into your 8-step plan.
PARTING THOUGHTS ON THE 8-STEP PLAN: In closing, make sure you pay close attention and adhere to as many of the 8 steps as possible. In doing so, you will achieve better and faster results. It is important to note that use of Step 1 will vary depending on your situation. If you are not diabetic, testing your blood sugar after meals a couple of times can still give you valuable information. If you have prediabetes or diabetes, Step 1 is extremely important to follow until you figure out what foods consistently put you out of the target ranges for blood sugar. sugar. The key to this 8-step program is consistency, and the enemy of the program is convenience. Preparing good food is time consuming, and getting fast food is convenient.
KEY POINT: Consistency is your friend with the 8-step plan. Convenience is the enemy. Spend a couple of hours on a weekend to prepare a large quantity of food for your lunches the following week. Soups and stews work well because they are relatively easy to make in large quantities. We will cover more of these ideas in the Strong Medicine Nutrition: Individualized Strategies chapter near the end of the book. Over time, consistency with the 8-step plan will lower chronic inflammation and oxidative stress, fix your leptin signaling, restore insulin sensitivity, and help you achieve achieve your weight loss and blood sugar goals go als without counting calories and being constantly hungry.
“BREAKING THE LINK” The Strong Medicine 8-Step Program for Obesity and Insulin Resistance will “break the link” in the chain between between obesity/insulin obesity/insuli n resistance r esistance and chronic chro nic disease, thus defeating the “enemy within.”
“MILITARY INTELLIGENCE” INT ELLIGENCE” (REFERENCES): Ahima RS. Di gging deeper into obesity. obesity. J Clin Invest 121 (2011): 2076-2079. Al le n DL, Hi ttel DS, & M cPherron AC. Expression andfunctio functio n of myostatin i n obesi obesi ty, diabetes, diabetes, and and exercise adap adaptation. tation. ˆ 43 (2011): 1828-1835. Neurosci 7 (2013): 51. Amitani Amitani M , Asakawa A, Ami tani H, & Inui Inui A . The role of le ptin ptin in the the control control of insuli insuli n-glucose n-glucose axis. Front Neurosci Food (2013). Bahad Bahadoran oran Z , Mi rmiran P, & Azi zi F. Potential Ef fi cacy cacy of Broccoli Sprout Sproutss as a Unique Unique Suppleme Suppleme nt for Manageme Manageme nt of Type Type 2 Di abete abete s and and Its Compli Compli cations. J Med Food (2013). Sci (Lond) 121 (2011): 43-55. Barlovi c DP, Soro-Paavonen Soro-Paavonen A, & Jandel ei t-Dahm KA. RA GE biol ogy, atheroscle rosis and diabete diabete s. Clin Sci (Lond) World J Gastroenterol 19 (2013): 1166-1172. Basaranogl anogl u M, Basaranoglu Basaranoglu G, Sabuncu ncu T, T, & Senturk Senturk H . Fructose as a ke y player i n the deve lo pment of fatty l iv er dise ase. World World J Gastroenterol 19 (2013): 1166-1172. Basaranogl anogl u M, Basaranoglu Basaranoglu G, Sabuncu ncu T, T, & Senturk Senturk H . Fructose as a ke y player i n the deve lo pment of fatty l iv er dise ase. World Neurosci 6 (2012): 49. Beel er J A, F razie r CR, & Z huang ang X. Putting Putting desi re on a budget: dopamine and and energy ex penditure, reconcil ing rew ardand and resources. resources. Front Integr Neurosci Berridge KC, H o CY, Ri chard chardJM , & Di Fe li ceantonio ceantonio AG , The tempted brain brain eats: ple asure asure anddesire ci rcuits i n obesi ty andeati ng diso diso rders. rders. Brain Res 1350 (2010): 43-64. Brandt C, et al. Pl asma and andmuscle muscle myostatin in rel ation to type 2 diabetes. PLoS One 7 (2012): e37236. Buxton OM, et al . Adverse metaboli c consequenc consequences es i n huma humans ns of prolonged sl ee p restriction combined with circadian circadian disruptio n. Sci Transl Med 4 (2012): 129ra43. Cai W, et al . Oral advanced gly cation endproduc roducts ts (AGEs) promote insuli n resistance anddiabetes by deple ting the antiox idant def def enses A GE receptor-1 and sirtuin sirtuin 1. Proc Natl Acad Sci U S A 109 (2012): 15888-15893. Cavalot F, e t al. Postprandial bl ood glucose i s a stronger stronger predictor of cardio cardio vascular vascular ev ents than than fasting blood gl ucose ucose i n type type 2 diabetes mel li tus, particu particularly larly in wome n: lesso ns from the San Luigi Gonzaga Di abete abete s Study. J Clin Endocrinol Metab 91 (2006): 813-819. Chan KH, et al. Adiponectin is protective against oxidative stress induced cytotoxicity in amyloid-beta neurotoxicity. PLoS One 7 (2012): e52354. Chapu Chaput J P, Doucet E, & Tremblay A . Obesity: a dise ase or a biol ogi cal adapta adaptation? tion? An update. date. Obes Rev 13 (2012), 681-691. Chavali Chavali V, Tyagi SC, & Mi shra shra PK. Predictors and preventi on of diabetic cardio myopathy. Diabetes y. Diabetes Metab Syndr Obes 6 (2013): 151-160. Thromb H aemost 109 (2013). Chmelar J, Chung Chung KJ, & Chavaki Chavaki s T. The role o f i nnate immune cell s in obese adipose adipose ti ssue infl ammation and anddevel opment of i nsuli n resi stance. stance. Thromb Cruje Cruje iras AB, Di az-L agares A, Carrei Carrei ra MC, Ami l M , & Casanu Casanueva FF. Oxi dativ dativ e stress associated to dysfunctional adipose tissue: a potential l ink betwee n obesi obesi ty, type 2 diabetes me ll itus and and breast canc cancer. er. Free Radic Res 47 (2013): 243-256. Cui H, Kong Y, Y, & Z hang hang H. Oxidative stress, mi tochond tochondrial rial dysfunction, andaging. J Signal Transduct (2012): (2012): 646354. Clin Nutr Nutr 67 (2013): 455-461. Davidenk o O, Darcel Darcel N, F romentin G, & Tome D. Control of protei n and andenergy i ntak ntak e - brain mechan mechanisms. isms. Eur J Clin Longev (2013): 564961. De M archi archi E, Baldassari Baldassari F, Bononi A, W ie cko wsk i M R, & Pi nton P. Oxidative Stress i n Card Cardio io vascular vascular Di seases and Obesi Obesi ty: Ro le of p66Shc and and Protei Protei n Kinase C. Oxid Me d Cell Longev Neuroendocrinology 93 (2011): 9-18. Donato JJ, Cravo RM , Frazao R, & Eli as CF. CF. Hypothalamic Hypothalamic si tes of l eptin action action li nki ng metabol ism and reprodu reproduction. ction. Neuroendocrinology Drong AW, AW, Li ndgren CM, & M cCarthy cCarthy MI. The ge netic and epige netic basis of type 2 diabetes and obesity. Clin Pharmacol Ther 92 (2012): 707-715. Egecioglu E, et al. Hedonic and incentive signals for body weight control. Rev Endocr Metab Disord 12 (2011): 141-151. El ias CF, & Purohit Purohit D. Leptin si gnaling and circuits circuits i n pub puberty andfe rtil ity. Cell Mol Life Sci 70 (2013): 841-862. Redox Signal 7 (2005): 1040-1052. Evans JL, M addu addux BA, & Gol dfine ID . The mole cular cular basis basis f or oxidative stress-i nduced uced insuli insuli n resi stance. stance. Antioxid Redox Faraut B, Boudjel tia K Z , Vanhamme hamme L , & Ke rkhofs M . Immune, i nflammatory and and card cardio io vascular vascular consequences of sle ep restricti on and and recovery. Sleep Med Rev 16 (2012): 137-149. Galvi n JE . O Optimiz ptimiz ing diagnosi diagnosi s and manan manangeme geme nt in mil d-to-moderate alzhei mer’s disease. Neurodegener Dis Manag 2 (2012): 291-304. Gi ll en JB, et al . Acute Acute high-i ntensity interval e xercise reduces the postpr postpran andial dial gl ucose ucose response and and preval preval ence of hypergly- caemia in patie patie nts wi th type 2 diabetes. diabetes. Diabetes Obes Metab 14 (2012): 575-577. Gil lum MP, et al. Si rT1 regulates regulates adipose adipose ti ssue ssue i nflammation. nflammation. Diabetes 60 (2011): 3235-3245. Toxicol Pathol 64 (2012): 503-508. Guerrero-Bel tranCE, Calderon-Oli ver M , Pedraza-Chaverri Pedraza-Chaverri J , & Chirino YI, Protective ef fe ct of sulfo raphane hane against oxidative stre ss: recent advan advances. Exp Toxicol Gulati M , et al. He art rate response response to exe rcise stress testi ng in asymptomatic asymptomatic women: the st. J ames women take heart heart proje proje ct. Circulation 122 (2010): 130-137. Guldbrand H, et al. In type 2 diabetes, randomisation to advice to follow a low-carbohydrate diet transiently improves glycaemic control compared with advice to follow a low-fat diet producing a similar weight loss. Diabetologia Diabetologia 55 (2012): 2118-2127. 263 Gutteridge Gutteridge JM , & Hall iwe ll B, Antioxidants: Mol ecule ecule s, medicines, and and myths. Biochem Biophys Res Commun 393 (2010): 561-564. Hall iw el l B. F ree radicals and and antioxi antioxi dants: dants: updating dating a personal personal vi ew. Nutr Rev 70 (2012): 257-265. Clin Pharmacol 75 (2013): 637-644. Halliwell B. The antioxidant paradox: less paradoxical now? Br J Clin Nutr 88 (2008): 578S-581S. Hayes D P. Adverse e ff ects of nutriti onal i nadequ nadequacy and excess: a hormetic model . Am J Clin Nutr Henrik sen EJ, Di amond-Stanic -Stanic M K, & Marchio Marchio nne EM , Oxidative stress and the etio lo gy of i nsuli n resi stance stance and and type 2 diabete diabete s. Free Radic Biol Med 51 (2011): 993-999. Hittel DS, Berggren JR, Shearer Shearer J, Boyle K, & Ho umar umard d JA, I ncreased secretion secretion and expression of myostatin myostatin in sk el etal muscle muscle from extremely obese women. Diabetes 58 (2009): 30-38. Howitz KT, & Sinclair DA. Xenohormesis: sensing the chemical cues of other species. Cell 133 (2008): 387-391. Inflam (2011): 720926. Itoh M, Sugana Suganami mi T, Hachiya R, & Ogawa Y. Adipose ti ssue remodel ing as homeostatic i nflammation. Int J Inflam (2011): Je on MJ , et al . Mi tochondrial drial dysfunction and and activati activati on of i NOS are are responsible responsible for the palmi palmi tate-i nduced uced decrease decrease i n adipon adiponectin ectin synthesi synthesi s in 3T3L 1 adipocytes. adipocytes. Exp Mol Med 44 (2012): 562-570. Ji ao P, et al . FFA- induced induced adipocyte i nflammation andinsuli n resi resi stance: stance: i nvolve ment of ER stress and and IKKbeta pathways. pathways. Obesity Obesity (Silv er Spring) Spring) 19 (2011): 483-491. Jo urnel urnel M , Chaumon Chaumontet tet C, Darcel N , Fromenti n G, & Tome Tome D. Brain responses responses to high-protei high-protei n die ts. Adv Nutr 3 (2012): 322-329. Keating S, & El-Osta A. Epigenetic changes in diabetes. Clin Genet (2013). (2013). Kenny PJ. R eward mechan mechanisms isms in obesi ty: new i nsights and future directi ons. Neuron ons. Neuron 69 (2011): 664-679. Metab (Lond) 8 (2011): 75. Kl eme nt RJ , & Kammerer U . Is there a rol e f or carboh carbohydr ydrate ate restricti on in the treatment and andpreve preve ntion of cancer? cancer? Nutr Metab (Lond) Landry D, Clo utier F, & Martin LJ . Impli cations of l eptin in neuroend neuroendocrine ocrine regulati on of male reprodu reproduction. ction. Reprod Biol 13 (2013): 1-14. Lei dy HJ, Ortinau Ortinau LC, Douglas SM, & Hoe rtel HA . Benefi cial e ff ects of a hig her-protei her-protei n break break fast on the app appeti tive , hormona hormonal, l, and neural si gnals controll ing energy intake regulatio n in overwe ig ht/obese , “breakf astNutr 97 (2013): 677-688. ski pping,” l ate-adole ate-adole scent scent girl s. Am s. Am J Clin Nutr
Li ttle JP, et al. Lo w-v ol ume hig hig h-intensity i nterval training reduc reduces es hyperglycemi a and increases increases muscle mi tochondrial drial capacity i n patie nts with type type 2 diabete diabete s. J Appl Physiol 111 (2011): 1554-1560. Logue J , et al . Obesi Obesi ty is associ ated with fatal coronary coronary heart heart dise dise ase i ndependently ependently o f traditi traditi onal risk factors and deprivati on. Heart 97 (2011): 564-568. Acta (2013). Louie SM, R oberts LS, & Nomura DK. M echanisms l ink ing obesi ty and and can cancer. cer. Biochim Biophys Acta (2013). Lumeng CN. Innate Innate i mmune activati on in obesity. Mol obesity. Mol Aspects Med 34 (2013): 12-29. Lumeng Lumeng CN, & Saltiel AR. Inflammatory Inflammatory li nks between obesity an and d metabolic metabolic disease. J Clin Invest 121 (2011): 2111-2117. Mul le r JE, e t al. Carbohyd Carbohydrate rate restricted die t in conjunct conjunctio io n with metformi n and and li raglutide is an eff ecti ve treatment in patie patie nts with dete riorated type type 2 diabetes me ll itus: Proof-of -concept study. Nutr Metab (Lond) 8 (2011): 92. Rev M ol Cell Biol 9 (2008): 193-205. Muoio DM, & Newgard CB. Mechanisms of disease: molecular and metabolic mechanisms of insulin resistance and beta-cell failure in type 2 diabetes. Nat Rev World J Gastroenterol 16 (2010): 2579-2588. Nsei r W, Nassar F, & Assy N, Soft drinks consumptio n and nonalcoholi c fatty li ver dise ase. World Okwan-Duodu D, U mpierrez G E, Brawle y OW, & Diaz R . Obesi ty-drive n inflammation andcancer risk : role of mye lo id derive d suppressor cell s and and alte alte rnately rnately activated macrop macropha hages. ges. Am J Cancer Res 3 (2013): 21-33. Olefsk y J M. IKKe psil psil on: a bridge between obesity obesity and and inflammation. inflammation. Cell 138 (2009): 834-836. Rev I mmunol 11 mmunol 11 (2011): 85-97. Ouchi chi N, Parke r JL, Lugus JJ, & Walsh K. Adipok ines i n inflammation and and metaboli c dise ase. Nat Rev Longev 2 (2009): 270-278. Pandey KB, & Ri zvi SI. Pl ant ant polyphenols as die tary antiox idants idants i n huma human n heal heal th and dise dise ase. Oxid Med Cell Longev Paul L. Diet, nutrition and telomere length. J Nutr Biochem 22 (2011): 895-901. Qi Y, Y, et al. A diponecti diponecti n acts acts i n the the brain to decrease body wei ght. Nat ght. Nat Med 10 (2004): 524-529. RahmanI, Bi swas SK, & Ki rkham PA. R egulati on of i nflammation and and redox redox si gnaling by die die tary pol yphenol yphenol s. Biochem Pharmacol 72 (2006): 1439-1452. Ri stow M , & Sch Schmei mei sser S. Extending Extending li fe span by increasing increasing oxi dativ dativ e stress. Free Radic Biol Med 51 (2011): 327-336. Ri stow M , & Zarse K. Ho w increased oxidative stress promotes lo ngevi ty and and metaboli c heal th: The concept concept of mitochondrial hormesi s (mitohormesis). Exp Gerontol 45 (2010): 410-418. Atheroscler Re p 14 (2012): 563-569. Ri vel le se AA, Giacco R, & Costabile Costabile G, Di etary etary carboh carbohydrates ydrates for diabetics. Curr Atheroscler Ro el ofse n H, Priebe M G, & Vonk Vonk R J. T he interactio interactio n of short-cha short-chain in fatty acids with adipose adipose tissue: rel evance for preventio preventio n of type 2 diabetes. Benef Microbes 1 (2010): 433-437. Sandovici I, H ammerle CM, Ozanne Ozanne SE, & Constancia M . De vel opmental opmental and and environmental environmental epige netic programming programming of the endocrine endocrine pancreas: consequences sequences fo r type 2 diabetes. diabetes. Cell Mol Life Sci 70 (2013): 1575-1595. Santos FL, E steve s SS, da Costa Perei Perei ra A, Yancy ancy WSJ , & Nunes Nunes J P. Systematic revi ew and meta-analysi s of cl ini cal trials of the eff ects of l ow carbohydrate diets on cardiovascular cardiovascular risk risk factors. Obes Rev 13 (2012): 10481066. Savini I, Catani MV, Evangelista D, Gasperi V, & Avigliano L. Obesity-associated oxidative stress: strategies finalized to improve redox state. Int J Mol Sci 14 (2013): 10497-10538. 264 Neurobiol 44 (2011): 192-201. Scapa Scapagnini gnini G , et al . M odulati odulati on of Nrf2 /AR E pathway by food polyphenols: a nutriti onal neuropr neuroprotecti otecti ve strategy for cogniti ve and neurodege eurodege nerative di sorders. sorders. Mol Neurobiol Schmid SM, e t al. Di sturbed sturbed glucoregulatory glucoregulatory response to food intake after moderate sle ep restriction. Sleep 34 (2011): 371-377. Seyfri ed TN, et al . M etaboli c management of brain can cancer. cer. Biochim Biophys Acta 1807 (2011): 577-594. Seyfri ed TN, M arshJ, Shel Shel ton LM, H uysentruyt uysentruyt LC, & Muk herjee P. Is the restri cted ke togeni c die die t a viable alte rnative rnative to the standa standard rd of care care f or managing managing mali gnant brain brain cancer? Epilepsy Res 100 (2012): 310-326. Metab (Lond) 7 (2010): 7. Seyfri ed TN, & Shel ton LM. Cancer Cancer as a metabol metabol ic dise ase. Nutr Metab (Lond) Enteral Nutr 32 (2008): 638-644. Shah Shah A, M ehta N, & Rei ll y M P. Adipose i nflammation, i nsuli n resi resi stance, stance, andcardiovascular cardiovascular dise ase. JPEN J Parenter Enteral Nutr Shammas MA. Telomeres, lifestyle, cancer, and aging. Curr Opin Clin Nutr Metab Care 14 (2011): 28-34. Shen Shen J, Obin M S, & Z hao hao L. T he gut microbio microbio ta, obesity and and insuli insuli n resi resi stance. stance. Mol Aspects Med 34 (2013): 39-58. Sie s H, e t al. Protection by fl avanol avanol -rich foo ds against against vascular dysfunc dysfunction tion and oxi dativ dativ e damage: 27th Hohenheim Co nsensus Conference. Adv Nutr 3 (2012): 217-221. Singh S, Vrishni S, Singh BK, Rahman I, & K akk ar P. Nrf2- AR E stress response mechanism: a control point i n oxidative stress-me diated dysfunc dysfunctio tio ns and chronic infl ammatory ammatory dise ases. Free Radic Res 44 (2010): 12671288. Siow R C, & Mann GE. Di etary isof lavo nes and vascu vascular lar protectio protectio n: activation of cel lul ar antio antio xi dant dant defenses by SERM s or hormesi s? Mol Aspects Med 31 (2010): 468-477. Obesity (Sil ver Spring) Siri- Tarino Tarino PW, Wi ll iams PT, Fernstrom HS, Rawl ings RS, & Krauss Krauss RM . Re versal of small , dense dense LDL subclass phenotype henotype by normali normali zatio n of adiposity. Obesity (Sil Spring) 17 (2009): 1768-1775. Speci Speci ale A , Chirafisi J , Saij a A, & Cimi no F. Nutriti Nutriti onal antio antio xi dants dants and adap adaptive tive cel l responses: an update. date. Curr Mol Med 11 (2011): 770-789. St-Onge St-Onge M P, Bosarge A, Goree LL, & Darnel Darnel l B. M edium chain trigl yceride oi l consumption consumption as as part part of a weig ht loss diet does not lead to an an adverse adverse metaboli c profi profi le when compa compared red to oli ve oi l. J Am Coll Nutr 27 (2008), (2008), 547-5 52. Lipidol (2013). Stanhope hope KL, Schwarz Schwarz J M, & Have l PJ . Adverse metaboli c eff ects of die tary fructose: results from the recent epidemi ol ogi cal, cli nical, and and mechanisti anisti c studies. Curr Opin Lipidol (2013). Endocrinol 366 (2013): 215-223. Stark Stark R, Ashle y SE, & Andrews Andrews Z B. AM PK and and the neuroendocrine neuroendocrine regulati on of appeti appeti te and energy e xpenditure. Mol Cell Endocrinol Stevenson DE, & Hurst RD . Poly phenoli c phytochemicals- -j ust antioxi antioxi dants dants or much more? Cell Mol Life Sci 64 (2007): 2900-2916. Stout Stout R D, e t al. M acroph acrophages ages se quential ly chan change ge thei r functional functional phenotype phenotype i n response response to changes changes i n microenvironmental microenvironmental infl uences. uences. J Immunol 175 (2005): 342-349. Sugana Suganami mi T, & Ogawa Y. Adipose tissue macrophages: thei r role in adipose ti ssue remodel ing. J Leukoc Biol 88 (2010): 33-39. Res (2012): 824305. Suzuki Suzuki K, J ayasena CN, & Blo om SR. Obesity and appetite appetite control control . Exp Diabetes Res (2012): Szasz T, Bomfi m GF, & Webb RC. T he infl uence uence of perivascular adipose adipose tissue on vascular vascular homeostasis. Vasc He alth Risk Manag 9 (2013): 105-116. Lab Invest 90 (2010): 1117-1127. Tak Tak euchi euchi M, et al . Immunologi cal detectio n of fructose-deriv ed advanc advanced ed gl ycation end-prod end-produc ucts. ts. Lab Tana Tanak k a H, Mo naha nahan n KD, & Seals DR . Age -predicted maximal heart rate rate revi site d. J Am Coll Cardiol 37 (2001): 153-156. Thund Thundyi l J , Pavlovsk i D , Sobey CG, & Arumugam TV. Adiponectin Adiponectin receptor signalli ng in the the brain. brain. Br J Pharmacol 165 (2012): 313-327. Tremblay A, & Chapu Chaput JP. Obesity: the all ostatic lo ad of we ig ht lo ss dieti ng. Physiol Behav 106 (2012): 16-21. Tsuji H, e t al. D ie tary medium-chain medium-chain triacylgl ycerol s suppr suppress ess accumulation accumulation of body body fat i n a double ouble -bli nd, control control le d trial trial in healthy men and and women. J Nutr 131 (2001): 2853-2859. U padh padhyay M , Samal J , K andp andpal M, Singh OV, & Vi vek anan ananda dan n P. The Warbu Warburg ef fe ct: insig hts from the past decade. Pharma Pharmacol col Ther 137 (2013): 318-330. U ribarri ribarri J , et al. A dvanced gly cation end products in foo ds and a prac practical tical guide to thei r reduction i n the the die t. J Am Diet Assoc 110 (2010): 911-16.e12. U zi el O, et al. Telome re dynamics dynamics in arterie arterie s and and mononuc mononucle le ar cel ls of diabetic patie patie nts: ef fe ct of diabete diabete s and and of gl ycemi c control. Exp Gerontol 42 (2007): 971-978. Vach Vachha harajan rajanii V, & Granger Granger DN . Adipose tissue: a moto r for the i nflammation associated wi th obesi obesi ty. IUBMB Life 61 (2009): 424-430.
Vand Vander He iden M G, Cantley LC, & Thompson CB. CB. U nderstanding erstanding the the Warbur Warburg g ef fe ct: the the me tabol tabol ic requirements of ce ll prol prol if eration. Science 324 (2009): 1029-1033. Vl assara assara H, et al . Protection against lo ss of i nnate defe nses in adulthood by low advanced advanced glycati on end produ products cts (AGE) intake : role of the antii nflammatory AGE re ceptor-1. J Clin Endocrinol Metab 94 (2009): 4483-4491. Rev Endocrinol 7 (2011): 526-539. Vl assara assara H, & Strik Strik er GE. AG E restrictio n in diabete diabete s mel li tus: a para paradigm digm shift. Nat Rev Well en KE, & Hotamisl igi l GS. Inflammation, Inflammation, stress, stress, and and diabetes. diabetes. J Clin Invest 115 (2005): 1111-1119. Wellen KE, & Thompson CB. Cellular metabolic stress: considering how cells respond to nutrient excess. Mol Cell 40 (2010): 323-332. Westerterp-Plantenga MS, Lemmens SG, & Westerterp KR. Dietary protein - its role in satiety, energetics, weight loss and health. Br J Nutr 108 Suppl 2 (2012): S105-12. Sportsmed 39 (2011): 172-178. Wroble wsk i AP, Amati F, Smile y MA , Goodpaster Goodpaster B, & Wright V. V. Chronic Chronic exercise prese prese rves l ean muscle mass i n masters athlete athlete s. Phys Sportsmed Yu JH , & Kim M S. Mol ecular mechanisms anisms of appetite appetite re gulatio n. Diabetes n. Diabetes Metab J 36 (2012
KNOWING KNOW ING YOUR ENEMY III: III:
CHRONIC STRESS: THE SILENT SILEN T KILLER
Chronic psychological stress affects us all to varying degrees. Psychological stress is a serious problem that can lead to physical maladies. Sustained stress in particular causes tangible, medically definable harm to the body and brain. Chronic stress causes premature ageing while those who have conquer conquer ed str str ess look years younger than than their their chro nological nolo gical age. Very real physical changes occur to those who have continual chronic stress. Chronic stress can be overcome by using proven stress-relieving strategies and methods. Stress has been called the silent killer, but can be overcome with knowledge and a game plan. Chronic stress is a master assassin that kills with a thousand small cuts over time. He will worm his way inside your brain and wreak havoc. As you will see, this silent member of the Pentaverate will actually change your brain and affect your body fro m the inside. inside. The Strong Medicine training team has studied the ways of this killer and devised effective defenses against him.
CHRONIC STRESS AND DISEASE Recent research has linked chronic stress to a multitude of diseases. For many of these diseases, stress is either thought to be the actual cause of the disease, or at the very least, stress makes any disease worse.
DISEASES ASSOCIATED WITH CHRONIC STRESS
• Obesity • Diabetes • Alzheimer’s dementia and other neurodegenerative diseases • High blood pressure • Heart disease disease • Depression and anxiety • Chronic pain • Cancer Even with the association of chronic stress to the above diseases, most patients do not bring up their chronic stress when discussing their health concerns with their doctor, and most doctors don’t ask their patients about stress levels. There are ro adblocks for having having this this cr ucial discussion.. discussion... • Many physicians feel they they are ar e physical custodians, not mental custodians, and refuse to offer advice or recommendations regarding stress reduction. • Most physicians don’t have specific advice or recomm r ecommendat endatio ions ns to give gi ve their patients patients to effectively r educe str str ess. • Chro Chro nic stress is still not r ecognized as a serious serio us r isk factor factor leading to disease. disease. • Historically Histor ically there have been no go od medical tests tests to evaluate chro nic stress.
This is starting to change. change. • Mental health and physical health health are ar e still viewed viewed as separ separate ate and distinct and obviously obvio usly that is flawed fl awed thinking. thinking. Your mental health is really an extension of your physical state. Mind and body need be addressed as an organic whole. Chronic stress will prevent us fro
att ainin ainingg any and all all body-composition body-composition and fitness fit ness go als. als.
CHRONIC STRESS I
MIND AN A N D BODY: BODY: WA WA S DESCA DES CARTES RTES WRONG?
Rene Descartes (1596- 1650) French mathematician mathematician and philosopher Rene Descartes (1596 - 1650) was a brilliant 17th century mathematician and philosopher widely widely considered the father father of modern philosophy. philosophy. One One of his centr centr al philosophical tenets is the idea of dual nature—we have a mind and we have a body. Descartes proposed the theory of mind-body dualism—the body and the thinking,
conscious mind exist in separate parallel universes. For Descartes, the body was a material object following the laws of nature, while the thinking conscious mind was “nonmaterial,” and not subject to these laws. He contended that the body and mind can influence each other, o ther, but ultimately remain remai n separate separ ate and distinct. distinct. Descartes’s philosophy founded the idea that psychology and neuroscience are separate and distinct disciplines—and should remain that way. Psychology deals with the “non-material” thinking mind while neuroscience explores the actual mechanical workings of the physical brain. Increasingly, modern science is discovering that this is not how the mind and body function. Both form an intertwined, indivisible whole. New fields of study such as neuropsychology and psychoneuroendoncri psychoneuroendoncrinolog nolog y explore this this mind/body connection. connection.
UNION OF MIND MIND AND A ND BODY Our conscious co nscious and subconscious subconscious mind is r esponsible for so many things things on o n many levels. The brain is Command Central, Headquarters, the place where projection and reflection reside. It is able to switch tasks, compute, calculate, interface ongoing changes in our environment, then determine our next actions and reactions. Consciousness Conscio usness always occurs occur s in the exact present pres ent time. time. The brain monitors critical operations of the body, such as the second to second function of the heart and lungs for example. Though the brain itself is a physical organ, it has produced the non-physical consciousness of our mind and is able to manifest our intellect, personality and behavior. The actual physical brain is
constantly shaped, changed, and literally reconfigured, based on our experiences, thoughts and perceptions.
THE CHANGING BRAIN Ideas, thoughts, attitudes and perceptions can literally change the brain’s “hardwiring.” New technology now allows us to track these brain circuitry changes. Brain plasticity is not new age nonsense designed to fleece hippies—technical advances are allowing us to actually see how the human brain can rewire itself. If the rewiring is in response to repeated, ongoing physical and psychological stress, then it is a bad thing—but, if the rewiring is in response to activating new and exciting ar eas of the untapp untapped ed brain, brai n, then then it is a fabulous fabulo us thing. Change to the physical structure and function of the brain in response to internal and external stimuli is known as neuroplasticity. The original definition of the word plastic is, “Easily modeled or molded, capable of adapting to various
conditions.” The human brain is “plastic” as well, and can mold or adapt itself to various vario us conditions conditions throughout thro ughout a lifetime.
KEY POINT: Neuroplasticity refers to the brain’s ability to physically change its structure and function to adapt to changing environmental conditions. The most current research shows that the human brain contains approximately 86 billion nerve cells (neurons) and almost an equal amount of “support cells” (glial cells). There are about 25 times more cells in a single human brain than there are people on the planet. Even more mind-blowing is the fact that each of the 86 billion nerve cells can form up to 1000 connections with other cells in the brain. The total number of potential connections formed between nerve cells has been estimated at sever sever al hundr hundr ed tr tr illion. illio n. The possibilities are l iterally endless. Let us take a look at the nerve cells and how they make these trillions of connections. The synapses, or “connections” between axons and dendrites of neighboring nerve cells are “made” and “unmade” constantly, depending on environmental circumstances. The making and unmaking of these connections is the definition of neuroplasticity.
The picture picture above is a dr awing awing of o f a nerve cell (neuron): (neuro n):
• T he cell body of the neuron is the cell’s “control center” and the location of the the energy-producing energ y-producing machinery keeping the neuro neuron n alive.
• The dendrites receive signals from the other nerve cells. You can think of them them as satellite satellite dishes receiving incoming transmissions to the neuro neuron n cell body bo dy.. nerve cell to o ther ther nerve cells in • The axons transmit signals fro m the nerve the brain, and also to other cells (like muscle cells) in the body. The light blue “blocks” covering the axon in the picture above act as insulation allowing the signals transmitted by nerve cells to travel farther. This insulation is called myelin, and acts just like the insulative coating around electrical wires, which allows electricity to flow without “short circuits.”
THE ULTIMATE WIRING DIAGRAM Billions of nerve cells communicate with each other via the dendrite “receivers” and the axon “transmitters.” This graphic only shows 6 nerve Imagine t he com co mplexit plexit y cells (neurons) connecting and communicating. Imagine
of bill billions ions of nerve cells cells each formin formingg up to t o 1000 connections! The yellow glow at the connection (synapse) of o f an axon “transmitte “transmitterr ” betwe between en one neuro n to the dendrite dendrite “receive “r eceiver” r” of another another neuron illustrates the communication signal passed along the chain of neurons. This is how your brain communicates within itself and the rest of the body. When you want to move your leg, this is how the signals pass from the
brain all the way to your muscles to tell them to move. This system is also how the body communicates changes in your outside environment to the brain. This is how signals about touch, taste, smell, sight, hearing, heat, cold, and danger danger are communica co mmunicated ted from fr om body bo dy to to br ain.
KEY POINT: Neuroplasticity occurs because of nerve cells making and unmaking connections. This process pr ocess can start just minutes minutes after a new stimulus to the brain. Like a muscle, the human brain has a “use it or lose it” quality. When we stop perfor ming r egular physical physical activity activity,, our muscles shrink, and and bones become brittle. brittle. Stressing our body purposefully and intelligently with exercise halts these negative physical physical pro cesses. The brain is no different. Your brain will adapt to the challenges you give it by forming new connections. Without challenges, the circuit connections wither away. We challenge the brain by taking on new and mentally complex tasks outside our normal scope of activities. This includes difficult tasks like learning a foreign language, taking up a musical instrument, reading classical literature, composing poetry, sculpting, painting, or mastering another new and different skill. There are two elements critical to invoking positive brain plasticity. First, the new skill needs to be different from the skills you already possess—new skills activate new regions of the brain. Second, the skill needs to be sufficiently complex—we need intellectual stimulation, not moronic “stupefaction.” Mental challenges cause an “adaptive respo nse” to take place in the brain, just like a muscle. Challenges build axon-dendrite “transmitter-receiver” connections. Passive activities such as watching “reality” television do not stimulate or build these connections. We need to be actively involved with our activities, instead of being passive observers. Making and unmaking nerve cell connections (neuro plasticity) dictates dictates how well the brain can handle stress.
THIS IS YOUR YOUR BRAIN BRA IN ON STR STRESS ESS
Stress actually changes the brain’s structure and function through neuroplasticity. Brain cell changes and alterations will affect how you think, act and behave. The duration and intensity of psychological stress makes a huge difference in how the brain r esponds to to stress.
• Isolated, short-t short-t erm stresses such as an arg arg ument with with your friend fri end or spouse, final exam week at college, or an unexpected expense temporarily causing financial stress, str ess, can all actually lead to r esiliency esili ency.. Resiliency means that after the short-term stresses, you rebound and are able to deal with future stresses that come along much better. Think of the difference between a college freshman going through her first exams, versus a graduate student who has spent the last 45 years dealing deali ng with exams. The gr g r aduate aduate student student is much less stressed abo ut exams than the the freshman. fr eshman. The gr g r ad student student has has survived sur vived the short-term short-ter m final exam str str ess many times times before befor e and is now mor e resilient r esilient.. Her Her brain has made axondendrite “transmitter-receiver” connections that allow her to deal with the stress of final exams better. The freshman is just starting the process of building the brain brai n connections that enhance enhance exam resiliency. resi liency.
FLASHBACK Do a quick r eview of Centr Centr al Themes T hemes IV, IV, “Stress and the Response to Threat,” befor befor e you read on. The freshman has never encountered this level of exam stress before and her brain registers the exams as a significant threat. This produces the threat response. The graduate student’s brain, fortified against the stress of final exams from fro m years of o f experience, perceives perceives the the exams as far less o f a threat. Short-term, intermittent stressors of relatively low intensity will build resiliency to future stress and decrease the threat response.
KEY POINT:
Occasional, relatively low intensity intensity str str essors essor s will build resiliency r esiliency and prote pro tect ct you you from fr om future stress thro through ugh “re-wiring ” the the brain (neuroplasticity).
• Chronic Chronic stress, st ress, or high high intensity intensity stress st ress alters the brain much differ ently, ently, and much more radically—in a negative, detrimental way—than short term, low intensity stress. Chronic stress and high intensity stress (such as combat stress, auto accidents, or other traumatic events) alter brain “transmitter-receiver” connections that strengthen the stress response over time to threats. The connections that strengthen the stress response do not make you more resilient to future future stress; str ess; instead instead you become mo r e vulnerable to the effects effects of o f psychological psycholog ical stress. Intense trauma makes you more sensitive to threats in your daily life.
Many of us under chronic stress can relate to having “little things” set us off, and not being able to handle minor stresses that we used to take in stride. This feeling of being always always “stressed out” is because our brain’s thr thr eat syste system m has been rewired in r esponse to to chronic stress. str ess. From Fro m a strictly sur sur vival standp standpoint, oint, your br ain is trying to pr otect you from fr om a persistent persi stent threat. Remember fr f r om Centr Centr al Themes T hemes IV that that the the brain’s br ain’s thr thr eat response doesn’t know if your “threats” are a nasty boss at work, financial worries, or dealing with a troubled teenager. All it knows is that you are under a daily “threat” and it responds by strengthening your threat response. The problem is, the st rengthened long-t long-t erm threat response response
is not good go od for your health. health.
KEY POINT: Chronic stress “re-wires” the brain to strengthen the stress response to threat. This physical change in the brain will make you more sensitive to
future future stress with with poor poo r long-te long -terr m health effect effects. s. We will diagram the “re-wiring” of the brain to help you visualize what happens to certain regions of the brain during chronic stress. The Hypothalamic-PituitaryAdrenal axis (HPA (HPA axis) is i s a “hard-wir ed” stress r esponse system. The HPA HPA axis and the Sympathetic Nervous System produce stress hormones such as cortisol, epinephrine, and norepinephrine. These hormones are released when preparing for a “fight or flight” situat situation. ion.
THE HPA-AX HPA-AXIS IS:: HYPOTHALAMUS HYPOTHALAM US-PITUITARY-ADRENAL • T he fast pathwa pathwayy is trigg tr igg ered immediately immediately after the brain senses a threat. It bypasses the pituitary pituitary and sends a dir di r ect signal to the adrenals to produce epinephrine (adrenaline) and norepinephrine. This pathway immediately puts you in an alert state, and prepares you to “fight” or “flee” from danger. threats, but responds slowly slo wly,, • T he slow pathway is also trigg ered by threats, signaling the adrenal gland to to secr ete ete cor tisol. Cortisol helps you recover from the threat after it has passed.
cortisol, epinephrine, and norepinephrine The HPA axis induced hormones— cortisol, have the following actions on the body and brain: • They increase the the energy available available to the the body by increasing blood sugar. sugar.
• They increase heart r ate ate and blood bloo d pressure. • They increase blood bloo d flow to muscles • They pro duce hyper vigilant vigi lant behavior (watchfulness, (watchfulness, anxiousness, alertness) aler tness) The HPA axis—both slow and fast pathways—is triggered in response to any stress perceived as a threat by the brain. It is a well-designed system, but is only meant to operate o perate in response r esponse to “threats” “threats” in our o ur environment. environment.
pathway triggers the sympathetic nervous system (flight or fight). The The fast pathway result is the release of epinephrine (adrenaline), and a hormone that closely resembles epinephrine called norepinephrine. Both of these hormonal messengers increase alertness, release stored glucose from the liver into the bloodstream, increase heart rate, stop digestion, and increase blood supply to the muscles—all in anticipation of either fighting hard or running away fast. This particular pathway will make you jittery after a heated confrontation or disoriented after a car accident. The slow pathway goes through the pituitary gland on the way to the adrenal glands. This pathway is the most active about 30 minutes after the threat has passed. Cortisol is the primary hormone that helps you recover from the threat, and it prepares the body and brain for any future threats. Cortisol releases glucose from the liver to ensure the brain has enough fuel to deal with the threat. Cortisol will also “assist” in breaking muscles down (muscle cannibalism) so the amino acids in the muscle protein can be used to make more glucose for the brain. In certain circumstances, cortisol helps the body eat itself. One reason many marathon and ultra-marathon runners look emaciated is they are awash in cortisol to the point that caloric calor ic shor tfalls tfalls ar e fed with with the runners’ own muscles. muscles.
As far far as our brain is concerned, many of us are
“chased by bears” daily. This system was never meant to be used daily. A majority of the population overuses and over -works this system system in r esponse to to modern threats threats such as abusive abusive bosses, snarled snarled traffic, domestic relationship and and financial financial problems pr oblems or poor sleep. As far as our brain is concerned, many of us are “chased by bears” daily. While the degr degr ee to which the the system is activated activated will not r egister egi ster as hig h as actually being chased by a bear or an assailant, we still activate it in lesser degrees when responding to the constant daily stresses of modern life. Our stresses add up to the proverbial “death of a thousand cuts.”
THREA THRE AT AN AND D THE TH E STRESS RESPONSE RESPONSE What determines if the HPA axis is activated to produce the stress response? Anything the brain perceives as threatening from within the body or from our external envir onment will activate the the HPA HPA and pro duce a stress r esponse. • Potential Potential threats arising ar ising within within the body include infection, injury injur y, toxins or sickness. Internal Inter nal threats do not have to t o be processed by higher levels l evels of the subco nscious per ceives the inter internal nal threat and tr tr igger ig ger s the HP HPA axis to brain. The subconscious greater and lesser degrees. • Higher levels levels of the the brain pr pr ocess external external threats threats that that arise in our environment and ente enterr into into our consciousness. Exte Exterr nal threats threats require requir e a series ser ies of “decisions” “decisions” which need be made—the seriousness of the threat is assessed, and a course of action is devised.
KEY POINT: Potential Potential threats threats from fro m our external external enviro nment nment are fir st processed by higher levels of the brain befor e they they are determined determined to be threatening threatening or non-threatening. Degree of threat and threat response will vary radically from individual to individual. What is perceived as threatening to one person is considered no threat
whatsoever to a harder type. The difference between individuals in the perception of threat is experiential: a Navy SEAL under fire during combat will show a lower threat response and less agitation than a distraught teenager dumped by a boyfriend or girlfriend. girlfriend.
For simplicity’s sake, our discussion will be limited to the three parts of the higher brain instrumental in perceiving threats and initiating the stress response. The workings of the brain are staggeringly complex, and the following is substantially simplified from the current science of the brain and threat response. Let’s Let’s meet the the main player s in this g ame:
• T he Prefrontal Cortex (PFC) (PFC) • The Hippocampus • The Amygdala
THE PREFRONT PREFRON TAL CORTEX CORTEX (PFC) The PFC is the ar ar ea in the the front fr ont of your brain (behind your your for ehead) ehead) r esponsible esponsibl e for fo r what brain brai n scientists call “executive “executive function.” Execut Executive ive function is the description given for tasks such as: • Assigning Assigning “value” to to something (“goo d” versus versus “bad”). “bad”). • Paying attent attentio ion n to something. som ething. • Contro Contro lling your behavior (yo u lose this this when when you are drunk). • Solving complex co mplex pr pr oblems, oblems , and task switching switching (commonl (com monly y called multimultitasking). • Distinguishing “same” versus “differ ent” when viewing two two objects. obj ects.
executive T he PFC can help help stop st op a st ress response by the t he HPA HPA if executive function is intact i ntact.. The PFC is one of o f the brain structures str uctures that separates us from fr om animals. It It helps us evaluate evaluate a potential environmental envir onmental threat by “thinking” about it before deciding if it is threatening or not. Animals don’t have the executive executive function, and r eact to potential threats instinctively without without “thinking” about it.
THE HIPPOCAMPUS
This part of o f the brain is thought to to be responsible for fo r functions functions such as: • Puttin Putting g short-term memor memor y into into long-term memor y (learning). • Forming For ming memories memor ies of “new “new”” situat situations ions or enviro nments. nments.
The hippocampus is one of the only areas in an adult brain that regularly grows new nerve cells. The hippocampus also helps helps stop sto p stress responses from the HPA axis by recalling memor ies about your environment when you come across a potential threat you have seen before.
THE AMYGDALA The amygdala is an area of the the brain in charge o f: • Forming For ming memories memor ies associated associated with with strong emotions. • Contro Contro lling aggr essive behavior. behavior.
• Contro Contro lling emotional emotional reactions.
T he amygdala amygdala can activate t he stress st ress response respo nse by the t he HPA HPA axis. axis. It is also the str str ucture ucture o f the brain r esponsible for “learned fear.” fear.” For example, example, hearing a bell does do es not provoke provo ke fear for fo r most people. However, However, if every every time you you heard a bell r ing you r eceived eceived a painful painful electr electr ic shock soon soo n after, after, you would quickly learn to “fear” the sound of a bell. This is an example of a learned fear produce pro duced d by the the amygdala. When working properly, the PFC hippocampus and amygdala act together to produce stress responses appropriate to the threat. The three will also halt the stress response when the danger has passed—an overactive stress-response system is counterproductive and detrimental.
T he PFC and and hippocam hippocampus pus can stop sto p the st ress response by using executive executive function and memory to determine that something is not really a “threat.”
The amygdala triggers the stress response to external stimuli in the environment that are ar e perceived per ceived to be “threats.”
This is the nor mal “threat-st “threat-strr ess circuitry” in the brain of o f a healthy healthy person.
executive T he PFC and and hippocam hippocampus pus can stop sto p the st ress response by using executive function and memory to determine that something is not really a “threat.”
The amygdala triggers the stress response to external stimuli in the environment that are ar e perceived per ceived to be “threats.”
CHRON IC STRESS REWIRES CHRONIC REWIRE S “THREA “THRE ATSTRESS” CIRCUITRY The hippocampus is especially sensitive to over-activation of the HPA-axis. Over time, the high levels of cortisol from chronic stress will actually shrink the hippocampus, reducing its function. Studies using special types of MRI have shown that people under chronic stress (and people with depression) have smaller, shrunken hippocampi, which are decidedly smaller than those in healthy people. The mechanisms and rationale for how and why stress shrinks the hippocampus include: • Decreased dendrite “receiver “r eceiver”” and axon “transmitter” connections between between bundles bundles of nerve cells. • Decreased for fo r mation of new neuro ns in the hippocampus. The hippocampus is one of the few regions in the adult brain that regularly produces new nerve cells (neur (neur ons). The hippocampu hippocampuss r elies on the for mation mation o f new ner ner ve cells to maintain its numbers. When fewer new nerve cells are formed, the overall population decreases, shrinking the entire hippocampus. The shrinking hippocampus results in poor short-term memory and problems when coping with new situations and environments. A shrunken hippocampus is woefully ill prepared to deal with stress, and does a poor job of controlling the activation activatio n of o f the HPA HPA axis. The nerve cells in the prefrontal cortex (PFC) also shrink. The dendrite “receivers” shrink, due to high cortisol levels released by chronic stress. When the dendrite “receivers” shrink, they cannot form as many connections with other nerve cells. These connections are critical for cell communication. The “executive function” of the PFC is also diminished. Without good executive function, we have trouble paying attention, controlling our behavior, solving complex problems, or ganizing thoughts and and distinguishing distinguishing “go od” from fr om “evil.” “evil.” Chronic stress changes the amygdala in a opposite way as compared to the PFC and the hippocampus. “Receiver-transmitter” connections between nerve cells in the amygdala will grow stronger and more numerous in response r esponse to to cont co ntinual inual chronic stress. High fear and anxiety levels increase the activation of the HPA-axis. The str str engthened engthened amygdala amygdala can r esult in increased agg ressive behavior. Physical changes due to chronic brain stress include:
• Non-threatening stimuli are ar e perceived percei ved as “threatening” to the stressed-out stressed-o ut brain. brai n. Tension and stress provoke the HPA-axis stress response causing a decrease in function of o f the PFC and and the hippocampus. Stress strengthens str engthens the amygdala and these effects combine to create stress responses to events that were previously non-threatening. Many of us in modern society are “set off” over trivialities, which which causes causes us to to engage engag e in aggr essive behav behavior ior like “road “ro ad rage”, overreacting, over reacting, or snapping snapping at friends and and family over minor mino r issues. • The poor poo r ly functioning PFC PFC and hippocampus do not allow allo w us to evaluate situations well using our higher brain functions. We start reacting to things much like animals do. One way to view the physical changes of chronic stress is that our brains will function function in a more “animal-like” way. • Mor e stress leads to higher threat perceptions, per ceptions, which leads to mor e activatio activation n of the HP HPA-thr A-threat eat system. system. Mor Mor e HPA-axis HPA-axis activity leads to hig her cor tisol and adrenaline, which leads to poorer function of the PFC and hippocampus. This is a vicious cycle of chronic stress and has real health consequences.
THE “STRESSED-OU “STRESSED-OUT T BRAIN” Notice the shrinking of the PFC PFC and the the hippocampus along al ong with the the strengthene streng thened d amygdala. These changes will r esult in an over active thr threat eat response respo nse and HP HPA-axis
activation. The environment can physically alter our brain. It not only affects our physical health, but can alter our behavior and even our personality. If Descartes were living in our modern age, would he change his assessment based on what modern science has discovered in respect to the mind/body?
FIRST PRINCIPLES PERSPECTIVE: PERSPECTIVE : STRESS TRESS AND BRAIN CHANGES CHA NGES
What advant advantage age would woul d physical changes in the brain br ain in r esponse to chronic stress g ive us? If If you take us us out of mo dern society for a minute minute and think about what chronic stress might mean in a different environment, these brain changes may make more sense. If an individual from a primitive society was under a constant threat from his or her environment—predators, aggressive neighboring tribes—it would make sense for the brain to change to help this person survive. If the brain changes to interpret most things in the environment as a potential thr thr eat (whet (whether her they they are or not), the the person will never be caught off guard. guar d. They will always be alert and anxious about every noise in the woods at night, and it would be unlikely that a predator or human enemy could sneak up and kill them. They are always ready for “fight or flight.” In this primitive, survival situation, it seems better for them to react to the unknown like an animal, instead of using any higher brain functions (PFC and hippocampus) to further fur ther evaluate the “threat.” “threat.” In In the long-term, long -term, this is is
bad for their overall health, but it could certainly help them live another day in a dangerous environment envir onment..
CHRONIC STRESS II
STRESS AND AN D HEAL HEA LTH
THE “NEGATIVITY BIAS” Human beings are hard-wired to react more strongly to negative things in our environment than positive things. Due to our higher brain function, we are generally much more capable at evaluating potential threats than an animal, but we still carry a “negativity bias.” In psychology, a negativity bias means that a negative stimulus (pain, conflict, criticism) will elicit a much stronger reaction and memory formation than a positive stimulus (comfort, reassurance, compliment) of equal intensity. Many of us intuit intuitively ively know this this is true fr om our own personal experiences. • One critical comment from fr om a superviso supervisorr can erase ten ten previous compliments compliments from your mind. • One argument ar gument or fight fi ght with a friend fr iend can end a friendship fr iendship that has existed for years. • We learn lear n mo morr e from fr om making mistakes than we do by by “getting things r ight. ig ht.”” The negativity bias exists, and our brain reacts this way for a reason.
FIRST PRINCIPLES PERSPECTIVE: PERSPECTIVE : NEGA NE GATIVITY TIVITY BIAS We already discussed the survival advantage for the brain changes from chronic stress. These changes can be thought of as an extension of the negativity bias. The negativity bias helps us survive when exploring a new environment or situat situation. ion.
If a situatio situation n is perceived per ceived by the the brain br ain to have an equal amount of neg ative and positive characteristics—such as a potential source of food located close to an aggr ag gr essive bear bear ’s home—the home—the potential potential danger danger from fr om the bear gets a stronger strong er r esponse from fro m the brain than than the the potential potential benefit of getting the food. Even though food is necessary for survival, the potential danger from fr om the bear bear may stop stop you from fr om pursuing this food source. sour ce. Starvation is surely a threat, and acquiring the food is a powerful positive reward, but the bear is potentially an immediate danger to life and limb. The negativity bias wins the day for immediate survival. Knowing about the negativity bias may help you moderate your reactions to negative events and stimuli. Our higher brain functions allow us to override systems like the negativity bias, o nce we understand them. Many of us know people whom seem unfazed by genuinely stressful situations. “Nerves of steel,” “courageous” and “crazy” are how others view the rare few who have learned how to put non-life threatening and life-threatening stresses into the proper context. Let’s not have a total freak-out over a traffic jam; or grossly overr eact when when confront confro nted ed by everyday everyday modern stressor s.
KEY POINT: Under Understanding standing the negativity bias bias can help you r eact less negatively to things things that are not no t life or limb dangers.
EA RLY EARL Y LIFE LIFE EX EXPERIENCES PERIENCES SHAPE SHA PE THE STRESS RESPONSE Traumatic events experienced in childhood (abuse, loss of a parent, hunger, neglect) have a profound impact on a child’s developing brain—especially the developing stress-threat system. As these children enter adulthood, they are disproportionally afflicted with depression and anxiety. Their brains are physically and functionally different than a normal adult who did not have traumatic childhood experiences. The developing brain of a child is much more susceptible to stress— fro m childhood into adulth adulthoo ood. d.
FLASHBACK Do a quick review of Central Themes II, “The Gene-Environment Connection,” before continuing further.
CENTRAL CENT RAL THEMES THEMES CONNECT CONNECTION: ION: Early Early life l ife Stress and Epigene Epigenetics tics In Central Central Themes T hemes II “The Gene-Envir onment Connection,” we discussed
how epigenetic changes alter how a gene is expressed. Some changes “bookmark” the gene, causing it to be turned on all of the time, and other changes “stick the pages of the recipe together,” in effect turning the gene off.
Early Early life life stress st ress causes these t hese types of o f epigenetic changes in the areas of t he brain brain involved involved in in the st ress-threat ress-t hreat syst em. em. Specifically, early life stress “turns on” many of the genes involved with making the HPA-axis HPA-axis function mor e often. o ften. This leads the HPA-axis HPA-axis to be very sensitive to any “threats” in the environment, and will turn on very easily. Adults with a history of significant early life stress can have their stress systems turned on most of the time, even in response to minor stresses. Remember from the previous section that the prefrontal cortex (PFC) and sto p the stress response response of the hippocampus normally function to help stop the HPA-axis. Adults with a history of early life stress have epigenetic changes that inter interfer feree with nor nor mal PFC and hippocampus hippocampus function. For these people, the PFC PFC and the the hippocampus don’t do n’t stop the str str ess response r esponse well, and it can get out of control. Research has also shown that children raised with abuse or other significant stresses have epigenetic changes affecting the function of the amygdala, making it strongly trigger the stress response of the HPA-axis. Recent research shows how continual and repeated stress rewires the brain to make it even more susceptible and inclined to trigger stress. There are epigenetic mechanisms responsible for these changes. Epigenetic changes can be reversed over time. If you are an adult with a history of childhood stress, seek to normalize the stress-threat system. This is accomplished with consistent and dedicated brain plasticity training. The adult brain is still very “plastic” or changeable, if you give it the right rig ht inputs. inputs.
BRAIN CHANGES CHAN GES AND “MENT “MENTAL AL HEALTH” Epigenetic changes to the brain of those afflicted with chronic stress (particularly childhood stress) have been shown to increase depression, anxiety and other mental health conditions. The brain is a physical organ that is adversely affected, literally changed by chronic stress. This leads to mood and behavior changes. Thus, “mental
health” is just another aspect of your physical health and should be treated as such. Supporting this notion, people with major depression have been shown to have smaller hippocampi than non-depressed individuals. These are physical brain changes associated with depression and other mental health disorders, not just a “mental” defect. It should be no surprise that many of the self-treatment approaches covered in following sections for chronic stress, have also been shown to be effective in treating treating disorders disor ders tradit tr aditionally ionally thought of as mental mental health pr pr oblems.
STRESS ST RESS AN AND D CHRONIC CH RONIC DISEASE
The long-term health consequences of chronic stress are primarily related to chronic inflammation and oxidative stress. It is therefore no surprise that chronic stress has been linked to... • Heart disease • Diabetes • Accelerated aging agi ng • Autoi Autoimmune mmune disease • Cancer • Obesity • DepressionDepression- new new r esearch is showing that that depression is an inflammator inflammator y disease!
CENTRAL CENT RAL THEMES THEMES CONNECT CONNECTION: ION: A primar y mechanism mechanism behind behind how long-te long -term rm stress leads to to chronic inflammation and oxidative stress is over-activity of the sympathetic (“flight or fight”) nervous system. We covered this at the beginning of the book boo k in Central Themes IV, IV, but it bears r epeating. Act Act ivation of t he
“flight or fight” (sympathetic) part of the nervous system can lead to an increase in inflammation and oxidative stress. Short-term activation of the sympathetic nervous system from stimuli such as exercise produces short-term inflammation and oxidative stress, which is beneficial for health health through hormesis, hor mesis, as we have have discussed extensively. Long-term, low level activation of the sympathetic (flight or fight) nervous system system fr om chronic chro nic stress leads to to the the chronic chro nic inflammation inflammation and oxidative stress that is the underlying cause of many diseases. Cortisol produce pro duced d as part of the the stress response r esponse is supposed to to help with with recovery reco very by decreasing inflammation and oxidative oxidative stress, after after a shortshor tterm stress such as exercise, injury, or escaping a predator. In short, cortisol “puts the brakes on” inflammation and oxidative stress produced by the “flight or fight” system after the “danger” has passed. This system of checks and balances between the the sympathetic sympathetic nervous ner vous system system (inflammation) and cor tisol (anti-inflammation) (anti-inflammation) works wor ks extremely extremely well with short-term stressors. The problem lies when cortisol (HPA-axis) is activated constantly. New research proposes that the body develops
“cortisol resistance” similar to insulin resistance and leptin resistance. Simil Similarly arly,, it also leads to t o uncont roll ro lled ed inflamm inflammation. at ion.
TECHNICAL NOTE: Cortisol receptor r esistance esistance is a relat r elatively ively new area o f r esearch, but but the the idea seems concept co nceptually ually sound. so und. Receptor Receptor r esistance—as found with insulin receptors in diabetes, diabetes, and leptin leptin recept r eceptor or s in o besity—is besity—is commonly fo und in bodies with disease. It is not surprising that another hormone, like cortisol, cor tisol, could follow fol low this same theme. theme.
DIGGING DEEPER:
Corti Cortisol sol Receptor Receptor Resistance Resis tance Chro Chro nic stress and resistance resistance to the the effects effects of cortisol cor tisol is a new area of of research. resear ch. As discussed discussed before, befor e, cor tisol usually has anti-inflammatory anti-inflammatory effects on inflammation produced by cells of the immune system (both the “innate guardian” guar dian” and “adaptive assassin” types). To To make this antiinflammator inflammator y effect happen happen,, cor tisol binds to r eceptor eceptor s on o n the immune immune cells to to sig nal for them them to to stop pro ducing ducing inflammatory messengers (cytokines). Remember fr om the Obesity chapter, chapter, we discussed how in insulin resistance, resistance, the the insulin receptor receptor stops wor wor king and the the normal signal fr om insulin does not get thr thr ough to the the cell. Cor Cor tisol r esistance esistance is similar to insulin resistance in this manner. With chronic stress, the receptors for cortisol cor tisol on o n the immune immune cells start functioning functioning insufficiently insufficiently over time. When this happens, the immune cells no longer get the signal to “turn off” inflammation after a threat has passed. This results in long-term uncontr uncontr olled inflammat i nflammation ion and oxidat o xidative ive stress leading to chronic chro nic diseases such as hear t disease, diabetes, obesity, obesity, autoimmune disease and cancer. In summary, chronic stress causes the “flight or fight” sympathetic nervous system system to to trig ger chronic chro nic inflammation inflammation from fro m our immune cells. cells. The normal anti-inflammatory “checks and balances” produced by cortisol cor tisol are wor king insufficiently insufficiently due to to cor co r tisol resist r esistance. ance.
FLASHBACK Remember the hunger communication system with its food reward in the obesity chapt chapter? er? High levels of cortisol cor tisol pro duced duced by chro chro nic stress stress also trigg er the the foo d reward pathwa pathway y. This causes causes hunger hunger and cravings for fo r high-calorie, high-calor ie, palatable palatable foods. This makes since since from fr om a survival perspective. As far as your yo ur brain is concerned, cortisol means that that you just survived a significant stress stress and need to to refuel. High High calor calo r ie sour ces of fuel would be desirable to prepare yo u for the the next “fight or flight.” flight.” Unfor Unfor tunat tunately ely in moder n society, society, most of our “threats” “threats” don’t require r efeeding feeding fo r recovery. reco very. The stressed out brain is more “animal-like” and gets the signal to refeed anyway. When you are stressed, recognize what is happening and don’t “feed the beast.”
BODY AFFECTS BRAIN; BRAIN; BRAIN AFF AFFECTS ECTS BODY Fro m the Gut Chapt Chapter, er, we saw that that problems pro blems with our body can affect the functio function n of our brain. Recent research shows that metabolic diseases such as diabetes can affect both the str str ucture and function o f the brain brai n over time. Studies Studies have shown that diabetes can have the same “shrinking” effects on the hippocampus as chronic psycholog psycholog ical str str ess. This should not be too surprising as diabetes is an “internal” physical stress recognized as a threat by the brain, in the same way as a chronic “external” environmental stress is seen as threatening. Diabetics experience experi ence chronic activation activat ion of the HPA-axis because the brain thinks the body is starving since the leptin and insulin signals not getting through to the brain. The inflammatory “threat” of diabetes perceived by the brain creates a vicious cycle… • The internal internal threat threat of inflammation inflammation trigg ers the the HPA-a HPA-axis, xis, producin pro ducing g cortisol. This pr ocess shrinks shr inks the the hippocampus. hippocampus. • High cortisol cor tisol trigg ers the the hunger hunger communication communication system, system, signaling you you to eat
more. • Eating Eating mo morr e makes the diabetes condition conditio n worse. wor se. • As the diabetes gets worse, wor se, it pro duces mor e inflammatio n, which trig ger s the HPA-axis, HPA-axis, ad infinitum.. infi nitum.... Diabetes makes people more susceptible to depression since a shrunken hippocampus and inflammation are indeed contributors to depression. The physical brain changes generated by continual chronic external stress are made worse with the the addition addition o f chro nic internal internal stress fr om diabetes diabetes..
KEY POINT: No matter matter the the source sour ce (external (external or o r inter inter nal), chr chr onic stress makes the the brain change in i n ways that activates activates the threat-stress system (HPA(HPA- axis) mor e often. This leads to chronic diseases and increased susceptibility to future stress—a vicious cycle.
CHRONIC STRESS AND PREMATURE AGING Chronic stress has been associated with accelerated aging in humans. Chronic stress activates the HPA-axis/sympathetic nervous system’s threat-stress response system. Long-term and continual activation of the threat-stress response system leads to chronic inflammation and oxidative stress. One of the consequences of chronic inflammation and oxidative stress is damage to the protective “caps” (telomer (telomer es) on your chromoso chro mosomes mes (DNA). (DNA). Losing telomer telomer es leads to DNA DNA damage. Damaged DNA eventually stops your cells from dividing to regenerate the tissues and organs in your body. When your tissues and organs can no longer regenerate, they star startt to fail—leading fai l—leading to death. Chronic stress accelerates this process. Many of us know people who’ve seemed to age before our eyes during a period of intense stress. The perfect example of this is how a U.S. President will appear to rapidly age during their term in office.
The most health-damaging health-damaging and age-accelerating aspects aspects of o f chronic chr onic stress are two two rumination and worry. str str ess behavior behaviors— s— rumination
STRESS FROM “NOTHING”— RUMINATION RUMINA TION AND AN D WORR WORRY Y Rumination and worry are stress-related behaviors that amplify the negativity bias. The stress-threat system perceives rumination and worry as two sides of the largest contrib co ntributo utors rs to chronic chronic st st ress. same coin. These behavior behavior s are ar e t he largest
Rumination is defined as having persistent negative thoughts about past experiences. Rumination is a negative process that adversely impacts self-image and self-worth. Rumination can be caused by critical comments or embarrassing situations. Insecurity triggers rumination. If you find yourself mired in continual and ongoing rumination, be aware that this will have a devastating impact on your mental and physical health over time. Rumination is in some ways “stress over nothing.” Rumination is created in the mind, and in the same way, the mind can kill rumination by not engaging in it, or silencing rumination before it has an opportunity to fester and grow. We want to avoid reliving stressful situations over and over in the mind, since this prolongs activation of the HPA-axis. The ruminator is creating “stress from within” when there there is no r eal stress curr ently ently present in the the envir environment onment..
Worry is the opposite side of the same stress coin. Worry is the anticipation of a future stressful or threatening event. With worry, the stressful event has not actually
happened yet, yet, but you ar e activating the stress-threat r esponse system when the the brain br ain “worries” about the future event.
CENTRAL CENT RAL THEMES THEMES CONNECT CONNECTION: ION: Hormesis ormes is and Chronic Stress Stress The arrow below should look familiar. It was taken from Central Themes III, III, Hor Hor mesis. The stress of rumination and wor wor r y follo ws a hormesis-like response: r epresentss an individual individual with with no wor ry or rumination. Finding Finding a Point A represent human without any worry or rumination would be extremely difficult. Many animals fall into this category. As previously discussed, having no worr y or r umination umination would not be a survival advant advantage. age.
Point B represent r epresentss an individual individual with with occasional, shor t-term t-term worr y and rumination. This “hormetic “hor metic dose” dose” of worr y and rumination rumination provides pr ovides a survival advantage by making this individual more resilient against future stress. r epresentss an individual individual with with chro chronic nic daily wor wor r y or rumination. Point C represent The stress-threat str ess-threat system (HPA-axis) (HPA-axis) is co nstantly nstantly activated by “str “str ess fr om nothing”, leading to chronic diseases such as heart disease, diabetes, obesity, depressio n and anxiety. anxiety. Scientists Scientists call this the anticipatory threat response. In In effect, we are anticipating anticipating a future stressful event, but causing a stress response in the present moment—without
an actual actual environmental environmental stressor. This is why we also classify worr y as “stress from fr om nothing.” A certain amount of short-term periodic rumination or worry can make us resilient to future stresses. Rumination and worry provide humans a survival advantage over animals. With reasonable and appropriate worry, we anticipate and prepare for fo r future stresses.
RESEARCH UPDATE: Recent research has shown that anticipatory stress (worry) activates the stress-threat system more than experiencing the actual future stressful situat situation ion you yo u are worr ying about! Ruminat Rumination ion and worry wor ry are ver y hard to control with the environmental stresses of modern society.
THE 24-HOUR NEWS NEW S MEDIA, CHRONIC STRESS STRESS,, AND AN D THE NEGA NE GATIVITY TIVITY BIAS The modern moder n news news media is now operating o perating 24/7, constant constantly ly repor r eportin ting g on war, murders, plane crashes, abductions, economic forecasts, and other negative events events and subjects to to anyone anyo ne tuned tuned in. Negativity br br ings go od ratings and feeds our negativity bias. Over time, habitual watchers of the modern news media have increased chronic stress that keeps their “flight or fight” system constantly in low-level activity. Worriers seem to be the most affected. Most people don’t even know what has happened to them until they “unplug” for a period of time. Many people who voluntarily restrict their viewing viewing of o f the the 24-hour 24-hour news news cycle for a week or so repor t lower lower levels of anxiety and depr depressive essive thoughts. thoug hts. Taking a “news holiday” hol iday” is always al ways a goo d idea. idea.
Rumination allows us to learn from past threats—specifically, how to adapt and better deal with similar threats in the future. But, long-term, chronic rumination and worry over-activa over-activate te your stress-threa stress-t hreatt system (HPA-axis), fill your stress cup and eventually lead to chronic disease.
Modern stresses amplify our inborn, human negativity bias to such a degree that our health is negatively impacted by the thoughts, ideas, projections, and reflections which occur in our consciousness. Understanding this mental stress is the first step. The second step is developing “mental antidotes”. Awareness of potential triggers or mental land mines, that over-activate the stress-threat system empower you to avoid, temper, or alleviate stress when it first appears.
CHRONIC STRESS III
MIND MI ND INTER IN TERVEN VENTIONS TIONS
BRAIN-TRAIN: WHERE EASTERN MEDITATION TACTICS MEET WESTERN HIGH TECHNOLOGY The previous chapters showed that chronic stress physically changes the structure and function of the human brain by over-activating the stress response, filling the stress cup to overflowing, contributing to age acceleration, and developing chronic disease. What if there was a mental approach or strategy that you could consistently use to relieve stress, and minimize projection, reflection, rumination and worry? Additionally, this same brain-train mind method can be used to improve discipline, adherence, steadfastness and human performance.
Training the brain will have a beneficial beneficial carry-o car ry-over ver to physical physical effects with with the body. body. Tr Tr aining the body will beneficially beneficial ly affect the structure and function of the brain.
We live in the information age where there are no more secrets. If you want to learn lear n details about anything anything under the sun, just Goo gle gl e it. Mental tr tr aining techniques techniques used by Eastern mystics and shrouded in mystery for centuries are now available to anyone. Want to learn Dogen Zenji’s tactical approach to meditation? No problem! Want to learn about the breakthrough mental preparation of elite athletes in the old Soviet Union? Google Dr. Aladar Kogler and read about his pioneering work with autogenic and auto-suggestive practices. Experts in the East and West have offered up complex and effective systems for transforming the human mind from an individual’s worst enemy into their best friend. Our user-friendly mind methodology is a blend of Eastern contemplative techniques and Western athletic and technological techniques and tools. All the religiousness and supernatural aspects of Eastern meditational techniques, and overly mechanistic shortcomings of the uber-rational Western approach have been stripped away. Our synthesis of East and West—with understanding and practice— will be immediately immediately applicable applicable for you in your current curr ent life situat situation. ion. View the the interventions in this chapter as mental m ental exercise—we are literally liter ally training tr aining the brain in the same way we train to make our bodies stronger and more resilient with with physical exercise. exer cise. Just as we need consistency in our physical exercise, exer cise, we need consistency consistency in our br ain-tr ain-tr ain protocols. The three main interventions are: 1. Mindfulness Mindfulness practice 2. Biofeedback 3. Physical exercise exerci se
I. MINDFULNESS PRACTICE Mindfulness training originated in traditional Buddhist meditation practices, but has been used used extensive extensively ly in mo dern medicine for well well over 20 years.
WHAT IS MINDFULNESS? In its simplest definition, mindfulness means focusing your attention and awareness on o n the present moment. With mindfulness, you ar e aware of of internal internal pr ocesses like br eathing, eathing, and external external stimulus stimulus fr om the the environment—while not “holding on to” any thoughts or experiences after they pass from the present moment.
Seamus the “mindful cat” Focusing your attention and awareness to the present moment sounds easy until you try it for a couple of minutes. At first, it is common for beginners in mindfulness training to have intrusive or distracting thoughts—that have nothing to do with the the present moment—p mo ment—pop op into i nto their heads. Thinking about what you need to get at the store for tonight’s meal, or the jerk that cut you off on the way home from work, will take you away from your focused attention on the present moment. You can be aware of what goes on in your environment moment to moment, but don’t hold on to or make judgments on these stimuli, just label them as what they are and let them pass. For instance, during mindfulness practice you can be aware of the sound of a jet passing overhead, but don’t think about how annoying the sound is, or how you wish you hadn’t bought a home so close clo se to to the airpor t. Being consistently mindful for even a couple of minutes can be challenging at first. Try this simple breathing exercise to get you started.
MINDFUL BREATHING Many mindfulness meditation techniques involve focusing on your inhalation and exhalation during slow breathing. The way you breathe in these exercises is critical to the desired effect on your nervous system. It is important that you primarily breathe “into your belly” instead of your chest. In other words, we are trying to almost exclusively use our diaphragm for breathing instead of the chest and neck muscles. There ar e scientific scientific r easons for breathing breathing in i n this this specific way: way:
• Inhal Inhalat ation ion (breathing (breathing in) activates t he sympathet sympathetic ic nervous nervous system syst em.. Breathing in using your chest and neck muscles strongly activates the flight or fight sympathetic system. This makes sense when you are running away from danger danger or fighting—you will will take in huge huge gulps g ulps of air by using using your yo ur chest and and neck muscles to assist your diaphragm. This helps your muscles get the maximum amount amount of oxygen o xygen dur dur ing the physical physical str str ess of a flight fli ght or fight situation. T he brain brain associates “chest and neck neck breathing” breathing” with the t he flight flight or sympathetic ner vous system activatio activation. n. Many Many fight fight response response and incr eases sympathetic people under chronic stress habitually breathe this way without the presence of immediate danger to life and limb. Breathing this way causes chronic low-level sympathetic sympathetic nervous ner vous system activation. We We have previousl pr eviously y mentioned that constant high levels of sympathetic flight or flight activation result in high alert levels, increased inflammation, and oxidative stress that can lead to chronic disease. For this reason, don’t use your chest and neck muscles for breathing.
• Exhala Exhalatt ion (breat (breat hing hing out) out ) activates the t he parasym parasympathet pathetic ic nervous system. system. We want you to breathe br eathe with with slow slo w exhalatio exhalations ns that are ar e longer lo nger than inhalatio inhalation n so we can tip the balance of your autonomic nervous system in favor of the parasympathetic system, which has anti-inflammatory and calming effects on breathing o ut for a longer long er time than than breathing breathing in, we are your body bo dy.. By breathing
spending spending a longer t ime ime activa act ivatt ing ing t he parasympathet parasympathetic ic system and and a short er t ime ime activa act ivatt ing ing t he sympathet sympathetic ic system syst em.. The effect over time is less activation of the str str ess-threat system that we discussed in the previo us section. Try to practice breathing like this throughout the day so it becomes a natural way to breathe. Many Many of us with chronic chro nic stress have fallen into i nto the “chest and and neck” breathing pattern without even realizing it.
• Find a comfor table table position, eithe eitherr seated seated or somewhat somewhat reclined. • While you ar ar e first learning to breathe cor rectly, rectly, place place one hand hand on your belly and the the other on o n your chest. chest. • Breathe in slowly slo wly through thro ugh your nose, no se, and and make sure sur e that that you mostly feel the the hand on your belly move during inhalations, inhalations, and only minimal movement in the chest area. • Exhale slo wly. T he time time spent breathi breat hing ng out o ut (exhal ( exhalation) ation) should s hould be be longer t han the tim t imee spent breathing in (inhal (inhalation). ation). If you are having problems pro blems exhaling exhaling slo wly, wly, purse your lips at the the beginning of the the exhalation. exhalation. This makes your mouth smaller and it will be easier to co ntr ntr ol the the air passing out of your mouth. • Focus on the the sensat sensation ion of the air passing in thro through ugh your nostrils, nostri ls, filling your belly, belly, and then then passing passing out o ut of your mouth. Mentally count each cycle o f inhalation inhalatio n and exhalation, attempting attempting to r each 10 without without any “intr “intr uding” thoughts thoug hts other than the the sensation of of breathing. If you find your mind has wandered before you get to 10 breaths, start over. • Focusing on the sensation of breathing without without letting letting your mind wander wander with with distracting thoughts has the benefit of directly attacking rumination and worry. Remember that your prefrontal cortex is involved with maintaining attention. By focusing attention on breathing, you are strengthening the connections in this area of the brain. By not allowing rumination, worry, and negative thoughts —“stress —“str ess fr o m nothing no thing”—we ”—we decrease decr ease activatio activa tion n of the stress stres s respo r esponse. nse. Decreasing chronic activation of the threat-stress system over time with this type of mindful attention attention to the present moment mo ment and br br eathing will strengthen str engthen the the prefrontal cortex and hippocampus while weakening the amygdala. The downstream downstream effects effects of o f this seemingly seemingly small breathing breathing exercise exer cise performed perfo rmed
ro utinely utinely over time can slowly slowly physically physically r ebuild the the stressed brain so it functions functions normally nor mally again.
With proper breathing, we can maximize our time with high parasympathetic activation, activation, and only using the high level activation of o f the sympathetic “flight or fight” system sparingly when necessary. Review Central Themes IV for more on the balance of the autonomic nervous system. The following graphic shows the “rebuilding” process of the brain through daily mindful mindful breathing breathing exercises: • Decreased r umination and worr wor r y, which decreases the the activatio activation n of the the threatstress system. • Decreased activatio activation n of the the sympathetic sympathetic system with increased incr eased activatio activation n of the the parasympathetic system system caused by slow “belly br eathing” with long exhalations, exhalatio ns, reduces overall activation of the threat-stress system. • Pro longed lo nged r eductio eduction n of the stress-threat stress-thr eat system activatio activation n allows allo ws the prefr pr efrontal ontal cortex and hippocampus to strengthen their connections.
The bottom picture illustrates how regular mindfulness breathing restores the healthy healthy brain over o ver time. The pr pr eviously overactive amygdala fro m the top top image imag e of the “stressed out brain” is now “shrinking” and has a smaller activation signal to the stress-threat system. Now that the prefrontal cortex and hippocampus are strengthened, they can stop the stress response better with stronger inhibition signals. This will give you more resilience against future stress. Mindfulness not only helps with present time stress reduction, it prepares you to cope with future stress by physically rebuilding and restoring the stress-threat system to a healthy state. This is how brain training with mindfulness practice is similar to strength training fo r your muscles. In both cases, cases, regular r egular training causes beneficial beneficial physical physical changes.
KEY POINT: Regular Regular mindfulness mindfulness practice can physically physically rebuild r ebuild your brain in i n the same way that regular strength training can build your body. Start out by trying to spend at least 10 minutes each day with mindfulness breathing, working up to 30 minutes a day over time. You may begin to sleep better, have less depression and anxiety, and cope with daily stresses more easily. Make time for mindfulness breathing whenever you can. The benefits are too great to be
ignor ig nor ed. Make the time time to pr actice.
STRONG MEDICINE TACTICS: Start with 10 minutes a day of mindfulness breathing practice and work your way up to 30 minutes a day over time.
THE BODY-SCAN This is not a high-tech device at airport security checkpoints! Body scanning refers to systematically visualizing and “paying attention” to each part of your body. Like mindful breathing, you can perform this exercise in a relaxed seated or reclining position. Start by focusing your attention on one of your big toes for 20-30 seconds and register all of the sensations coming from this toe. Don’t let any “intrusive thoughts” take hold and cause your mind to wander. Move on from your big toe to the rest of your foot and proceed slowly up your ankle, leg, knee, and thigh. At all times, focus on the sensations coming from those specific areas. Then start at the big toe on the other foot and do the same thing until you get to the waist area. Next, move up your torso with the same focus on your abdomen, rib cage, and chest. When you get to your neck, start with individual fingers on one hand and move up the arm to the shoulder. Then begin with the other hand, moving up to the shoulder on that side. Lastly, move up the neck into your head until you reach the top of your scalp.
STRONG MEDICINE TACTICS: Add the body-scan technique as part of your mindfulness training after you have worked up to 20-30 minutes of mindful breathing practice. The body scan may seem strange, but it is similar to the mindful breathing
exercise. Both exercises involve being in the moment while focusing on the immediate sensations coming from your body. While doing the body scan, if your mind wanders—especially with negative thoughts of rumination and worry—stop, then star startt again at the big toe. Focusing on the three dimensional space in and around your body during the body scan is an additional strategy recommended by Dr. Les Fehmi in his book, The Open-Focus Brain. In this approach, with your eyes closed, imagine the three dimensional space occupied by each body part as well as the distance between them. Dr. Fehmi asserts that focusing on 3-D space further assists the mindful-state and enhances the body scan. The body-scan technique is a somewhat advanced mindfulness technique, and should be added after you have trained with the mindfulness breathing technique for several weeks or months. Once your breathing technique has become automatic, you can continue continue breathing breathing pr operly operl y while while perfo rming rmi ng the body scan. scan. With either the mindfulness breathing or the body-scan, you should attempt a total 20-30 minutes of mindfulness training daily. This is just the very tip of the iceberg with mindfulness training. You may find many other techniques that work better for you. There are some fantastic mindfulness systems and books to explore if you like the results you get from the basics:
• Jon Kabat-Zinn, PhD, br ought mindfulness practice into into mainstream mainstream medicine. He founded the Mindfulness-Based Mindfulnes s-Based Stress Stre ss Reduction (MBSR) ( MBSR) course current curr ently ly taught taught around aro und the the world. His His boo ks and progr prog r ams are excellent resources. and author author of Buddha’s Buddha’s Brain. He • Rick Rick Hanson, PhD, is a neuropsycholog ist and has some excellent audio-based mindfulness programs that are definitely worth looking into. He also discusses the science behind mindfulness in a very clear and easy to understand way. scientist in the the field of neurofeedback • Les Fehmi, Fehmi, PhD, Ph D, is a pioneering scientist (biofeedback (biofeedback for the the brain) and the auth author or of The Open-Focus Brain. His scientific scientific perspective perspective on mindfu mi ndfulness lness is a g reat place for a beginner to star star t. Mindfulness “brain training” is no longer just for Buddhist monks or Zen masters. It It has become mainstream mainstr eam in a big way over the past 10-15 year yearss along alo ng with very strong scientific evidence for health benefits. This type of training interrupts
the vicious negative mental thought cycles of chronic rumination and worry. As rumination and worry are large contributors to chronic stress, it’s no surprise that recent research shows very very pr omising results with with mindfulness mindfulness training training for chronic chro nic “body” diseases such as diabetes, heart disease, high blood pressure, and autoimmune disease.
You can’t try mindfulness exercises once and decide “they don’t work for you.” T hat would be lik likee goin go ingg t o t he gym once and saying saying “exercise doesn’t doesn’t work for me.” This is brain training, and daily mindfulness practice is key if you want to rebuild a stressed brain.
II. BIOFEED BIOFEEDBACK BACK Biofeedback is a technique for stress reduction in which you use devices to monitor your body’s heart rate, muscle tension, or skin conductance in the attempt
to exert some type of control over these processes. A biofeedback device will give you instant “feedback” so you can be aware of your body’s state in real time. For instance, a device monitoring your muscle tension can give you instant feedback to your stress state, since increased muscle tension equals increased stress. You can also monitor the sweat response in your skin with skin conductance biofeedback. Increased stress leads to increased sweating, causing increased electrical conductance measurable by the device. Monitoring muscle tension and skin conductance provides a real-time window to your current state of stress—second by second. The idea of biofeedback is to use real-time information in an attempt to change your stress level. If the device shows increased muscle tension—that you might not be aware of—then you can actively try to relax your muscles to change the muscle tension readings. You will be able to change your behavior based on the feedback.
KEY POINT: Biofeedback Biofeedback uses monitoring devices devices to train you to r educe educe stress-relat stress-r elated ed body responses. Many of us walk around during the day with high amounts of muscle tension from underlying stress. We may “carry” the stress in our neck or chest muscles. Biofeedback brings this muscle tension to your awareness so you can change it by relaxing. Once we are aware of the behavior, we can eventually “catch” ourselves and stop the the tensing behavior without without using the biofeedback bio feedback device. Monitoring muscle tension and skin conductance can require expensive equipment and technical expertise. These types of biofeedback sessions are best done in a clinic with a biofeedback professional. A type of biofeedback many of us can perform at home with relatively inexpensive equipment monitors something called heart rate variabi variabili litt y. Heart rate variability (HRV) does not measure the slowing down and speeding up of the heart rate as the name might imply. HRV measures the variation in the time between each heartbeat.
The best way to illustrate this concept is to show how the heart behaves in a person with a resting heart rate of 60 beats per minute (one beat every second).
between Low Variabilit ariabilit y: the heart beating exactly once ever y second. The time between each beat is exactly the the same (in this case 1 second). seco nd). This machine-like m achine-like pr ecision ecisio n is ho w a healthy perso n’s heart beats. Low variability variabilit y is a marker mar ker of poor health. heal th. not how
ever y second. Sometimes High Variability: the heartbeats do not happen on exactly every the time time between between heartbeats is less than a second, or mor e than a second. This perso n would still have 60 heartbeats in a minute on averag e, but would not have a heart beat exactly every second. High variabili vari ability ty is a marker m arker of good health. heal th.
LOW HRV = BAD Low HRV, the machine-like heart, has been linked to a high amount of sympathetic sympathetic nervous ner vous system s ystem (“fight (“fig ht or flig ht”) activity activity. Low Low HRV HRV is seen in people with chronic diseases and indicates poor health overall. Chronic stress and activation of o f the str str ess/threat system causes the the heart to beat in a more “machine-like” way, causing low HRV.
HIGH HRV = GOOD High HRV corresponds to higher activation of the “rest and digest” parasympathetic nervo us system. Hig High h HRV HRV is asso ciated with with go od physical health and low stress str ess states. New technology has allowed for portable HRV biofeedback devices that you can use at home. These devices monitor your HRV moment to moment by tracking your
pulse with different types of sensors. Using the mindful breathing techniques covered earlier in this section, biofeedback can track how proper breathing reduces “flight or fight” syste activation and raises your HRV. The device will also alert you if your attention drifts into worry or rumination which both raise your anxiety levels and lowering your HRV. Biofeedback devices that use HRV are useful for daily practice at home to reduce your stress levels. There are plenty of portable systems on the market, but our current favorite personal HRV biofeedback system is Inner Balance made by HeartMath. HeartMath. It is an application and ear sensor that works wor ks with the the iPhone. iPho ne. With biofeedback, you can train your brain to maintain low stress states with real effects on your body. Give it a try...
STRONG MEDICINE TACTICS: Try a personal HRV biofeedback device to reduce chronic stress and raise your heart rate variability. Use it daily for maximal health benefits.
III. EX EXERCISE ERCISE Similar to mindfulness practice, exercise decreases activation of the stressthreat system (HPA-axis). But, it also helps to regrow stress-shrunken brain structures such as the hippocampus by stimulating the release of Brain Derived Neurotrophic Neurotrophic Factor (BDNF).
DIGGING DEEPER: Exercise, BDNF, and the Hippocampus Exercise stops the shrinking hippocampus by not just decreasing the
excess cor tisol fr f r om stress activation of o f the HP HPA-axis, but by stimulating the growth of the hippocampus by an additional mechanism. Exercise is a potent stimulator of Brain Derived Neurotrophic Factor BDNF is a pro tein that that stimulates stimulates nerve cell cel l gr g r owth and is a (BDNF). BDNF central player in neuroplasticity (adaptive brain changes to environmental stimuli). Exercise stimulates BDNF BDNF,, which stimulates the the gr g r owth of nerve cells in the hippocampus, rebuilding this part of the brain that was “shrunken” by stress. stres s. Recall Recall that the the hippocampus is i s a key player in preventing preventing the the stress-thr stress-thr eat syste system m fr om getting getting out of control. control . Regr Regr owth owth is goo d for contro contro lling stress. stress.
Exercise has proven to be beneficial for stress relief. Recent research shows that exercise specifically decreases rumination and worry—both major contributors to chronic stress. Exercise has been shown to be extremely effective for reshaping the stressed brain through neuroplasticity. Reshaping the brain connections with exercise is thought thought to be r esponsible for helping the anxiety anxiety and and depression-r elated elated symptoms that often accompany chronic stress. Exercise is a true mind-body intervention. While you can train both the body and the the brain dir ectly ectly,, not all exercise is optimal for tar tar geting brain training.
COACH’S CORNER: We love out o utdoor door exercise such as chopping chopping wood, runn r unning ing or o r biking steep steep mountain mountain trails, r unning unning along the the seashore, swimming, intense intense games g ames and sports. Think big athletic cardio—not being stuck indoors like a gerbil ger bil riding ri ding or operating an aerobic stationar stationary y bike or machine while while
watc watching hing the built-in built-in TV to to distract you fr om the horro hor ro r of the the mindless activity activity you are doing. Meanwhile eanwhile the the mountain biker biker or r unner—tearing unner—tearing alo ng wooded woo ded trails trails of serene ser ene natur natur al beauty—is beauty—is having a transcendental, alter altered-stat ed-statee experience experi ence while while wor king his lungs until until they sear and g enerating enerating innumerable innumerable rivulets of sweat. Outdoor exercise gives maximum stimulus from the environment. It is superior for keeping you in the moment, mindful of what you are doing. It is easy to fall back into worry or rumination when you are plodding away on a treadmill or elliptical machine.
The author authorss engaged in “physical mindfulness” Chris has always been drawn to sports such as mountain biking, rock climbing, trail running, and surfing. There is no room for rumination or worry while flying downhill on a narrow mountain bike trail, or when dropping in on a big wave. Marty is a life-long powerlifter. He is not thinking about anything but the present moment mom ent while while pulling pulli ng a 500lb deadlift. Both Both of us have been drawn to to spo r ts such as these because because of the mindful aspects built in to the perfo r mance of these activities. You certainly do not have to engage in powerlifting or rock climbing to tap into physical mindfulness activities. A short hike in the woods can quickly reset your stress-threat system. Also, yoga and the ancient Chinese internal martial art of T’ai chi ch’uan (known as tai chi in the West) are embodiments of physical mindfulness and can be practiced by anyone regardless of fitness level or athletic experience.
STRONG MEDICINE TACTICS: Get regular exercise for stress relief. Outd Outdoo oorr exercise and “phys “physical ical mindfulness” mindfuln ess” activities activities are espec especially ially beneficial to r everse stress-r elat elated ed brain changes. Let Nature be your trainer, get outdoors!
COMING ATTRACTIONS >>> There will be extensive coverage on the Strong Medicine exercise approach appro ach in Part Par t 3, Batt Battle le Plan.
KNOWING YOUR ENEMY IV:
CONCLUSION
Chro Chro nic stress causes causes structural and functional changes in the brain that “link” to significant health consequences and leads to premature aging. The human mind and body are ar e not separate separ ate entities, entities, but tied tog tog ether inextricably inextri cably..
Chronic stress can also affect other organs such as the gut, multiplying chronic inflammation inflammatio n and oxidative stress. Remember Remember the Gut-Brain Axis?
The triumvirate of brain training—mindfulness, biofeedback, and exercise—will repair the damage of the stressed brain and combat chronic disease by reducing inflammation and oxidative stress. If you still think this is all new-age nonsense, be aware that recent research using sophisticated brain imaging techniques has shown that brain training does indeed physically reshape the brain. Several studies show that people who exercise and practice mindfulness mindfulness regularl r egularly y have structurally and functionally different brains than those who do not. People who exercise and practice mindfulness also have much lower rates of stress-induced chronic disease and mental health disorders. Just as weightlifters grow their muscles, and runners improve their cardiovascular fitness fitness thro thro ugh training, br ain training does the same for the the brain. In our stressed-out modern moder n world, brain br ain training can help prevent chronic disease and is truly part of the fountain of youth for your mind and body.
BREAKING THE LINK The Brain Training Triumvirate (mindfulness, biofeedback, and exercise) can stop chronic stress in its tracks, “breaking the link” between chronic stress and chronic disease. The Str Str ong Medicine Defensive Tactics Tactics in i n this section will expose the lurking “Silent “Silent Killer Killer”” and stop his subver subver sive plan to destro destro y your health. health.
“MILITARY INTELLIGENCE” INT ELLIGENCE” (REFERENCES): Aschbacher K, e t al. M aintenance of a posi posi tiv e outlo ok during acute stress protects against pro-i pro-i nflammatory reactivi ty andfuture future depressi depressi ve sy mptoms. Brain Behav Immun 26 (2012): 346-352. Psychoneuroendocrinology (2013). Aschbacher K, et al . Go od stress, badstress andoxi dativ dativ e stress: Insights from antici patory patory cortisol reactivi ty. Psychoneuroendocrinology (2013). Berk M , et al. So depressi depressi on is an infl ammatory ammatory disease, but where does the inflammatio n come come from? BMC Med 11 (2013): 200. Brown KW, & Ryan RM . The benefi ts of being present: present: mindfulness mindfulness and and its rol e i n psychol ogi cal wel l- being. J Pers Soc Psychol 84 (2003): 822-848. Natl Acad Sci U S A 109 (2012): E1312-E1319. Buss C, et al. Mate rnal rnal cortisol over the course of pregnanc pregnancy and subsequent child amygdala and hippocampu ippocampus vol umes andaffe ctive proble proble ms. Proc Natl Campbell Campbell CM, & Edwards Edwards R R. Mi nd-body interactions i n pain: pain: the neurophysiol ogy of anxi anxi ous and and catastrop catastrophic pain-related though thoughts. ts. Transl Res 153 (2009): 97-101. Chiesa A, & M ali nowsk i P. Mi ndfulness- based based approach proaches: es: are they all the same? J Clin Psychol 67 (2011): 404-424. Cohen S, S, et al . Chronic Chronic stress, gl ucocorticoi ucocorticoi d receptor receptor resistance, i nflammation, anddisease risk . Proc Natl Acad Sci U S A 109 (2012): 5995-5999. Danese A, & McEwen BS. Adverse childhood experiences, allostasis, allostatic load, and age-related disease. Physiol Behav 106 (2012): 29-39. Neurosci 15 (2012): 689-695. Davidson RJ , & McEwe n BS. Social Social infl uences uences on neurop neuroplasti lasti city: stress and and interventions to promote we ll -bei ng. Nat Neurosci Dedovi c K, Duchesne Duchesne A, Andrews Andrews J , Engert V, & Pruessner JC. The brain brain andthe stress axis: the neural neural correl correl ates of cortisol regulati on in response response to stress. Neuroimage 47 (2009): 864-871. Neurosci 7 (2013): 66. Dery N , et al . Adult hippocamp hippocampal al neurogenesis reduces memo ry interfe rence in humans: mans: opposi opposi ng eff ects of aerobic exe rcise and depression. Front Neurosci Clin Immunol 4 (2008): 2-11. Dhabhar har FS. Enhan Enhancing cing ve rsus rsus Suppr Suppressi essi ve Eff ects of Stress on I mmune Functio Functio n: Impli cations for Immunoprotection Immunoprotection ve rsus rsus I mmunopathol ogy. Allergy ogy. Allergy Asthma Clin Dhabhar har FS. Psycholo gi cal stress and and immunoprotection immunoprotection ve rsus rsus i mmunopathol ogy in the sk in. Clin Dermatol 31 (2013): 18-30. Dhabhar har FS, Mal arkey WB, N eri E , & McEw en BS. Stress- induced induced redistri redistri bution of i mmune cel ls—f rom barr barracks acks to boulev ards to battle battle fi el ds: a tale of three hormones—Curt hormones—Curt Ri chter chter Award wi nner. Psychoneuroendocrinology 37 (2012): 1345-1368. Di ng Q, Q, Vaynman Vaynman S, Souda Souda P, White le gge J P, & Gome z- Pinil la F. Exe rcise aff ects energy me tabol tabol ism and neural neural plastici ty-rel ated protei ns in the hippocampu hippocampus as reveale d by proteo proteo mic analy analy sis. Eur J Neurosci 24 (2006): 1265-1276. Dishman Dishman RK, e t al. Ne urobiology of e xercise. Obesity Obesity (Sil (Sil ver Spring) Spring) 14 (2006): 345-356. Engert V, Efanov SI, De dovic K, D agher A, & Pruessner JC. Increased cortisol cortisol awake ning response and afternoon/evening cortisol output output in heal heal thy young adults w ith l ow e arly l if e parental parental care. Psychopharmacology (Berl)
214 (2011): 261-268. Esch T, T, & Stefano GB. E ndoge ndoge nous rew rew ard mechanisms and thei r importance in stress reductio n, exe rcise andthe brai brai n. Arch Med Sci 6 (2010): 447-455. Eyre H, & Baune BT. Neuroimmunological effects of physical exercise in depression. Brain Behav Immun 26 (2012): 251-266. Neuroendocrinol 27 (2006): 180-192. Fe nogli o KA , Brunson Brunson KL, & Baram TZ . Hi ppocampal ocampal neuroplasti neuroplasti city i nduced uced by early-l if e stress: f unctional and mol ecular aspects. Front Neuroendocrinol Fj orback orback LO. M indfulness and and bodil y distress. Dan Med J 59 (2012): B4547. Fj orback orback L O, et al. M indfulness therapy therapy for somatiz ation disorder and functional somati c syndromes: analy analy sis of e conomic consequen consequences ces alo ngside a randomize d trial trial . J Psychosom Res 74 (2013): 41-48. Fl ak J N, Ostrander MM , Tasker J G, & H erman JP. JP. Chronic Chronic stress-i nduced uced neurotran neurotransmitte r plasti plasti city i n the PVN . J Comp Neurol 517 (2009), 156-165. Neurobiol 81 Fumagalli F, Molteni R, Racagni G. & Riva MA. Stress during development: Impact on neuroplasticity and relevance to psychopathology. Prog Neurobiol 81 (2007): 197-217. Hypertens (2012): 453465. Geri n W, et al. R uminatio uminatio n as a mediator of chronic chronic stress e ff ects on hypertensio n: a causal model . Int J Hypertens (2012): Glei DA, Goldman N, Chuang YL, & Weinstein, M. Do chronic stressors lead to physiological dysregulation? Testing the theory of allostatic load. Psychosom Med 69 (2007): 769-776. Gray JD , M il ner TA, TA, & M cEwen BS. Dynamic plastici ty: the role of gl ucocorticoi ucocorticoi ds, brain-derived brain-derived neurotroph neurotrophic f actor and andother trophic trophic factors. Neuroscience 239 (2013): 214-227. Hamli n J K, Wynn K, & Bloom P. P. Three-month-olds show a negativi ty bias in thei r social ev aluations. Dev Sc i 13 (2010): 923-929. Front Hum Neurosci Neurosci 3 (2009): 31. Herculano-Houzel S. The human brain brain in numbers: a li nearly nearly scaled-up primate primate brain. brain. Front Herman JP, & Cull inan WE. Ne urocircuitry urocircuitry of stress: ce ntral ntral control of the hypotha hypothalamolamo- pituitary-adrenocortical pituitary-adrenocortical axis. Trends Neurosci 20 (1997): 78-84. Neuroendocrinol 24 (2003): 151-180. Herman JP, et al. Central Central mechanisms mechanisms of stress i ntegration: hie hie rarch rarchical ical circuitry controll controll ing hypothalamo-pi hypothalamo-pi tuitary-adrenocort tuitary-adrenocortical ical responsiv responsiv eness. Front Neuroendocrinol Herring M P, Jacob ML, Suveg C, Di shman shman RK, & O’Connor PJ. Fe asibil ity o f ex ercise traini ng for the short-term treatment treatment of ge nerali nerali ze d anxi anxi ety disorder: a randomize d contr control ol le d trial . Psychother Psychosom 81 (2012): 21-28. Herring M P, Puetz Puetz T W, O’Connor O’Connor PJ, & Di shman shman RK. Ef fe ct of exe rcise training on depressiv depressiv e symptoms among among patie patie nts wi th a chronic chronic il lness: a systemati c revie w and meta-analysi s of randomize randomize d contr control ol le d trial trial s. Arch Intern Med 172 (2012): 101-111. Hi ll man CH, Erick son KI, & Kramer AF. Be smart, exercise y our heart: heart: exe rcise ef fe cts on brain brain and cogniti on. Nat Rev Neurosci 9 (2008): 58-65. Biobehav Rev 37 (2013): 1346-1362. Ho N, Somme rs MS, & Lucki I. Ef fe cts of diabetes on hippoca hippocampa mpall neurogenesi s: Link s to cognitio n and anddepressi depressi on. Neurosci Biobehav Cell Neurosci 6 (2012): 18. Hunter Hunter RG . Epige netic ef fe cts of stress andcorticosteroi ds in the brain. Front brain. Front Cell Hunter Hunter R G, & M cEwen BS. Stress and and anxiety anxiety across across the l if espan: espan: structu structural ral plastici ty andepig eneti c regulation. Epigenomics 5 (2013): 177-194. Ito TA, Larsen JT, Smith NK, & Cacio Cacio ppo JT. Ne gative informatio n weig hs more heavil y on the brain: brain: the negati vi ty bias in evaluative catego riz ations. J Pers Soc Psychol 75 (1998): 887-900. Ito TA, Larsen JT, Smith NK, & Cacio Cacio ppo JT. Ne gative informatio n weig hs more heavil y on the brain: brain: the negati vi ty bias in evaluative catego riz ations. J Pers Soc Psychol 75 (1998): 887-900. Ivanoff J , Branning Branning P, & M arois R . M apping apping the path pathways ways of informatio n processing f rom sensation to action in four disti disti nct nct sensorimotor task s. Hum Brain Mapp 30 (2009): 4167-4186. Am J Physiol Regul Integr Comp Comp Physiol 299 (2010): R343-R351. Janko rd R, et al . Stress activation of IL- 6 neurons neurons in the hypothalamus. othalamus. Am Karatsoreos Karatsoreos IN, & McEwe n BS. Psychob Psychobio lo gi cal all ostasis: resistance, resi resi li ence and vulnerabil vulnerabil ity. Trends Cogn Sci 15 (2011): 576-584. F1000Prime Rep 5 (2013): 13. Karatsoreos, IN, & McEwen BS. Resilience and vulnerability: a neurobiological perspective. F1000Prime Kuo LE, e t al. Chronic Chronic stress, combined wi th a hig h-fat/hig h-fat/hig h-sugar h-sugar diet, shi fts sympatheti sympatheti c sig nali nali ng toward neuropeptide europeptide Y and le ads ads to obesi ty and the metaboli c syndrome. Ann N Y Acad Sci 1148 (2008): 232-237. Kuo LE, e t al. Neuropeptide Neuropeptide Y acts acts directly in the periphery on fat tissue and mediates stress- induced induced obesity and and metabol metabol ic syndrome. Nat Med 13 (2007): 803-811. Neuroimage 47 (2009): 1135-1140. Lane RD, & Wager TD. T he new new f ie ld of Brain-Body M edici ne: what what have have w e l earned and and where where are we headed? headed? Neuroimage Neurosci 6 (2012): 34. Luders Luders E, e t al. T he unique brain anatomy anatomy of meditati on prac practiti titi oners: alterations i n cortical cortical gyrif icatio n. Front n. Front Hum Neurosci Luders Luders E, Toga A W, Le pore pore N , & Gaser C. The underl yi ng anatomical correl ates of lo ng-term meditati on: larger hippocamp hippocampal al and frontal vol umes of g ray matter. matter. Neuroimage 45 (2009): 672-678. Lupie Lupie n SJ, et al . Larger amygdala but no change ange i n hippocampa ippocampall v ol ume in 10- year-ol d chil chil dren dren exposed to maternal maternal depressi ve sy mptomatol mptomatol ogy si nce nce birth. Proc birth. Proc Natl Acad Sci U S A 108 (2011): 14324-14329.
Neurosci 7 (2013): 8. Mal inowsk i P, Neural Neural mechanisms of attentional control control i n mindfulness meditati on. Front on. Front Neurosci Manenschijn L, et al. High long-term cortisol levels, measured in scalp hair, are associated with a history of cardiovascular disease.
J Clin Endocrinol Endocrinol Metab 98 (2013): 2078-2083.
Marcovecchio M L, & Chiarell i F. The e ff ects of acute and chr chronic onic stress on diabetes control. Sci Signal 5 (2012): pt10. Maroi s R, & Ivanoff J . Capacity Capacity li mits of i nformation processing in the brain. brain. Trends Cogn Sci 9 (2005): 296-305. McEw en BS. Mood disorders and andall ostatic l oad. Biol Psychiatry 54 (2003): 200-207. McEw en BS. Central Central e ff ects of stress hormones hormones i n heal heal th and anddisease: U nderstanding erstanding the protectiv protectiv e and damaging damaging ef fe cts of stress and stress mediators. Eur J Pharmacol 583 (2008): 174-185. McEw en BS. The brain brain i s the central organ of stress and ada adapta ptatio tio n. Neuroimage n. Neuroimage 47 (2009): 911-913. McEw en BS. Brain Brain on stress: how the social environment gets under the sk in. Proc Natl Acad Sci U S A 109 Suppl 2 (2012): 17180-17185. Neuropharmacology 62 (2012): 3-12. McEw en BS, Eil and and L, Hunter RG , & Mi ll er M M . Stress and anxiety anxiety : structu structural ral plastici ty and and epigeneti c regulation as a consequenc consequencee of stress. Neuropharmacology McEwen BS, & Getz, L. Lifetime experiences, the brain and personalized medicine: an integrative perspective. Metabolism 62 Suppl 1 (2013): S20-S26. McEw en BS, & Gi anaros anaros PJ. Stress and all all ostasis i nduced uced brain brain plastici ty. Annu Rev Med 62 (2011): 431-445. McEw en BS, & Kali a M. The rol e of corticosteroi ds and andstress in chronic chronic pain pain conditio conditio ns. Metabolism ns. Metabolism 59 Suppl 1 (2010): S9-15. McEw en BS, & Magarinos AM. Stress and hippocampal ocampal plasti city: i mplicatio ns for the pathophysi ophysi ol ogy of affe ctive disorders. Hum Psychopharmacol 16 (2001): S7-S19. Neurosci 12 (2009): 342-348. McGo wan PO, et al. E pigeneti c regulatio n of the gl ucocorticoi ucocorticoi d receptor in huma human n brain brain associates wi th chil dhood abuse. abuse. Nat Neurosci Neurosci 6 (2012): 18. Mo ore A, Gruber Gruber T, Derose J , & M ali nowski P. Re gular, brie brie f mindfulness meditati meditati on practice practice improves el ectrophysi ol ogi cal mark mark ers of attentio attentio nal nal control control . Front Hum Neurosci Moylan S, et al. Exercising the worry away: how inflammation, oxidative and nitrogen stress mediates the beneficial effect of physical activity on anxiety disorder symptoms and behaviours. (2013): (2013): 573-5 84.
Neurosci Biobehav Rev 37
Clin Exp Pharmacol Physiol 34 (2007): 377-384. Muel le r PJ. Exe rcise training and and sympath sympatheti eti c nervous nervous system activi ty: evi dence dence f or physical physical activi ty dependent neural neural plastici ty. Clin Novak M, e t al. Perceiv ed stress and incidence of Type 2 diabetes: a 35-y ear fol lo w-up stud study of mi ddle -aged Swedish men. Diabet Med 30 (2013): e8-16. O’Donovan A, et al. Pessi mism correlate s with leuk ocyte tel omere shortness shortness and and el evated interle uki n-6 in post-me nopau nopausal sal wome n. Brain Behav Immun 23 (2009): 446-449. O’Donovan A, et al . Stress appraisals praisals and cel lul ar agi agi ng: a k ey rol e f or antici patory patory threat threat in the relati onship onship betwee n psychologi cal stress and and telome re l ength. Brain Behav Immun 26 (2012): 573-579. Ossewaarde Ossewaarde L, e t al. Stress-i nduced uced reduction reduction i n reward-rel ated prefrontal prefrontal cortex f unction. Ne uroi uroi mage 55 (2011): 345-352. Aging Neurosci Neurosci 2 (2010): 9. Penner Penner MR , Ro th TL, Barnes Barnes CA, & Sweatt JD . An epig epig eneti c hypoth hypothesi esi s of aging-re lated cogniti ve dysfunction. dysfunction. Front Aging Pereg D, e t al. Hai r cortisol cortisol and and the risk for acute acute myocardial myocardial infarction in adult adult men. Stress 14 (2011): 73-81. Rev Neurosci 13 (2012): 22-37. Popoli M, Yan Z, M cEwen BS, & Sanacora Sanacora G. The stressed synapse: synapse: the i mpact mpact of stress and and glucocorticoids on gl utamate utamate transmissi transmissi on. Nat Rev Puterman E, et al. The power of exercise: buffering the effect of chronic stress on telomere length. PLoS One 5 (2010): e10837. Puterman Puterman E, et al . Physical activi ty moderates eff ects of stressor- induced rumination on cortisol cortisol reactivi ty. Psychosom Med 73 (2011): 604-611. Re iche EM , Nunes Nunes SO, & Mori moto HK. Stress, depressio n, the i mmune syste m, and and can cancer. cer. Lancet Oncol 5 (2004): 617-625. Roth TL, & Sweatt JD. Epigenetic marking of the the BDNF gene by earlyearly- li fe adverse experiences. Horm Behav 59 (2011): 315-320. Russel l E, Ko ren G, Ri eder M , & VanU um S. Hair cortisol as a bio bio lo gi cal marke r of chronic stress: current current status, future future dire ctions and and una unanswered nswered questions. questions. Psychoneuroendocrinology 37 (2012): 589-601. Sei tz R J, F ranz M , & Azari NP. Value judgments and and sel f- control control of acti on: the role of the medial f rontal cortex. Brain Res Rev 60 (2009): 368-378. Thaker PH, Lutgendorf Lutgendorf SK, & Sood AK. The neuroendocrine neuroendocrine i mpact mpact of chronic chronic stress on cancer. cancer. Cell Cycle 6 (2007): 430-433. Thayer JF, Ahs F, F, Fredrik son M, Soll ers JJ , & Wager Wager TD. A me ta-analysi ta-analysi s of heart rate variabil variabil ity and neuroi maging studie s: impli cations for heart heart rate rate variabil ity as a mark mark er of stress and health. Neurosci Biobehav Rev 36 (2012): 747-756. Tomiyama AJ, e t al. Doe s cell ular agi ng rel rel ate to patterns patterns of al lo stasis? An examination of basal andstress reactive HPA axis activi ty and and telome re le ngth. Physiol Behav 106 (2012): 40-45. Vaish A, Grossmann T, & Woodward A. Not all emotions are created equal: the negativity bias in social-emotional development. Psychol Bull 134 (2008): 383-403. Van Van Wi ngen GA, e t al. Persiste nt and reversibl e consequences consequences of combat combat stress on the meso frontal circuit and cogniti on. Proc Natl Acad Sci U S A 109 (2012): 15508-15513. Van Van Wi ngen GA, Ge uze E, Vermetten E, & Fe rnan rnandez dez G . Consequences Consequences of combat combat stress on brain brain functio functio ning. Mol Psychiatry 16 (2011): 583. Vaynman S, & Gomez-Pinilla F. Revenge of the “sit”: how lifestyle impacts neuronal and cognitive health through molecular systems that interface energy metabolism with neuronal plasticity. J Neurosci Res 84 (2006): 699-715. PLoS One 8 (2013): e61038. Wei GX, GX , et al . Can tai tai chi re shape the brain? A brai brai n morphometry morphometry st udy. udy. PLoS Wi ll iams LM , et al. ‘ Negativi ty bias’ in risk for depression andanxie anxie ty: brain-b brain-body ody fear circuitr circuitry y correl correl ates, 5-HTT-LPR and early li fe stress. Neuroimage 47 (2009): 804-814. Z occola PM, & Di cke rson SS. Assessing the relati onship onship betwee n rumination rumination and cortisol cortisol : a revi revi ew. J Psychosom Res 73 (2012): 1-9.
KNOWING KNOW ING YOUR ENEMY IV IV
CIRCADIAN DISRUPTION: THIEF IN THE NIGHT
Our body and mind follow a natural rhythm of activity and rest that few of us appreciate or follow. The modern environment is at odds with this ancient internal rhythm that that developed developed at the the or igin of our species. species. Failure to follow this circadian rhythm creates dissonance and disruption in the internal workings of our body—with profound consequences to our health that modern science is just now beginning beginning to appreciate. appreciate. Circadian Disruption is one of the more slippery members of the Pentaverate. He oper ates in ghostly g hostly silence sil ence and attacks attacks relentlessly. r elentlessly. You cannot touch, taste, taste, smell, or hear him. The only evidence of his attack is constant fatigue and the slow destruction of your health. We will show you how to spot him and stop him in his tracks. We have his number.
CIRCADIAN DISRUP DISRUPTION TION I
THE INTERNAL INTERN AL TIMEKEEPER TIMEKEEPER
A master clock resides deep inside the brain. It governs cycles of sleeping, waking, eating, fasting, body temperature, and controls the ebb and flow of the various vario us hormones hormo nes that that control o ur metabolism. metabolism. This clock is not constructed of metallic gears, it is a molecular clock made of genes and protein located within specific nerve cells of the hypothalamus. Recall that the hypothalamus is the control center of the brain that responds to signals from the environment. It controls many of the body’s processes, so it makes sense that the hypothalamus houses the master clock.
QUICK DEFINITION: Pr ocesses that that Circadian is from the Latin circa = “about” dies = “day”. Processes follo w circadian rhythm rhythm fluctuat fluctuatee over a time period o f approximat appro ximately ely 24 hours or “about a day.” The inner inner wor kings of our o ur master molecular clock clo ck are just now being being under under stood
by very sophisticated cutting edge science and will not be covered in Strong mplexity. Medicine due to the extreme co mplexity. Science has recently shown that most cells in the body contain their own circadian clocks, but only the master clock in the hypothalamus can maintain a circadian rhythm without external influences from the environment. Scientists have removed master clock cells and locked them away from environmental influences like light and dark, fueling and fasting, and yet they maintain their rhythm of slightly slig htly more mor e than a 24-hour 24-hour cycle (between (between 24.2 24.2 and 24.5 24.5 hours). hour s). The master clock in the hypothalamus regulates all of our major organs including the liver, lungs, heart, kidneys, gastrointestinal tract, and our muscles.
Each organ has its own internal clock that is influenced by the master clock. This ensures that each organ system is adjusted to meet the metabolic and functional demands demands of activity activity during during waking waking hours, hour s, and allows for “sleep mode” regeneration reg eneration during rest and sleep. This rhythm of the metabolic and physiologic ebb and flow allows for maximal efficiency efficiency in operation oper ation and repair of the the “flesh machine. machine.””
THE CONDUCTOR OF THE ORCHESTRA The master clock in the hypothalamus coordinates the activity and regeneration rhythms of the organs in the body. The individual organs’ clocks also communicate with with each other other thro thro ugh hor monal signals sig nals to coor coo r dinate dinate optimum functionalit functionality y for activity during the day, and repair and regeneration at night. This timing system system and the the or gans’ coordinat coor dinated ed rhythms rhythms are ar e crucial fo r ensuri ensuring ng precious energy is not wasted and each organ system is prepared to function individually and in harmony with the other organs. The whole system must be coordinated to deal with the extremes of the circadian cycle: full throttle physical activity during the day, and deep sleep during night time hours. The master master clock is the conduct conductor or of this this symphony orchest or chestrr a. The various vario us or gan clocks are the musicians who must listen to each other while following the conductor. One organ clock out of sync with the system is like a violist playing a different tune than the rest of the orchestra—disastrous to the overall performance, and in the body, this is disastrous to long-term health. Peripheral body “organ clocks” are set by the “master clock” in the
hypothalamus. Each organ clock controls organ functions during activity and cr ucial in ensuri ensuring ng the org an systems systems work together regeneration regenerat ion modes. modes. They are crucial in a synchronized manner. As we will see, desynchronized desynchronized (broken) clocks lead lead to to
chronic disease.
The adrenal gland’s clock helps maintain the timed secretion of cortisol in the the early mor ning to prepare fo r activity activity by increasing increasing g lucose release from the liver. It reduces cortisol levels in the evening and through the night to to promo pr omote te rest and and regeneration.
heart for daytime daytime by making making it mor e T he heart heart clock clock helps prepare the heart r esponsive to the demands demands of physical activity with with heart rate r ate and str str ength of contraction. At night, the clock allows the heart to be less responsive during sleep.
The liver clock helps control the “glucose banker” so that the liver can store glucose during daytime activity and meals, then release and make glucose at night during fasting to supply the brain.
T he pancreas pancreas clock sets insulin secretion at the highest during daytime activity to allow for energy storage. At night, insulin secretion is set low to ensur ensur e the the brain r eceives eceives a steady steady supply supply of glucose gl ucose for reg eneration.
hor mones adiponectin adiponectin and leptin. leptin. T he fat fat clock contro ls the release o f the hormones Adiponectin is higher during daytime activity to increase insulin sensitivity, allowing the storage of nutrients. Leptin is higher at night, delivering the “stop “stop eating” signal necessary for fasting fasting during dur ing regeneration.
The muscle clock helps prepare our muscles for optimum performance during the day. The clock sets a metabolic rhythm, making it easier for muscle to burn glucose during the day, then using fat for energy at night.
The immune clock has the immune system on alert for threats such as bacteria and vir vi r uses in the daytime, then at night the adaptive adaptive assassins assassi ns create “immune memories” for the threats encountered during the day.
The kidney clock helps control fluid and electrolyte balance in the body. To support daytime activity, blood pressure is increased, then at night there’s there’s a 10-20% 10-20% dr dr op in blood bloo d pressure during regeneration. reg eneration.
egulates gast g astro ro intest intestinal inal function function to increase dig estion, estion, The gut clock r egulates absorption of food, foo d, and and motility (movement (movement of digested food) foo d) during the day. It signals for repair of the gut lining at night when digestive processes are minimized.
Durin Duringg daylight daylight hours, hormone hormone levels are cont rolled by the mast master er clock in the t he hypothal hypot halam amus us to t o support increased increased physical physical activit activit y. incr eases glucose after after • Cortisol Cort isol level levelss are highest highest in t he morning. morning. This increases night-time fasting, making energy available for the brain and body. It also helps “wake you up”.
• Leptin levels levels are low in in the mor morning ning and during daylight hour hours, s, this this gives the brain the “GO” signal to eat. Hunger is high with low leptin levels, this this pro motes eating eating to satisfy the the energy r equir equirement ement for physical physical activity during the day. day.
• Melat Melatonin onin levels levels are suppressed by light light , which brings the brain and body out of resting/sleep mode to prepare the mind and body for activity.
• Growth Gro wth hormo hormo ne is low, low, suppressed by increased cortisol in the mor ning as the the body comes out of the the regeneration/repair reg eneration/repair mode of sleep.
Durin Duringg t he onset of night night,, horm ho rmone one levels levels are controlled cont rolled by the mast master er clock in in the t he hypothal hypot halam amus us to t o support repair repair and regeneration.
prepar e the the body and brain brain fo r • Cortisol Cort isol levels levels are lowest lowest at thi t hiss time time to prepare sleep. Low cortisol allo ws for g ro wth wth hormo ne secretion secretion during sleep. g iving the brain the signal to “stop • Leptin levels levels are high high at night, night , giving eating”. Hunger is low with high leptin levels, which promote fasting during the repair/r repair /regeneration egeneration phase and and allow for uninterr uninterr upted upted sleep (no (no need for midnight snacks). snacks). sets, giving givi ng the brain brai n and body • Melatonin levels levels start st art to t o rise as the sun sets, the the signal to slow down in preparation for fo r sleep and the the repair and regeneration that happens during this time. dur ing deep sleep in the the first fir st par par t • Growth Growt h hormone hormone is is high high especially dur of the the night. Growt Gr owth h hormone hor mone increases incr eases the the burning of o f body fat for energy during duri ng fasting, and increases muscle repair and regeneration. Because the organs in the body function differently if we are in the activity or regeneration phases of the circadian rhythm, are there optimal times to perform activities such as exercise and eating so these activities match up with the rhythm of organ function? • Is it bette betterr to to exercise exercise in the the mor ning or evening? evening? • Is a late night snack a go od idea? • Are there any health consequences to shift work? wor k? We’ll answer these questions in upcoming sections, but they are important to consider now.
LIGHT RESETS THE MASTER CLOCK While the master clock in the hypothalamus can keep running without any external influence, the clock can be reset to match the external environment through outside influences such as light. It is important to reset the clock daily as most people’s internal master clock runs in a cycles a bit longer than 24 hours. The majority of the general public has an internal timekeeper genetically set to about 24.5 hours. Some people may have longer cycles up to 26 hours. Without external cues from the environment (such as light), the internal timekeeper would slowly advance out of sync with the environmental 24 hour cycle ruled by the rising and setting of the sun. Most people’s internal time would end up being about 30 minutes off “environmental time” each day, adding up to over 3
hours out of sync in a week.
KEY POINT: Most people’s master clock is genetically set for a cycle of about 24.5 hours. We need external “cues” from the environment to “reset” our clock each day. The external environmental clock setters are called “zietgebers,” which is German for “time givers.” Light is the most powerful zeitgeber that resets our master master clocks on a daily basis.
KEY POINT: Light is the most powerful environmental cue to reset the master clock. The circadian master clock regulates our daily rhythm of activity and regeneration through key hormones as shown in the previous diagram. Of these hormones, melatonin is of particular importance to how we enter and exit the body’s body’s regeneration r egeneration mode. When light—especially short-wave length blue light—hits our eyes in the morning, specialized cells in the back of our eyes transmit this signal to the hypothalamus (master controller). The hypothalamus transmits the “light signal” to a tiny structure in the brain called the pineal gland, which is responsible for producing melatonin. The “light signal” tells the pineal gland to stop producing melatonin so we can enter enter the activity phase of the cir cadian cycle.
KEY POINT: Light signals the pineal gland to stop producing melatonin. Decreased melatonin levels send a message to the master clock and the organ clocks to prepare for the activity phase. After the physical and mental stress of our daily activities, the body and brain desperately need time to regenerate and repair. Our flesh machine enters regeneration mode primarily through the actions of the hormone melatonin. The dimming lig ht—w ht—with ith longer wavelengt wavelengths hs of red and or o r ange—in the the evening evening signals the hypothalamus to tell the pineal gland to start making melatonin. Melatonin production starting at twilight is the gateway into regeneration mode.
KEY POINT: The dimming light li ght of the evening evening sky signals sig nals the the pineal gland to start producing melatonin. Melatonin is the gateway into the regeneration phase.
MELATONIN: THE GATEWAY TO
REGENERATION MODE Melatonin is indeed the “gateway” hormone for entering the regeneration mode, and it is essential for overall health with multiple actions in the body: • Melatonin elatonin prepares the the brain and and body for sleep, allowing a smooth smoo th transition transition between between waking and sleeping. sl eeping. • Melatonin signals sig nals the or gan clocks clo cks to start shifting from fr om activity activity mo mode de into regeneration mode. • Melatonin is a potent antioxidant and gr eatly increases incr eases the body’s internal antioxidant defense system system to decrease decr ease oxidative stress. • Melatonin has anti-inflammator y proper pr oper ties that can counteract chro nic inflammation. • Melatonin elatonin is a crucial signal for cellular and DNA DNA r epair. This is impor tant tant because damaged cells and DNA contribute contr ibute to to acceler accel erated ated aging and cancer. Given the many actions of melatonin which enhance regeneration of the flesh machine, and protect against chronic disease, anything that decreases melatonin during the evening and night has the potential to cause health problems. Melatonin interacts with the master clocks as well as the organ clocks to help keep the flesh machine “orchestra” perfectly synchronized as the brain and body weave in and out of the activity and regeneration modes in the 24 hour circadian rhythm.
KEY POINT: Interrupting the natural cycle of melatonin secretion at night has farreaching health consequences and contributes to many chronic diseases. One of the gravest consequences of low melatonin at night is sleep disturbance. Poor sleep has emerged as one of the most important public health issues of the modern age. Chronic poor sleep doesn’t just result in fatigue during the day, it plays havoc on the regeneration mode at night. Recent research shows that poor sleep is a
major contributor contributor to chronic chro nic disease. disease. Building Building a perfect night’ night’s sleep is a challenge in a modern world polluted by artificial light. Read on for a description of sleep in its optimum optimum for m.
CIRCADIAN DISRUP DISRUPTION TION II
SLEEP ARCHITECTURE: BUILDING A GOOD NIGHT’S SLEEP
There is a lot happening in the body and brain from the time you lay your head down at night until you wake in the morning. Sleep is much more than escaping the conscious world when the lights go out. The health benefits of the regeneration mode happen during high quality sleep. An episode of sleep is actually a very structured process built on a cycle of sequential stages that repeat approximately every 90-120 minutes, with four to five total cycles during a night of sleep. The structured cycle of sleep is called sleep architecture.
BUILDING BLOCKS There are two distinct types of sleep that occur during the night—non-rapid eye movement sleep (NR ( NREM EM)) and r apid eye-movement eye-mo vement sleep (REM): (REM): o f total sleep time dur ing the night. It is • NREM sleep makes up about 75% of divided into 3 distinct stages: NREM-1, NREM-2, and NREM-3. As you fall
asleep you descend down through thro ugh the stages: awake NREM-1 NREM-1 NREM-2 NREM-2 NREM-3 NREM-3. The electrical activity of your brain slows as you descend through the stages to NREM NREM-3. -3. Br Br ain electrical electr ical activity is very slow slo w at NREM NREM-3, -3, also named slow slo w wave wave sleep (SWS). Slo Slow w wave wave sleep happens mostly mos tly in the first fir st part of o f the night.
TECHNICAL NOTE: Non-rapid Non-r apid eye movement sleep (NREM (NREM) was traditionally traditionall y bro ken up into into four separate separ ate stages. stages. In 2008, 2008, the the American Academy of o f Sleep Medicine merged stages three and four—both characterized by slow wave sleep (SWS)—into one phase. The NRE NREM M-3 we refer to in this boo k is the combination combi nation of stages three and four, fo ur, to be consistent consis tent with with the new classification system.
• REM sleep makes up about 25% of o f total sleep sl eep time. In this this type of sleep, the brain brai n shows electrical electri cal activity similar to waking states. REM sleep is also al so known kno wn as “active sleep.” sleep.” REM sleep is when most dreaming dreami ng takes place, The l ength of time spent in REM sleep incr eases at the end of the night.
IMPORTANCE OF SLOW WAVE SLEEP (NREM-3) Slow wave sleep (SWS) during the first part of the night has some very importan impor tantt funct functions ions in the the regeneration r egeneration mode o f circadian cir cadian rhythm: rhythm: • Most Most of the daily supply supply of gr owth owth hormone hor mone is r eleased during during slow wave sleep. Recall that growth hormone is essential for sparing muscle mass while while burning fat for energy during dur ing the fasting fasting period per iod at night. Reduced Reduced slow slo w wave wave sleep leads to r educed growth gr owth hormo hor mone. ne. Reduced Reduced gr owth owth hormone hor mone leads to muscle wastin wasting, g, and slows fat loss to a crawl. • Event Eventss from fr om the pr pr evious day are stored stor ed in long-term memor y dur dur ing slow wave wave sleep. This is especially true for storing new infor mation mation
learned duri during ng the day into long-term memor y for later later r ecall. • Much of the cellular and DNA repair in the body and brain is performed during slow wave sleep.
COACH’S CORNER: You will not no t achieve achieve your body fat reduction reduction o r muscle gain go als if you yo u are not getting getting enough eno ugh sleep—no sleep—no matte matterr how dialed-in your nutr nutr ition and exercise exerci se plans. Inadequate sleep = reduced slow wave sleep = reduced
growth gro wth horm ho rmone= one= poor poo r body fat f at loss and increased increased muscl musclee wasting.
THE FIRST HALF OF THE NIGHT—(NREM-3) The fir st half of the night is dominated domi nated by slow slo w wave wave sleep (NREM (NREM-3). -3). Notice that that as you descend into sleep, you spend a relatively r elatively brief bri ef time in NREM NREM-1 -1 and NREM NREM-2 -2 befor befo r e spending the majo r ity of time in the deep SWS of NREM-3. The mind is quiet with slow electrical activity.
Much of the restorative and healing processes of the regeneration mode happen during NREM-3 in the first part of the night. Disrupting NREM-3 has significant health consequences of which few are aware. T HE SECOND SECOND HALF HALF OF T HE NIGHT NIGHT—(REM) —(REM)
The second seco nd half of the night is dominated domi nated by REM REM sleep, when dr dr eaming takes place. During this time, the the mind is very active with with electrical activity similar to waking states. During REM REM sleep, althoug although h the mind is active, the muscles of the body are paralyzed.
REM REM sleep sleep is extremely extremely im important port ant for healt healt h, but for different different reasons t han SWS as we will will discu discuss ss short sho rtly ly.. Most people don’t appreciate appreciate t he potential pot ential healt healt h consequen co nsequences ces of o f reduced dreamin dreaming. g.
IMPORT IMPORTANCE AN CE OF REM SLEEP SLEE P The impor impo r tance of rapid r apid eye movement (REM) (REM) sleep to human health and function is less clear than that of slow wave sleep, but some theories are emerging emerg ing fr om r ecent research. resear ch.... • In REM REM sleep, we can play play out stressful stressf ul situations in the safe environment of dreaming. dr eaming. This process is thought thought to give g ive us resiliency resili ency,, leaving us less vulnerable to the effects of actual stresses encountered during waking hours. Recall from the Stress Chapter how stress can cause significant sig nificant health problems. pro blems. REM REM sleep may help shield us fr om actual stressful events events by “rehearsing” stressful str essful situat situations ions in i n our dreams. • REM sleep is thoug thought ht to significantly signif icantly enhance enhance creativity and pr pr oblem solving. Histor Histor ically, ically, gr eat wor wor ks of art and scientific scientific breakt br eakthro hroughs ughs have been reported as happening after dreaming. Recent science has shown us that REM sleep activates activates areas ar eas of the brain thought thoug ht to to be r esponsible for problem pro blem solving and creativity creativity. Sleep research is still in its infancy and we are only beginning to crack the surface of what happens at night in the mind and body when we leave the conscious world. But, the nasty health effects of sleep deprivation are already well defined. Before we launch into the health problems caused by poor sleep, it is crucial to understand what causes us to fall asleep, and the transition from activity mode to regeneration mode. We cannot fix sleep problems such as insomnia if we do not understand the internal processes that allow us to fall asleep under ideal circumstances.
THE DRIVE TO SLEEP There are two primary processes that work together to promote falling asleep and staying asleep. If these two systems are synchronized, we will enjoy a smooth plunge into a restful and regenerative sleep period. If these systems are uncoupled, insomnia and restless, fragmented sleep may occur.
SLEEP SLEE P DRIVE #1: # 1: THE THE CHEM CHEMICAL ICAL SYSTEM The first sleep system is the “chemical system” because it is primarily driven by the build up of a certain chemical— adenosine br ain. The name of this adenosine —in the brain. chemical chemical may seem familiar; it is part of the “ener “ener gy curr ency” ency” molecule adenosine the Metabolism Metabolism 101 section. triphosphate (ATP) intro duced in the
Recall that the brain is an “energy hog” and uses 20% of the body’s supply of ATP even though it is only 2% of the body’s weight. When adenosine triphosphate (ATP) is used for energy it loses its phosphates and becomes adenosine. Adenosine could be understood as an energy waste-product. The brain goes through a mountain of ATP during the high activity of waking hours. Adenosine, the energy use “waste-product,” begins to build up in certain parts of the brain. This build up o adenosine is the chemical signal that produces fatigue and drives sleep as night approaches.
KEY POINT:
The “energy waste product,” adenosine, accumulates in the brain during the day. Once adenosine builds up to a certain level in the brain, it triggers the drive to sleep.
Adenosine building up during the day is analogous to adding debt on an “awaketime credit card.” Once this credit card reaches its awake-time spending limit for adenosine, it must be paid off. The only way to pay off this credit card is by sleeping. After several hours of sleep, a large amount of the adenosine will have cleared out—the out—the “credit card” will be close to paid off, o ff, and waking waking is trigg tr iggered. ered.
SLEEP SLEE P DRIVE # 2: THE CIRCADIAN SYSTEM The second sleep system is the one driven by the circadian rhythm. The circadian sleep system follows the light-dark cycles of your environment and works side by side with the chemical (adenosine) (adenosi ne) system. The circadian system sets the threshold o how much adenosine can be accumulated on the chemical system’s “awake-time credit card” before triggering sleep. The circadian sleep system sets the adenosine threshold (“credit-limit”) primarily through the actions of melatonin. During darkness, the circadian system secretes melatonin and sets the adenosine “credit limit” low. Lower amounts of adenosine will easily trigger sleep with the lower “credit limit”. When daylight hits the eyes, the circadian system stops secreting melatonin and the adenosine credit limit is set higher. Now it will take higher amounts of built up adenosine to trigger sleep.
KEY POINT:
The adenosine “credit limit” is the amount of adenosine build-up necessary necessary to trigg tr igger er sleep. This “credit limit” is set by the circadian
sleep system. • A high “credit limit” limit” requires a larg e amount of adenosine to to trig ger sleep. • A low lo w “credit “cr edit limit” limi t” only needs a small amount amo unt of adenosine adenosi ne to to trigg tri gg er sleep.
The morning sunlight triggers the circadian system to stop secreting melatonin. The circadian sleep system issues a high credit limit “gold card” for adenosine for fo r
use during the day. The adenosine gold card issued by the circadian system allows the brain to accumulate relatively high amounts of adenosine during the day without triggering sleep.
As the sun sets, low light levels trigger melatonin. At this time, the circadian sleep system system issues a low cr edit limit “gr “gr ay card” for use at night night.. The low credit limit gray card issued by the circadian sleep system lowers the amount of adenosine adenosine necessary necessary to trigg tr igg er sleep. The card switch from gold to gray as the sun sets allows the amount of adenosine that accumulated during the daylight waking hours to trigger sleep under the low adenosine credit limit of the gray card. The gray card’s lower credit limit requires that the adenosine “debt” be paid immediately imm ediately by sleeping .
The card switch switch from fr om gr ay to go ld as the sun sun rises r ises allows the brain to accumulate accumulate adenosine during waking hours without reaching the high credit limit. The gold card’s high credit limit prevents the accumulating adenosine from triggering sleep during the day, so we can wait to pay the sleep debt.
SLEEP SYSTEM SYNERGY The chemical and circadian systems are synergistic for a reason. It makes sense to sleep when when the the master master clock and or gan clocks clo cks of the the circadian cir cadian syste system m ar e primed pri med for the regeneration mode. Using the circadian sleep system, the brain will allow sleep to be triggered more easily by the chemical sleep system if the master clock and organ clocks are prepared to enter regeneration mode. It also makes sense to wake up when the master clock and organ clocks are primed for activity mode. The brain will resist the chemical signal (adenosine) to sleep if the the circadian master master clock and organ or gan clocks are ar e primed for fo r activity activity mode. When working properly, the circadian system will keep you asleep under the effects of melatonin even though your levels of adenosine are decreasing during sleep. The regeneration mode of the circadian system will set the low gray card “credit limit” for adenosine. This means you can clear out adenosine to relatively low levels by sleeping and remain asleep because the low adenosine levels are still trigg ering sleep because because of the the “low cr edit limit. limit.” During waking hours the circadian system in activity mode counteracts the rising levels of adenosine as the day progresses, allowing you to stay awake. The circadian system in activity mode sets the adenosine “credit limit” high with the gold card so you can accumulate adenosine without falling asleep during the daytime. The two sleep systems ensure that our circadian clocks and organ clocks are optimized to our activity levels. We should be awake during the circadian activity mode and asleep during circadian regeneration mode. To do otherwise will cause significant stress on our mind and body. Out of phase sleep systems result in using a gold card at night and a gray card during daytime. This is called circadian disruption and leads to poor sleep and eventually chronic disease. We are going to cover the health consequences of inadequate sleep in the next section, but first we will describe how the circadian system gets out of sync with the chemical-adenosine sleep system. Before we can fix something, we have to know the cause of the problem. The alternative is to try treating sleep symptoms with medications without addressing the underlying causes.
CIRCADIAN DISRUP DISRUPTION TION III
EDISON’ EDISON’S S FOLL FOL LY? THE CONSEQUENCES OF A BROKEN CLOCK
Thomas Edison, American inventor
Thomas Edison, the prolific American inventor of the late 19th century, brought us the first electric light bulb suitable for widespread consumer use. Edison also patented an early electrical distribution system, paving the way for the accessible electrical power we enjoy in our homes and businesses today. There is no doubt that Edison’s contributions to the Industrial Age have allowed the transition to the modern Information Age, supported by trillions of kilowatthours of electrical power annually. Businesses can now operate around the clock, and we can engage in late night recreation because of the ubiquitous bright electrical lighting in our world. Prior to electric light, the world primarily woke and went to sleep with the light and dark cycles from the rising and setting of the sun. Prior to 130 years ago, our circadian rhythms were entrained with the sun since the origin of our species. Electric light has enabled us to live out of sync with our natural circadian rhythm by extending waking activity well into the night. It has also enabled us to start working well before the sun comes up in the morning. From a circadian perspective, the regeneration mode has been significantly shortened in exchange for extended activity time. Science is now starting to understand that the artificial disruption of the circadian system may not be so good for our health. Light is the most powerful stimulator of the circadian system. Natural light is broken up into a spectrum of different colors, each corresponding to different wavelengths. wavelengths. You You can see the light spectrum when it is refr r efracted acted by water water dr oplets in a rainbow or when viewed through a crystal prism. Otherwise, you cannot distinguish distinguish the full spectrum spectrum of colors colo rs hiding within within daylight. daylight. The short wavelength—primarily blue light—portion of natural light stimulates our circadian system. Blue light signals the brain to stop melatonin production and prepare us to enter the activity mode of the circadian cycle.
The blue light fro m the sun sun rising r ising in the mor ning signals sig nals the the master master clock and the the organ clocks to prepare the mind and body for the increased energy demands of activity. activity. Natural Natural light’ lig ht’ss effects on o n melatonin keep us in activity mo de during dur ing the day. day. The circadian system issues us a high credit limit “gold card” to prevent the build up of adenosine from triggering sleep.
KEY POINT: Blue light, the short wavelength part of natural light, is the primary stimulator of the circadian cycle. Blue light turns off melatonin production and signals the activity mode to start. Before incandescent light bulbs were widespread, the setting sun reduced the blue light signal that triggered melatonin production. The circadian system issued the “gray card” with the low credit limit as melatonin increased and the adenosine build-up triggered sleep. Light from candle flames and fire have less blue light in their spectrums and did not significantly affect the circadian circadian systems of preindustrial citizens. In modern times, widespread use of indoor electric light at night has effectively extended the daylight. Although indoor electric light is lower in intensity than sunlight, it still has a significant amount of blue in its spectrum. It does not take
much blue light to stop melatonin production, and recent science has shown that most nighttime indoor light significantly reduces melatonin production. This light the activity mode o f the circadian cir cadian cycle at the expense of the at night night (LAN) (LAN) extends the regeneration mode. Computer screens and television sets also give off significant amounts of blue light. Light at night (LAN) is not just from indoors. If you live in or around a metropolitan area, it will be difficult to see the starts at night. Many places in our country simply no longer have true darkness at night. Street lamps and illuminated signs shine through thro ugh bedroom bedro om windows, windows, potentially potentially disrupting disrupting melatonin melatonin pr oduction oduction light pollution pollution . and sleep. This constant outdoor electric light at night is known as light
FALLIN ALLING G ASLEEP ASLEE P WITH LAN The light at night (LAN) exposure many of us have produces an abnormally long activity mode with no gradual transition from wake to sleep. Without exposure to LAN, melatonin production starts approximately 2-4 hours after natural light starts to dim at sunset. This delay in melatonin production 2-4 hours after sunset corresponds well to bedtime for many people who do not have the influence of artificial light at night. Recent research has shown that exposure to artificial light at night not only delays
the onset of melatonin production, but also reduces the total amount of melatonin produced overnight. Many of us try to go to sleep right after exposure to artificial light for most of the evening hours. Even though we have turned off the lights, we will have to wait an additional 2-4 hours for melatonin production to start in full swing. Since melatonin is the gateway to the regeneration mode for the mind and body, we have delayed and shortened the time for recovery and repair. Light at night (LAN) also makes it difficult to fall asleep. Recall that melatonin generated by the circadian sleep system issues the low-credit limit “gray card” for the adenosine sleep system. In this way, melatonin allows the built-up adenosine to trigger sleep. If we have delayed melatonin production with LAN, we are still in the activity mode of the circadian sleep system. We are still carrying the high credit limit “gold card” for the adenosine sleep system while trying to fall asleep. The gold card credit limit will not allow the adenosine built up during the waking hours to trigger trig ger sleep. Insomnia Insomnia is the the r esult. esult.
Using the adenosine “gold card” at night = insomnia Compounding the problem, light at night decreases the melatonin produced when we finally enter the regeneration phase. The low levels of melatonin do not produce a strong “keep sleeping” signal as adenosine levels of the chemical sleep system drop during sleep. The result is frequent waking during the night, especially towards towards the early mor ning. Valuable sleep is lost. Many people in modern society wake before dawn to a home illuminated by low intensity artificial light. Then they go to offices with only low intensity artificial light which does not completely shut off melatonin production. To truly reset the circadian system in the morning and strongly enter the circadian activity mode, we need the the high intensity intensity natu natural ral light from fr om outdoors. outdoor s. Outdoo Outdoorr natural natural light has a high enough intensity and a significant amount of blue light in its spectrum to absolutely tur tur n off melatonin. melatonin.
KEY POINT: High intensity natural outdoor light is the best way to reset the circadian system and enter enter into activity mode. While anemic indoor light is enough to stall the start of melatonin production at night, it does not sufficiently shut off melatonin production in the morning once the regeneration mode has picked up steam during the night. The low intensity indoor lighting sends mixed signals to the master clock and organ clocks. The internal clocks do not fully initiate the activity mode, and your brain and body are not optimized to meet the the challenges challeng es of o f the day. day. Many people who who suffer from fr om disrupted disrupted circadian cir cadian syste systems ms and the resulting resulting poor sleep at night turn to stimulants like caffeine to keep them going during the day. The out-of-sync circadian sleep system lets relatively small amounts of adenosine build up and trigger an intense feeling of fatigue and need to sleep. It is no surprise that caffeine wor wor ks by interfer interfer ing with with adenosine signaling. A significant number of us carry around enough chronic adenosine sleep debt that we need caffeine and other stimulants on a daily basis to keep functio functioning. ning.
QUICK QUICK MEDICAL MEDICA L NOTE: Caffeine keeps you alert for activities such as all night study sessions, late night parties, parties, or to help you get thro through ugh your day after after poor sleep. It stimulates us and delays delays sleep by stopping the actio actions ns of adenosine in the brain. In effect, caffeine—and the the theophylline in i n tea—slows down the chemical sleep drive dr ive system, keeping keeping you awake. Unfortuna Unfor tunately tely you will have to pay your sleep debt at some point after the effects of the caffeine wear off.
LAN AND CIRCADIAN DISRUPTION The end result of high amounts of indoor light at night and the lack of outdoor natural light in the daytime is a broken circadian system. This shortens the duration of restorative sleep at night and leaves us struggling to survive the day without falling asleep. Over time, this pattern leads to chronic disease through allostatic overload. Noted scientists and chronobiologists Michael Terman, PhD, and Ian McMahan, PhD, PhD, state state in their their gr oundbreaking boo k Chronotherapy, “Most of us live a twilight existence.” They are describing modern life with no true daylight in indoor offices during the day, and light pollution obscuring true darkness at night creating perpetual twilight.
Circadian Circadian disruption disruptio n and poor sleep significantly significant ly fills fills your stress cup Circadian disruption and the accompanying lack of restorative sleep are major contributors to filling your daily stress cup. Light at night (LAN) allows us to uncouple the synergy between the circadian cycles of activity and regeneration modes, and our actual patterns of waking and sleeping. The long-term health effects of this circadian disruption cannot be underestimated—the clocks are broken.
CONSEQUENCES OF A BROKEN CLOC CLOCK K Long-term cir cadian disr disrupt uption ion o ften ften leads to to chronic chr onic poor poo r sleep with with significant health consequences. It is hard to separate the adverse health effects of circadian disruption from fr om those those o f inadequat inadequatee sleep as they so o ften ften occur together. together. Circadian disruption disruption leads l eads to to sleep problems, pro blems, and poo poorr sleep can negatively negatively effect the circadian system. Not all sleep disorders are caused by circadian disruption but these sleep problems do impact the circadian system. Trying to tease out the cause
of these long-term health effects is like the “chicken or the egg” argument. We do know that long-term inadequate sleep is strongly associated with the following conditions:
• • • • • • • • •
Obesity Insulin Insulin r esistance and diabetes Cancer High High blood pressure Incr Incr eased susceptibility to infectious disease Heart Hear t and vascular disease Depression Depression Aggr avated symptoms of autoimmune disease Accelerated aging agi ng
The chronic disruption of the circadian system seen in long-term night shift workers has also been associated with all of the conditions listed above. This supports the strong reciprocal link between sleep disruption and circadian disruption r egarding egar ding health consequence consequences. s.
THE MALFUNCTIONING MASTER CLOCK When the master circadian clock in the hypothalamus is “broken”, it has far reaching effects on the mind and body. Recall that the hypothalamus is the master controller for many functions of the flesh machine including: metabolism, reproduction, stress-threat response, hunger, thirst, and body temperature. The master circadian clock orchestrates the timing of all of these crucial processes in the hypothalamus hypothalamus based on anticipated activity activity and reg eneration eneratio n cycles. When the master clock is out of phase it affects the body’s organ clocks as well. With overall direction by the hypothalamus, the organ clocks are finely tuned with functions optimized to activity or regeneration, depending on their place in the circadian cycle. Exercising when the organs clocks are in regeneration mode, or sleeping during activity mode places stress on the body.
When the organ clocks are out of sync with your waking and sleeping activity, they are not prepared to function optimally to support your activity. Waking activity during cir cadian regeneration reg eneration mode leads to to poor po or physical physical and ment mental al performance perfo rmance as well as wear and tear on the body. Attempting to sleep in circadian activity mode promotes pro motes poor mind and and body repair and regeneration. Some possible scenario scenarioss are outlined belo w.
Cortisol timing is off and may peak when when you are trying to g o to bed at night instead of the normal time—just before waking. Cortisol at night is stimulating to the mind and body and will disrupt sleep.
A heart clock still in regeneration mode while you begin the increased activity of the day is not prepared to respond to the increased demands of physical activity. Wear and tear on o n the t he heart is the result.
A liver clock still in r egeneration mode while you are ar e having a meal in the mor ning will cause the the liver to mishandle glucose or fat. Insulin resistance, diabetes and fat t y liver liver disease disease are possible long-term consequences.
A pancreas pancreas clo ck still still in i n regeneration r egeneration mode during duri ng the day may not not pro duce adequate adequate insulin to handle food fo od intak i ntake, e, contribut contri buting ing to diabetes. If the clock is in activity mode while you are sleeping, the inappropriate insulin release may make your bloo blood d sugar too low at night.
A disrupte disr upted d fat clock clo ck will cause adiponectin adipo nectin and leptin leptin to be r eleased at the wrong times. The result will be hunger at night, disrupting sleep and loss
of insul insulin in sensit sensit ivit ivit y leading leading t o diabetes. diabetes.
A muscle clock still in regeneration mode during physical activity will poo r athl at hlet etic ic perfo perform rmance. ance. Muscle lead to poor Muscle clock clo ck dysfunctio dysfunction n can also cause improper glucose handling leading to insulin resistance resistance and diabetes.
A broken immune clock can lead to a poor defense against “invaders” during the the day and poo poorr for mation mation o f long-term lo ng-term immunity. immunity. It It may also lead to out of control cont rol inflam inflamm mation at ion which which contrib cont ributes utes t o heart disease, disease,
diabetes, cancer, cancer, and autoim aut oimm munity.
A broken bro ken kidney kidney clock can cause cause poor poo r regulat reg ulation ion o f fluid and electro electro lyte lyte balance balance contri contribut buting ing to high bloo d pressure, a risk factor for heart
disease disease and stro ke.
A gut clock still in reg eneration mode during a meal can lead to poor digestion and poor movement of food through the GI tract. A gut clock in activity activity mode during sleep leads to to poo r intest intestinal inal barrier barr ier regeneration reg eneration contributing contributing to chronic inflammation.
TECHNICAL NOTE: The organ clocks can adopt circadian rhythms independent of the master clock with signals such as food intake and exercise. This can cause problems pro blems with with vari various ous org o rg an clocks being on their their “own schedule schedule,” ,” and out of sync with with each another. That is why the the or chestrating function o f the master master clock is so impor tant tant,, it ensures ensures that that the the or gan clocks wor k together optimally.
THE MELA M ELAT TONIN CONNECTION? CONN ECTION? One of the primary ways exposure to artificial light at night may slowly destroy your health and vitality is through diminishing the amount of the hormone melatonin. We previously described the potent effects melatonin has during the regeneration mode as a powerful antioxidant and antiinflammatory agent. In addition to acting as a direct antioxidant to scarf up free-radicals, it also strongly stimulates the body’s own antioxidant defense system, protecting against oxidative stress. Melatonin has been shown to protect against cancer and accelerated aging. There are melatonin receptors (“docks”) in almost every type of cell in the body. Melatonin truly has a long reach, potentially affecting every part of the mind and body during its activity activity after after dark as the gateway gateway hormone hor mone to r egeneration. The benefits of melatonin are not a surprise given its protective effects against oxidative stress and inflammation. Diminished melatonin at night due to circadian disruption and reduced sleep is likely a primary mechanism through which sleep and circadian disruption contribute to chronic inflammation and chronic oxidative stress. These two processes are the well-known deadly duo leading to chronic disease. This is not to say that melatonin deficiency is the sole cause of all chronic diseases arising from circadian disruption and poor sleep. It is a likely major contributor, but circadian disruption and poor sleep activate the brain’s stress-threat system on their own. The stress-threat system greatly increases the flight or fight sympathetic nervous system activity level, resulting in inflammation and oxidative stress.
KEY POINT: Circadian disruption disruption and poor poo r sleep result in decreased melatonin melatonin production, chronic activation of the stress-threat system, and physiologic “wear “wear and tear” on the the internal internal o rg ans. This all adds to the the gr owing pool poo l of o f chronic chro nic inflammation inflammation and oxidative oxidative stress which lead to chronic disease.
CIRCADIAN DISRUPTION, SLEEP, AND DIABETES When the body’s organs are forced to operate out of phase with their own individual circadian clocks, the resulting metabolic derangement and physiologic stress causes additional inflammatory responses and oxidative stress. This is especially true of the liver, muscles, and the pancreas. Disruption of the natural daily rhythm of these three organs is thought to contribute significantly to the development of insulin resistance leading to diabetes. The effects effects of o f cir cadian disr disrupt uption ion and poo r sleep on the development development of insulin resistance and diabetes can be profound. Several recent scientific studies have shown that even a couple nights of poor sleep can increase insulin resistance to rediabetic rediabetic levels in healthy young people. It was found that the loss of slow wave sleep (NREM-3) is the biggest contributor to insulin resistance.
KEY POINT: A couple nights of poor sleep have been shown to increase insulin resistance in healthy young people to prediabetic ranges. Loss of slow wave sleep seems to be the most damaging. If circadian disruption and reduced slow wave sleep can give a healthy young person insulin resistance to prediabetic levels, imagine what metabolic havoc poor sleep can have on an obese or diabetic person. For diabetes, we often focus on nutrition and exercise to help control blood sugar levels. This is hugely important, but a diabetic with disrupted sleep will have great difficulty meeting blood sugar goals go als no matte matterr how good go od they are doing with with their their nutri nutrition tion and exercise. exercise.
QUICK QUICK MEDICAL MEDICA L NOTE: If you are o bese and/or and/or diabetic, diabetic, fixing your sleep must be a top prio rity ri ty.. Good Goo d nutr nutr ition and exer exer cise are a gr eat start, start, but but you you most mo st likely be unable to reverse type II diabetes without mastering your circadian rhythm and getting recuperative sleep. The next section will give the Strong Medicine Tactics to fix your sleep.
OTHER EFFECTS OTHER EF FECTS ON THE BRAIN AND A ND BODY
Circadian disruption and sleep loss result in poor long-term memory formation and difficulties with concentration. Both can also lead to anxiety and depression due to their effects on the brain. Slow wave sleep (NREM-3) and REM sleep are crucial for the brain’s recovery after a day of activity. During sleep, memories and information are stored, emotional events are processed to promote resiliency, and irrelevant ir relevant “menta “mentall debris” from fr om the the previous previo us day is cleared clear ed away away.. Circadian disruption tears away the carefully structured sleep architecture, often reducing slow wave sleep and REM time in favor of lighter sleep stages such as NREM-1 and NREM-2. This results in light, non-regenerative, restless sleep. You can get a full eight hours of this non-recuperative sleep and still feel like a truck hit you in the the morning. mor ning.
BODY FAT, MUSCLE, AND SLOW WAVE SLEEP Remember Remember that slow wave wave sleep is the primary primar y time for gr owth owth hormone hor mone release. Growt Gr owth h hormone hor mone is a major majo r player player in fat burning, burning, muscle gr owth, owth, and muscle muscle repair r epair during duri ng the regeneration reg eneration mode. Cir Circadian cadian disruption disruption leads to r educed slow wave sleep, a one-way ticket ticket to to bo dy fat gain and muscle wasting. You will not no t reach your body composition g oals unless you fix your yo ur sleep. A night of poor sleep will limit your productivity the next day, make it difficult to concentrate or make decisions, and will decrease your ability to handle stress. Your reaction time will slow to the equivalent of having a blood alcohol level above the
legal limit. A sleep-deprived driver can be just as dangerous as a drunk driver with impaired ability to react in traffic. Make sure you get your slow wave sleep before you drive.
QUICK FACT: A sleep-deprived driver can be just as dangerous as a drunk driver. Studies have shown that sleep deprivation results in reaction times as slow or slower than a perso person n with with a blood bloo d alcohol level above the legal limit of 0.08 g/dL. It’s likely that there are many more sleep-deprived drivers than drunk drivers driver s on o n the the road. r oad. Dr Dr iving while sleep-deprived sleep-deprived is a r eal safety safety concern and public health issue. Spending time to fix circadian disruption can be especially important for people suffering with depression. One of the interventions shown to be effective for improving depressive symptoms is bright light therapy (BLT). We will discuss BLT in the next section as a method to reset the circadian rhythm. The anti-depressive effect of BLT in the morning supports the theory that a significant contributor to depr depr ession may in fact be be circadian cir cadian disruption. disruption. A final note to dieters strugg ling to control contro l cr avings and foo d intake. intake.—circadian —circadian disruption and sleep loss stimulate the drive to eat. The threat/stress response that results from poor sleep puts the food reward system into overdrive. Poor sleep results in a strong drive for palatable and rewarding foods that are often the same foods a dieter is trying to avoid. Fixing your sleep and circadian system will put the reigns on foo d cravings. cravings.
KEY POINT: Circadian disruption and poor sleep put the food reward system into
overdrive. Your goals of sustained lifestyle change will be sabotaged by cravings if i f you do not addr addr ess circadian and sleep issues. issues.
SHIFT WORK: A CIRC CIRCAD ADIAN IAN NIGH NIGHTMARE TMARE Part of the formal training in Occupational and Environmental Medicine (OEM) includes chronobiology. Chronobiology is simply the study of natural biological rhythms such as the circadian system. OEM physicians apply the knowledge of chronobiology to shift workers. As much as 20% of the U.S. workforce participates in some type of shift work. Night time shift work is the ultimate circadian nightmare. It puts the worker at complete odds with the natural cycle of the sun’s rising and setting for activity and sleep. • The night-shift night-shift worker starts his or her day during the the darkness of night. They are gearing up for physical and mental activity when the mind and body should be ente enteri ring ng regeneration r egeneration mode. • They are exposed exposed to relatively low-intensit low-intensity y indoor light lig ht during their their wor wor k shift. This somewhat suppresses melatonin but does not give the strong circadian signal for activity mode that high-intensity natural light provides. They often rely on caffeine to block the sleep promoting effects of the adenosine which accumulates while they are working. • The night-shift worker wor ker often finishes their their wor wor k shift as the sun r ises in the mor ning. During During their their drive home, the high intensit intensity y outdoor light is stops melatonin pr oduction and places them in the circadian cir cadian activity mode. The circadian system issues them a “gold card” for adenosine with a high credit limit, and prevents the accumulated adenosine in the brain from their time at work from trig gering sleep. sleep. • The worker wor ker will will go home and and attempt attempt to sleep while their circadian system system is in activity mode. The outside daylight seeps into their home during sleep and decreases melatonin. The adenosine build up becomes so high that it is able to override the circadian system to fall asleep but only for a short while. Most night shift workers report only getting 5-6 hours of sleep at best in the daytime. The sleep they do get has a significantly disrupted sleep architecture with shortened slow wave recuperative sleep. • The night-shift worker wor ker wakes wakes in the afternoon afterno on and prepar es for the physical and
mental activity activity of their upcoming “day”. The sun sets during the hours when they are preparing preparing for work. • These workers worker s often eat their their meals during the the r egeneration mode of the the circadian system, system, a time that that the the or gans are ar e not prepared to process pro cess and stor stor e nutrients from food. This leads to metabolic derangement such as insulin resistance. The extreme circadian disruption and poor sleep of the shift worker results in significant health consequences. Night-shift workers are at greater risk for developing chronic diseases such as diabetes, obesity, high blood pressure, heart disease, depression, accelerated aging, and cancer. In fact, the World Health Organization has classified shift work as a carcinogen (cancer-promoting). Many people have no choice but to perform shift-work to make a living and provide for their families. In the next section, we will show some easy strategies shift workers can implement to minimize the circadian disruption of and improve their health.
EDISON’S FOLLY? The point of this section was not to blame circadian disruption in modern society on Thomas Edison’s amazing invention. There is no doubt that artificial light in the modern world has dramatically altered how we live our lives and has allowed increased productivity and an exponential rate of technological advancement over the past century. Unfortunately, substantial negative impacts to our individual and public health have resulted from this advancement as a tradeoff. Modern problems require modern solutions. We will now provide some very simple and science-based interventions that can go a long way in fixing your broken clocks and r estor estor e the the healing power power of cir cadian r egeneration mode.
CIRCADIAN DISRUP DISRUPTION TION IV
MODERN SOLUTIONS TO A MODERN PROBLEM
U.S. citizens are working longer hours than the citizens of any other industrialized nation in the world. We are taking full advantage of artificial light at night to to wor k longer hours, making us especially vulnerable vulnerable to circadian cir cadian disruption. disruption. Many other countries are not far behind us, with sleep disorders and circadian disruption emerging as a worldwide public health problem—if not an epidemic. Fueled by artificial light, our recreational activities are extending further into the evening hours as well, with time spent in front of computer and television screens constantly increasing. Statistics from the National Sleep Foundation support the notion of inadequate sleep as a public health epidemic. • Over 60% 60% of American American adults adults exper exper ience sleep disruption on two two or more mo re nights per week. • Appro Approximat ximately ely 40 million millio n Amer Amer icans report repo rt chronic chro nic sleep problems. pro blems.
• Appro Approximat ximately ely 30% of Americans Americans r eport r outinely outinely getting getting only 6 hours or less sleep per night. Additionally, the increased hours Americans are working do not translate into increased productivity on the job. Sleep deprived workers are not efficient or productive. An estimated $18 billion is lost every year in decreased productivity from fr om sleep loss lo ss in the U.S. U.S. alone. alo ne. We rely on stimulants such as caffeine during the day to keep us going while adenosine levels keep piling up in the brain. Caffeine does not solve the problem and we carry the accumulated adenosine as sleep debt, since we’ve artificially stopping the sleep trig ger. Most Most of o f us put off of f this sleep debt all week with with stimulants and try to r epay it on the weekends weekends by “sleeping in.” This patter patter n is hard har d on the body and brain, brain, and overfills overfil ls our stress cup (allostat (allostatic ic overload). over load). We switch off the bright lights as we hit the bed, already well into the night. Then we are frustrated that we can’t fall asleep immediately, as we struggle against a circadian system disrupted by light at night. We resort to alcohol or prescription drugs as sleep aids instead of fixing the underlying problem, a disrupted circadian rhythm. Alcohol and many of the drugs used to help people fall asleep dramatically alter sleep architecture. Slow wave restorative sleep time (NREM-3) is reduced and replaced by an increased time in the “light sleep” stage of NREM-2. You may fall asleep faster, but you are missing the period of slow wave sleep crucial for your health.
KEY POINT: Alcohol and many of the sedative prescription medications alter sleep architecture, reducing time spent in slow wave sleep. Sending your circadian system the right signals at the right times can reset your clock and will help break the cycle of using stimulants to keep you going and sedatives to make you sleep. Stop fighting your broken internal clock. There are some simple ways to realign your internal clock with your personal wake-sleep
needs, even if you are a shift-worker.
FIXING FIXIN G YOUR CLOCK CLOCK We can use light (even artificial light) to “train” your circadian system to match up with your waking and sleeping schedule. Training the circadian system with light exposure is what chronobiologists call entrainment. The timing of meals, body temperature, and exercise can also be used to entrain the circadian rhythm, but light remains the most powerful powerful “trainer “trainer”. ”. The goal of training your circadian system is having your activity mode fall inline with your time awake, and the regeneration mode synchronized with your sleep. This is more difficult with extreme situations such as night-shift work, but still doable to some extent. We will begin by showing you how to use light as a “circadian trainer.”
KEY POINT: Fixing your clock involves getting the activity mode of the circadian cycle to fall inline with your time awake, and the regeneration mode synchronized with your sleep.
LIGHT AS THE MASTER-TRAINER Recall that short-wavelength light in the “blue range” is a potent signal to turn off melatonin and start the activity mode of the circadian system, while the dimming light at the end of the day will trigger melatonin release in preparation for regeneration. reg eneration. The following foll owing interventions interventions will g et you started started in becoming a master master of your circadian rhythm...
Dawn Dawn simulator si mulator
• Use a dawn dawn sim simulat ulator or t o make make the transi t ransitt ion from sleepin sleepingg t o waking waking gentle g entle and natural. Most people people experience a startling startling transition transition fr om sleeping sleeping to waking with the piercing sound of an alarm clock. Often they are in the middle of REM REM sleep and the sudden sudden loud noise no ise r ips them out of their dream state, state, leaving them disoriented disor iented and with with an elevated elevated stress/threat stress/thr eat system system response. r esponse. This is no t an ideal way to to start star t your day. day. A r elatively new technolo technology gy allo al lows ws a light to gradually increase in intensity starting about 20-30 minutes before you plan to wake. This technology is called a dawn simulator and is very valuable for those who have to rise before the sun comes up. The idea behind using a dawn simulator is to provide a very gradual transition from darkness to light, mimicking the sun rising at your planned time to wake. The gr adual adual increase incr ease in light lig ht (even (even thro thro ugh closed clo sed eyes) signals the circadian system system to start shutting down melatonin production and prepare for activity mode. The decreasing melatonin from the slowly increasing light will naturally and gradually pull you out of sleep without the violent stimulus of an alarm clock. You can always set the alarm as a backup, but you will only rarely need it when using the dawn simulator. Philips makes a great dawn simulator.
• Get as much much bright bright natural light light as possible possible in the first hours ho urs after aft er wakin wakingg g ently tr tr ansitioning to the waking waking state state with the the dawn simulator, up. After gently continue to get exposure to bright natural spectrum light. Ideally this “natural” light would be the sun, but realistically many of us will need to resort to artificial sources of light that mimic the broad spectrum light of the sun. The most practical way to do this in the mor mo r ning is i s to buy lig ht bulbs bulbs that emit a substantial substantial amount of “blue spectrum” light. Many of these light bulbs are advertised as “natural” light on the package and are r ated with with a scale called Correlated Color Temperature (CCT). The CCT CCT scale scal e relates r elates to the color of light produced and is measured in units of Kelvin (K). Low CCT lights emit more yellow and orange light (longer (long er wavelen wavelengths) gths) and high high CCT bulbs emit more blue light (shorter wavelengths). Look for light bulbs that are rated in
t he high high CCT range, between 5000K and 6500K 6500K on the t he CCT CCT scale for use in the morning . CCT in these ranges has a substantial amount of blue light in the spectrum and is the most similar to natural sunlight.
The left picture pictur e shows a low l ow CCT and high CCT CCT bulb next to each o ther. You can’t tell which is which which just by loo king at them. The picture o n the right rig ht shows the the bulbs in identical fixtu fi xturr es. You You can tell the difference differ ence when the the lig hts are o n in the picture on the right. The high CCT bulb is on the far right and the light emitted is “whiter” (representing more blue light in the spectrum) compared to the light on the left that looks yellow in comparison. Install 5000-6500K CCT bulbs in areas of your home where you spend the most time in the the mor ning get g ettin ting g r eady for work—the work—the bathro bathroom, om, bedroom, bedro om, and kitchen kitchen.. You can find these compact fluorescent light bulbs at most large home improvement stores and online as well. The blue light emitted from these bulbs is enough to provide a strong signal to the circadian system to start activity mode.
STRONG MEDICINE TACTICS: Install lig Install l ight ht bulbs with with a CCT between between 5000-6500K 5000-6500K in areas of your home where wh ere you yo u spend the the most time getting getting r eady for work in th thee mor ning to maximize your blue lig ht exposure exposure aft after er wa waking. king.
RESEARCH UPDATE: Recent r esearch esear ch has shown that that exposure to lig ht with with high blue spectrum content in the first few hours after waking increases alertness, decreases
feelings of fatigue, increases br br ain funct function ion for fo r problem pro blem solving, and enhances product pro ductivity ivity at wor wor k. This will help synchronize your initial waking time with the start of the circadian activity mode. Using high-range CCT artificial light just after waking is especially important if... • • • •
You do do not have time to spend outdoor outdoo r s in the mo morr ning sunlig sunlight. ht. You need to wake up befor e the sun r ises. You live in a r egion egi on predominated predomi nated by gr ay skies and r ain with little sunshine. You You work indoor s.
Giving a strong signal to start the circadian activity mode with blue spectrum light will ensure that your waking time is supported by the master clock and organ clocks, optimizing mind and body functions for the demands of the day. This simple intervent intervention ion will ensure your circadian system system issues you an adenosine “go ld card” to prevent fatigue fatigue during your waking waking hours. hour s. As your waking time draws to an end, we have to give an equally strong signal to start the circadian regeneration mode and prepare for sleep. The strategies to synchro synchronize nize entering entering regeneration reg eneration mode with your planned planned bedtime bedtime are ar e the opposite from the morning strategy. We need to eliminate blue spectrum light exposure.
• Elim Eliminate inate exposure expos ure to blue spectrum spectr um light light 2-3 hours prior to your planned You can still use artificial ar tificial lig l ight ht after after the sun goes do wn, but the the type type of bedtime. You light used is crucial to prevent circadian disruption. Recall that it will take about 2-3 hours after the the last blue spect spectrr um light exposure fo r melatonin melatonin levels to start to rise, r ise, signaling the start start of o f r egeneration mode. If If you can synchronize the start start of melatonin production with your planned sleep time, your transition into a deep recuperative sleep will will be effor tless. tless. The easiest way to avoid blue spectrum light but still have artificial light for evening activities is to use compact fluorescent light bulbs that are yellow/orange in color. colo r. These These bulbs are traditionally sold as “bug lights” l ights” in home improvement impr ovement stor stor es. The yellow/or ange bulbs should be installed installed in the areas of your home where where you yo u spend spend most of your yo ur lat l atee evening evening hour s. Appro Approximat ximately ely 2-3 hours befor e you plan to sleep, turn turn off o ff all the the light lig ht sources except for the yellow/orange “bug lights.” This will allow you to continue
evening activity without without disrupting melatonin m elatonin pr oduction. By the time time you yo u get ready to sleep, melatonin melatonin product pr oduction ion and the beginning beginning of o f r egeneration mode will have started. Sleep should come co me much easier.
SCIENCE SCIENCE TRIVIA Yellow ello w “bug lig hts” block most mos t of the blue spectr spectr um in visible light. lig ht. Bug lights do not repel insects as many people believe, they just do not attract bugs. Many insects are very receptive to short wavelength light (blue spectrum) and use it i t as a navigational navigatio nal aid. If If they detect detect blue spectr spectr um artificial ar tificial lig l ight ht at night they are dr awn to to it. i t. They will not no t detect detect the the light lig ht from the yellow bulbs because most of the blue spectrum has been blocked.
STRONG MEDICINE TACTICS: Install Insta ll yellow/or ange light bulbs (“bug (“bug lig ht hts”) s”) in areas of o f your home where you spend the most time in the late evening evening to elimi eliminate nate blue light spectrr um exposure 2-3 hour s befor e planned sleep spect sleep time.
QUICK TIP:
Many people spend a significant amount of time in some areas of the house in i n both the mor ning and the evening evening (kitchen, bathro bathro om om,, etc.). etc.). Many Many of these “dual use” areas have more than one light source. Take advantage of this and install install the high high CCT natural natural light l ight in one sour ce for mor ning use, and the “bug lights” in another source. This way you can use certain light switches for the morning to get blue light exposure and the other switches for turning on the “bug lights” in the evening to avoid blue light exposure befor e bedtime. bedtime.
• Use amber-tint amber-tinted ed glasses to t o eliminate eliminate blue lig lig ht exposure expo sure from fro m com co mputer put er monitors or TV screens. Modern computer and television screens emit LEDgener ated light with with a substantial substantial amount of blue light lig ht in the the spectrum. Staring Staring at these screens until bedtime will ensure that your circadian rhythm is disrupted by delaying delaying melatonin pro duction duction and r egeneration mode. There are ar e blue light filters you can purchase for television television and computer computer screens but a simpler simpler option is just to wear amber-tinted glasses to block the blue spectrum light. The glasses are a great option for people with family members or roommates that will not support the use of the “bug lights” at night. Just put the glasses on 2-3 hours before your planned bedtime to ensure melatonin production happens on schedule.
Amber-tinted glasses- an inexpensive circadian solution The amber-tinted amber-tinted glasses are ar e also very valuable for night-time night-time shift wor wor kers who have to drive home as the sun is coming up. The glasses will block the blue spectrum part of the morning sunlight and prepare you for sleep when you arrive home. Mor Mor e on o n this use to come. co me....
STRONG MEDICINE TACTICS: Wear glasses with amber-tinted lenses to block blue spectrum light from televisions and computer screens at night. The glasses are also valuable to shift-workers.
• Ensure your bedroo m environment environment is opt o ptim imum um for fo r sleep. These interventions are cr ucial for ensur ensur ing a night nig ht of regenerativ reg enerativee sleep. Your sleep enviro enviro nment nment should be similar to a cave. — Keep the bedroom cool (usually between 65-72 degrees depending on individual individual preference prefer ence). ). Part Part of o f the regenerat regener ation ion mo de is a slow slo w fall in body temperatu temperaturr e as the the night prog resses. A cool ro om encourages encour ages this natu natural ral fall in body temperature. — Keep the bedroom dark. dar k. Use “black-out” curtains to block outside light from neighbors’ porch lights and streetlights. You can buy black-out curtains at most major retailers. Cover any lig ht-emitt ht-emitting ing electro nic devices devices as well. — Move televisi tel evisions ons out of the t he bedroom. bedroom. Bedrooms should be dedicated to sleeping. If this is not an option, make sure you wear the amber glasses while watching TV before bed.
STRONG MEDICINE TACTICS: Make your nighttime sleep environment “cave-like” to ensure uninterrupted regenerative sleep. These relatively simple interventions strategically using light to train your circadian system are extremely effective. They all have been tested in research settings with positive results. Although light is the most powerful “trainer” of your circadian system, exercise can have dramatic effects as well as long as it is properly timed.
EXERCI EXE RCIS SE AND A ND THE CIRCADIAN SY SYST STEM EM
Your muscles, heart, liver, and adipose tissue are all directly involved in supporting exercise. Each has its own organ clock governing function during activity and regeneration modes. Obviously, exercise should take place in the activity mode of the circadian cycle, since the body is not optimally primed for exercise during regeneration mode. Most people do not wake up in the middle of their sleep to exercise, but many do perform exercise near the transition zones between activity mode and regeneration mode which can be problematic. The benefits of regular exercise can be obtained anytime during the activity mode of the circadian system. Exercise timing falls more to individual preference and schedule schedule requirements. There ar e two two g eneral guideline g uideliness to follow: fo llow: • Ensure that your body and brain brai n have r eceived a strong stro ng signal to enter activity mode before befor e exer exer cising fir st thing thing in the the mor ning. Use the the early mor ning light lig ht exposur exposuree strategies strategies discussed pr pr eviously to to ensure your yo ur cir cadian clocks clocks are ar e set to activity activity mode befor e starting exercise. • Avoid exercise exerci se 2-3 hour s befor e planned bedtime. bedtime. Exercise dur during ing this this time acts much like blue light and can delay the onset of melatonin production and delaying delaying entry into reg eneration mode.
STRONG MEDICINE TACTICS: Perform exercise consistently at the same time of the day. This will train your clocks to anticipate physical activity, and prepare your body to optimally suppor suppor t exercise.
RESEARCH UPDATE: Recent research has shown that muscle is able to generate the most force near the end of activity mode. Late afternoon or early evening exercise may be the natural time in the circadian cycle for peak performance.
This does not mean that exercise at different times of the day is less effective in promoting favorable adaptive gains in strength and fitness. The muscle clock can be “entrained” to anticipate exercise at different times during duri ng the activity mo mode de if you yo u consistently train at the same time time of of day. Consistency in training traini ng time seems s eems to be the best way to to ensure that your system system is prepared pr epared for exercise, whet whether her your training sessions ar e in the the mor ning, lunchtime, lunchtime, after after noon, or evening. evening.
COACH’S CORNER: If you are ar e a competit co mpetitive ive athlete and have have an upcoming upcomi ng event, adjust your daily training tr aining time to the event’s event’s time. If If your yo ur competitive event is at 4PM, 4PM, you should adjust your daily training time to as close to 4PM as possible, allowing your body clocks to support maximal perfo rmance at that that time. time. While exercising within 2-3 hours of planned sleep will delay entry into regeneration reg eneration mode, an exercise exercise session 4-6 hours befor e sleep (late (late afterno afternoon/early on/early evening) will have the opposite effect on the circadian system. Research has shown that late afternoon/early evening exercise can actually help stimulate melatonin product pro duction ion and the the beginning of r egeneration mode. Scheduling exercise 4-6 hours before planned sleep and avoiding blue light exposure will send a strong signal to enter regeneration mode, greatly aiding your transition to recuperative sleep.
STRONG MEDICINE TACTICS: Exercise 4-6 hour s befor e planned Exercise planned sleep time time to aid in pr iming melat melatonin onin produc pro duction tion and the the onset of r egeneration mode.
The sleep enhancing effects of exercising 4-6 hours before planned bedtime is the only r eason to advocate advocate a specific time for exercise. If your schedule will will allo w for it, this is a pretty good reason to switch over to late afternoon or early evening exercise.
MELA ME LAT TONIN SUP SUPPLEME PLEMENT NTA ATION? Recently there has been a substantial amount of research on melatonin supplementation and chronic disease. In some scenarios, supplementing melatonin may show some benefit, but the Strong Medicine approach is to support the body’s own production of melatonin with the proper environmental cues—light, exercise, etc. Most melatonin supplement dosage is well beyond what the body will produce naturally and may cause problems by inhibiting the body’s natural production of melatonin with long-term use. The other problem with melatonin supplementation is that it has a very shor sho r t half-life in the body. body. The melatonin melato nin only lasts l asts for about 20-40 minutes in the bloodstream before it is metabolized and eliminated. The pineal gland in the brain constantly produces new melatonin during the night so this is not an issue the during regeneration phase. However, a single supplement will only last for 20-40 minutes. You would have to take melatonin approximately every 30 minutes to mimic the pineal gland’s natural production during sleep. Supporting the natural cycle of melatonin production through the right environmental signals such as light and exercise is a much better solution to circadian problems.
MELATONIN MELATONIN SUPP SUPPLEMEN LEMENTS TS AND JET LAG Tempor Tempor ary use of o f melatonin can be useful useful for adjusting adjusting to rapid time changes from jet travel. Taking a low dose (usually 0.3 mg) of melatonin before bedtime bedtime after ar r iving in a new time zone may help you you fall asleep for the the first fir st couple of night nig htss as your circadian system system adjusts. adjusts.
RESEARCH UPDATE: A longer long er acting acting melatonin melatonin supplement supplement is curr ently ently being r esearched for use with the the elderly elder ly and those with Alzheimer ’s. As we age, melatonin production declines. There may be some benefit to using a long-acting melatonin melatonin fo rmulation to counteract counteract the declining declining melatonin melatonin pr oduction oduction to help restore nor no r mal sleep for the the elderly. Use of melatonin melatonin for Alzheimer’s (AD) patients is also an active area of research as AD also decreases melatonin product pro duction. ion.
SHIFT WORKER CASE STUDY The circadian disruption from nightshift work is very difficult to correct since the schedule is completely at odds with the natural cycle of light and dark that entrains the human circadian rhythm. With careful planning and smart use of light exposur exposuree strategies it is possible to improve impro ve the the quality quality of life—and likely the the longterm health—of the nightshift worker. One possible strategy: • Get blue spectrum light lig ht exposure exposur e upon waking and if possible, possi ble, during duri ng the fir st couple hours o f work. Some corpor cor porations ations have have installed installed high CCT CCT (more (mo re blue spectrum) lighting during night shifts to increase alertness and enhance productivity. If you are able to change the lighting in your work area yourself to this type of light, do it. There portable blue light emitters are available that can be powered by a USB USB port on o n your computer computer and can can be mounted mounted on your yo ur monitor or laptop. • Make sure sur e your eating cycles cor r espond to your waking time. Eat when you get up for work, eat “lunch” mid-shift at work, and eat a meal when you get home in the the mor ning. This will help keep keep your or gan clocks working wor king with with your master master clock. • When driving dri ving home after the the end of your shift, wear amber-tinted amber -tinted glasses gl asses to block the blue spectrum light from the rising sun. Keep the glasses on after work to block the blue blue spectrum spectrum light from fr om outside and and from fr om lighting inside the home. home. A nightshift worker has to be a little more aggressive with their time spent wearing wearing amber g lasses because because they they are working against daylight daylight permeating everything. • Ensure that no sunlig sunlight ht intrudes into your bedro om fro m outside. You will will have to be extr extr emely diligent about about blocking blocking the sun from your r oom oo m which which may require requir e covering coveri ng your yo ur windows windows with with opaque opaque materi material al in addition addition to using
blackout curtains. This is where shift workers often fall short in their attempts to sleep—even a little outside sunlight in the bedroom will stop melatonin product pro duction ion and bring bri ng them out of sleep. A similar strategy to the one outlined above was recently used in a research study with small groups of shift workers such as nurses and police officers. The results showed improved quality and duration of sleep time, and improved alertness and productivity. Much more research needs to be done in this area but the initial results are promising. These strategies are worth trying if you are a nightshift worker str str uggling uggli ng with sleep. sleep.
CONCLUSION Circadian disruption is widespread in modern society. Artificial light pollutes the total darkness that once existed during the night. Not all sleep disorders are primarily circadian problems, obstructive sleep apnea and anxiety are conditions that result in fragmented sleep without circadian disruption. However, it is very likely that optimizing your circadian rhythm will make treating these sleep problems pro blems easier. easier. Losing weight using the Strong Medicine Tactics in the obesity chapter will certainly help obstructive sleep apnea, and interventions from the chronic stress chapter will go a long way towards squashing anxiety. The integrative approach to chronic disease in this this book boo k will have have cro ssover effects, effects, often impr impr oving seemingly unrelated conditions. The mind and body are not a collection of separate organ systems; everything works together in harmony when everything is functioning correctly. This chapter hopefully illustrated the importance of the circadian system as a master conductor which ensures the synergy of the entire flesh machine. Incorporating the strategies in this section will go a long way towards helping you improve impro ve your overall health health and prevent chronic disease. By using the Strong Medicine Defensive Tactics in this section, you can reestablish the synchrony of your internal clocks with your waking and sleeping times—and master your circadian system. The “Thief in the Night” will no longer steal steal the the rest r estor or ative ative sleep so crucial fo r your health. health.
“MILITARY INTELLIGENCE” INT ELLIGENCE” (REFERENCES): Abel T, et al. Slee p, plasti city andmemory from mol ecules to whole -brain -brain networks. Curr Biol 23 (2013): R774-R788. Al brecht brecht U . The circadian clock , reward, and and memory. Front memory. Front Mol Neurosci 4 (2011): 41. Al brecht brecht U. Ti ming to perfecti on: the biol ogy of central central and peripheral peripheral ci rcadian rcadian clock s. Neuron 74 (2012): 246-260. Arch 463 (2012): 23-30. Al brecht brecht U . Ci rcadian rcadian rhythms and and sle ep—the metaboli c connecti on. Pflugers on. Pflugers Arch Anea CB, et al . Circadian Circadian clock control of nox4 and reactive reactive oxyge n speci speci es i n the vasculature. vasculature. PLoS One 8 (2013): e78626. Arjona A, et al . I mmunity ’s fourth dime nsion: appr approach oaching ing the ci rcadian rcadian-i -i mmune connection. Trends Immunol 33 (2012): 607-612. Balak rishnan A, et al. Ci rcadian rcadian clo ck ge nes and and impli cations for intesti nal nal nutrie nutrie nt uptak ptak e. J Nutr Biochem 23 (2012): 417-422. Bechtel W. From mol ecule s to behavi behavi or and the cl inic: Integratio n in chr chronob onobio io lo gy. Stud Hist Philos Biol Biomed Sci (2012). Arch 463 (2012): 121-137. Besedovsk y L, et al. Sl ee p and and immune functio functio n. Pflugers n. Pflugers Arch Boiv in DB, et al. Photic resetti ng in nig ht-shift work : impact on nurses’ urses’ sle ep. Chronobiol Int 29 (2012): 619-628. Boiv in DB, e t al. Phototherap Phototherapy y andorangeorange- tinted goggl es fo r nig nig ht-shif ht-shif t adap adaptation tation of poli ce off ice rs on patrol. patrol. Chronobiol Int 29 (2012): 629-640. Circ Physiol 294 (2008): H1036-H1047. Bray MS, et al. D isruptio isruptio n of the the ci rcadian rcadian clo ck wi thin the cardio myocyte i nfluences myocardial contractil e function, metabol metabol ism, and gene e xpression. Am J Physiol Heart Circ Broussard BroussardJL , et al . Impaired insuli n signali ng in human adipocytes adipocytes after ex perimental sl ee p restri restri ction: a rand randomi ze d, crossove r study study. Ann Intern Med 157 (2012): 549-557. Buxton Buxton OM, OM, et al. Slee p restriction for 1 wee k reduc reduces es i nsulin nsulin sensitivi ty i n healthy healthy men. Diabetes 59 (2010): 2126-2133. Cai DJ , et al. R EM, not incub incubation, improves improves creativity by priming priming associative associative network network s. Proc Natl Acad Sci U S A 106 (2009): 10130-10134. Physiol (1985) 110 (2011): 1432-1438. Cajochen C, et al. Eve ning exposure to a l ig ht-emi tting diodes (LED)-backl it computer screen screen affe cts circadian circadian physi ol ogy and cogniti ve performance. performance. J Appl Physiol (1985) Brain Res 190 (2011): 119-133. Chell appa appa SL, et al. Can li ght mak mak e us bright? bright? Effe cts of l ig ht on cogniti on and and sle ep. Prog Brain Chell appa appa SL, et al. No n-visual ef fe cts of li ght on mel atonin, atonin, ale rtness rtness andcognitiv e performance: performance: canblue-e nriched nriched li ght kee p us alert? PLoS One 6 (2011): e16429. Chell appa appa SL, et al . Acute exposure to eve ning blueblue- enriched lig ht impacts impacts on huma human n slee p. J Sleep Res 22 (2013): 573-580. Endocrinol 380 (2013): 2-15. Di ckme is T, et al . The circadian clock and and glucocorticoi glucocorticoi ds—interactio ds—interactio ns across across many many time scale s. Mol Cell Endocrinol Physiol (1985) 92 (2002): 852-862. Di jk DJ , & Lockl ey, SW. Integration of human human sle ep-wak e regulati on and and circadian rhythmicity. J Appl Physiol (1985) Donga E, et al. A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects.
J Clin Endocrinol Metab 95 (2010): 2963-2968.
Duffy J F, & Cze isl er CA. Effe ct of Light on HumanCircadian Circadian Physi ol ogy. Sleep Med Clin 4 (2009): 165-177. Faraut B, et al. N euroendocrine, euroendocrine, immune and and oxidative stress i n shif t work ers. Sleep Med Rev 17 (2013): 433-444. Faraut B, e t al. Immune, Immune, infl ammatory ammatory and card cardio vascular vascular consequences consequences of sle ep restricti on and and recovery. Sleep Med Rev 16 (2012): 137-149. Endocrinol 382 (2013): 926-937. Favero G, e t al. M el atonin and and its atherop atheroprotec rotective tive eff ects: A revie w. Mol w. Mol Cell Endocrinol Endocrinol 349 (2012): 51-55. Firsov D, et al. Role of the renal circadian timing system in maintaining water and electrolytes homeostasis. Mol Cell Endocrinol Fonken LK, & Nel son RJ. Il luminating luminating the the dele terious effects of l ight at night. F1000 Med Rep 3 (2011): 18. Froy O. M etaboli sm andcircadian rhythms—impli rhythms—impli cations for obesi ty. Endocr ty. Endocr Rev 31 (2011): 1-24. Froy O. The ci rcadian rcadian clo clo ck and metabol ism. Clin Sci (Lond) 120 (2011): 65-72. Froy O. Ci rcadian rcadian aspects aspects of e nergy metaboli sm andaging. Ageing Res Rev 12 (2013): 931-940. Gabel V, et al. Effects of artificial dawn and morning blue light on daytime cognitive performance, well-being, cortisol and melatonin levels. Chronobiol Int 30 (2013): 988-997. Garaule t M, & G omez -Abel lan P. Chronob Chronobio io lo gy and obesity. Nutr obesity. Nutr Hosp 28 Suppl 5 (2013): 114-120. Garaule t M, & M adrid adrid JA . Chronobiol ogi cal aspects of nutriti nutriti on, metaboli c syndrome and obesity. Adv Drug Deliv Rev 62 (2010): 967-978. Gool ey J J, et al . Exposure Exposure to room li ght bef bef ore bedtime suppresse presse s mel atonin atonin onset and shortens shortens mel atonin duration uration in human humans. s. J Clin Endocrinol Metab 96 (2011): E463-E472. Greer SM , et al . The i mpact mpact of sl ee p deprivati on on food desi desi re i n the human human brain. Nat rain. Nat Commun 4 (2013): 2259. Gujar N, et al. A role for REM sle ep in recali recali bratin brating g the sensitivi ty of the the human human brain brain to specifi specifi c emotions. Cereb Cortex 21 (2011): 115-123. Hardel Hardel and and R. M el atonin atonin i n agi agi ng and dise ase—multi ple consequences consequences of reduced reduced secretion, options andli mits o f treatment. Aging Dis 3 (2012): 194-225. Hardel Hardel and and R. M el atonin atonin andthe theori theori es of aging: a criti criti cal appr appraisal aisal o f me latonin’s rol e i n antiaging antiaging mechanisms. J Pineal Res 55 (2013): 325-356. Neurobiol 93 (2011): 350-384. Hardeland R, et al. Melatonin—a pleiotropic, orchestrating regulator molecule. Prog Neurobiol Haus EL, & Smolensk y M H. Shift wo rk and cancer risk : potential potential mechanisti mechanisti c roles of circadian circadian disrup disruptio tio n, li ght at at night, and slee p deprivatio n. Sleep Med Rev 17 (2013): 273-284. Huang W, e t al . Ci rcadian rcadian rhyth rhythms, ms, sl ee p, and and metaboli sm. J Clin Invest 121 (2011): 2133-2141. Endocrinol 349 (2012): 45-50. Jo hnston JD . A dipose ci rcadian rcadian rhythms: translati ng cel lular and animal studie s to human physiol physiol ogy. Mol Cell Endocrinol Jung Jung CM, et al. Acute effe cts of bright bright li ght exposu exposure re on cortisol cortisol l evel s. J Biol Rhythms 25 (2010): 208-216. Endocrinol 349 (2012): 20-29. Kalsbee k A, e t al. Circadian Circadian rhythms rhythms in the hypotha hypothalamolamo- pituitary-adrenal pituitary-adrenal (HPA) (HPA) axis. Mol Cell Endocrinol Kalsbee k A , et al. The hypoth hypothalami alami c clo clo ck andits control of gl ucose ucose homeostasi s. Trends Endocrinol Metab 21 (2010): 402-410. Kanathu Kanathur N, et al. Circadian Circadian rhythm rhythm sl ee p disorders. Clin Chest Med 31 (2010): 319-325. Kang JH, & Li n HC. Obstru Obstructive ctive sle ep apnea and the risk of autoimmune disease s: a l ongitudinal ongitudinal population-based population-based study study. Sleep Med 13 (2012): 583-588. Konturek Konturek PC, et al. Gut clock : impl icatio n of circadian circadian rhythms rhythms in the the gastroi ntestinal tract. J Physiol Pharmacol 62 (2011): 139-150. Lack LC, & Wri ght HR. Chronob Chronobio io lo gy of sl ee p in humans. mans. Cell Mol Life Sci 64 (2007): 1205-1215. Lamia KA, e t al. Physiol Physiol ogical si gnificance gnificance of a peripher peripheral al ti ssue ssue circad circadian ian clock. Proc Natl Acad Sci U S A 105 (2008): 15172-15177. Lange T, et al . Ef fe cts of sl ee p and circadian circadian rhyth rhythm m on the human immune sy stem. Ann N Y Acad Sci 1193 (2010): 48-59. Lef ta M, et al. Ci rcadian rcadian rhythms, rhythms, the mol ecular clo clo ck, and sk el etal muscle . Curr Top Dev Biol 96 (2011): 231-271.
Li n GJ , et al. M odulati odulati on by mel atonin of the pathogenesis pathogenesis of infl ammatory ammatory autoi autoi mmune dise ases. Int J Mol Sci 14 (2013): 11742-11766. Liti nsk nsk i M, et al. Influence Influence of the the Ci rcad rcadian ian System System on Dise ase Severity. Sleep Med Clin 4 (2009): 143-163. Endocrinol 349 (2012): 82-90. Logan RW, & Sarkar DK. Circadian Circadian nature of immune function. Mol function. Mol Cell Endocrinol Lowden A, & Ak erstedt T. T. Assessme nt of a new dynamic dynamic l ig ht regi men in a nucle ar power control control room wi thout thout windows on quickl y rotating shif shif twork ers—ee ff ects on heal th, wak wak ef ulness, and and circad circadian ian ali gnment: a pil pil ot study. Chronobiol Int 29 (2012): 641-649. Markwald R R, et al. Impact Impact of i nsufficient nsufficient sle ep on total total dail dail y e nergy nergy e xpenditu xpenditure, re, food i ntake, ntake, and and weig ht gain. gain. Proc Natl Acad Sci U S A 110 (2013): 5695-5700. Maury E, e t al. Circadian Circadian rhythms rhythms and metabol metabol ic sy ndrome: f rom experi mental ge netics to human dise ase. Circ Res 106 (2010): 447-462. Mazzo ccoli ccoli G, et al. Cl ock ge nes and clock-controll clock-controll ed genes in the regulation regulation of metaboli c rhythms. ythms. Chronobiol Int 29 (2012): 227-251. McEwen BS. Sleep deprivation as a neurobiologic and physiologic stressor: Allostasis and allostatic load. Metabolism 55 (2006): S20-S23. Moller-Levet CS, et al. Effects of insufficient sleep on circadian rhythmicity and expression amplitude of the human blood transcriptome. Proc Natl Acad Sci U S A 110 (2013): E1132-E1141. Endocrinol 349 (2012): 91-104. Mo rris CJ, e t al. Ci rcadian rcadian system, sl ee p and andendocrinolo endocrinolo gy. Mol gy. Mol Cell Endocrinol Brain Res 199 (2012): 337-358. Mo rris CJ , et al . The i mpact mpact of the circadian circadian timi ng system on cardiovascular cardiovascular and andmetaboli c function. function. Prog Brain Pflugers Arch Arch 463 (2012): 139-160. Morsel li LL, e t al. Sle ep and and metabolic metabolic function. function. Pflugers Narasimamurth Narasimamurthy y R , et al. Circadian Circadian clock protei protei n cryp cryptochr tochrome ome regul ates the expressio n of proi proi nflammatory cytoki nes. Proc nes. Proc Natl Acad Sci U S A 109 (2012): 12662-12667. Nguyen KD, et al. Circadian gene Bmal1 regulates diurnal oscillations of Ly6C(hi) inflammatory monocytes. Science 341 (2013): 1483-1488. Neuropsychobiology 64 (2011): 152-162. Pail G, et al. Bright-light therapy in the treatment of mood disorders. Neuropsychobiology Palagini L, et al. REM sleep dysregulation in depression: state of the art. Sleep Med Rev 17 (2013): 377-390. Pandi-Perumal SR, et al . Me latonin antiox antiox idative defense: therapeutical therapeutical i mpli cations for agi agi ng and andneurodegenerative neurodegenerative processe processe s. Neurotox Res 23 (2013): 267-300. Paul K N, e t al. T he role of re tinal photoreceptors photoreceptors in the regulati on of ci rcadian rcadian rhyth rhythms. ms. Rev Endocr Metab Disord 10 (2009): 271-278. Psychol 4 (2013): 474. Perogamvros L, e t al. Sle ep and and dreaming dreaming are fo r important important matters. Front matters. Front Psychol Peschke E , et al. M el atonin atonin andPancreatic Isl ets: Interrel ationships betwe en Me latonin, Insulin andGl ucagon. ucagon. Int J Mol Sci 14 (2013): 6981-7015. Pittman-Polletta BR, et al. The role of the circadian system in fractal neurophysiological control. Biol Rev Camb Philos Soc 88 (2013): 873-894. Laryngoscope 109 (1999): 1648-1654. Powell NB, et al. A comparative model: reaction time performance in sleep-disordered breathing versus alcohol-impaired controls. Laryngoscope Powell NB, et al. Sleepy driving: accidents and injury. Otolaryngol Head Neck Surg 126 (2002): 217-227. Reynolds AC, et al. Impact of five nights of sleep restriction on glucose metabolism, leptin and testosterone in young adult men. PLoS One 7 (2012): e41218. Arch 463 (2021): 169-176. Romei jn N, et al. Slee p, vigil ance, ance, and and thermosensiti ermosensiti vity. Pflugers vity. Pflugers Arch Roux FJ, & Kryger MH. M edication edication effe cts on sle sle ep. Clin Chest Med 31 (2010): 397-405. Ruger M , & Schee Schee r FA. Eff ects of circadian disruption disruption on the cardio cardio metaboli c system. Rev Endocr Metab Disord 10 (2009): 245-260. Santhi N, e t al. T he spectral spectral compositi on of e vening l ig ht and andindivi dual dif fe rences in the suppressi pressi on of mel atonin and anddelay of sle ep in human humans. s. J Pineal Res 53 (2012): 47-59. Neuropsychopharmacol Biol Biol Psychiatry 34 (2010): 1236-1242. Sassevil le A, & He bert M. U sing blue-gre en li ght at at night and and blue-block ers during the day day to improves adapta adaptatio tio n to nig ht work: a pilo t study. Prog Neuropsychopharmacol Sassevil le A, et al . Blue block er glasse s impede the capa capacity city of bright li ght to suppress press mel atonin produ production. ction. J Pineal Res 41 (2006): 73-78. Schee r FA, et al. A dverse metaboli c and and card cardio io vascular vascular consequences of circadian misal ig nment. nment. Proc Natl Acad Sci U S A 106 (2009): 4453-4458. Endocrinol 349 (2012): 38-44. Schmutz I, et al. The role of cl ock ge nes and rhythmicity rhythmicity i n the l iv er. Mol Cell Endocrinol Schroder roder EA, & Esse r KA. Ci rcadian rcadian rhythms, rhythms, ske le tal muscle mol ecular clocks, and exercise . Exerc Sport Sci Rev 41 (2013): 224-229. Schroeder AM, & Colwell CS. How to fix a broken clock. Trends Pharmacol Sci 34 (2013): 605-619. Shostak Shostak A , et al . Circadian regulatio n of adipose functio functio n. Adipocyte n. Adipocyte 2 (2013): 201-206. Slats D, et al . Re ciprocal ciprocal i nteractions nteractions betwee n slee p, circad circadian ian rhythms and and Al zhei mer’s dise ase: focus on the role o f hypocreti n and andmel atonin. Aging Res Rev 12 (2013): 188-200. Brain Res 199 (2012): 359-376. Stenvers DJ, e t al. Nutriti on and the circadian timi ng system. Prog Brain Talamini Talamini LM , et al . Sle eping worrie worrie s away or worrying worrying away slee p? Physiol Physiol ogical e vidence vidence on sle ep-emotion interaction interactions. s. PLoS One 8 (2013): e62480. Tasali Tasali E, et al. Sl ow- wave sl ee p and andthe risk o f type 2 diabetes in humans. mans. Proc Natl Acad Sci U S A 105 (2008): 1044-1049. Van Van Cauter Cauter E, et al. M etaboli c consequen consequences ces of sl ee p and andsle ep loss. Sleep Med 9 Suppl 1 (2008): S23-S28. Van der der He lm E, e t al. REM slee p depoten depotentiates tiates amygdala amygdala activi activi ty to previous emotional e xperie xperie nces. nces. Curr Biol 21 (2011): 2029-2032. Brain Res 199 (2012): 183-201. Van Van der Spek R, et al . Circadian rhythms rhythms in white adipose ti ssue. Prog Brain Vi ol a AU, e t al. Blue-e nriched nriched white white l ig ht in the the work place improves sel f- reported ale rtness, rtness, performance performance and and sle ep quali uali ty. Scand J Work Environ Health 34 (2008): 297-306. Brain Res 185 (2010): 49-68. Walk er MP. Sle Sle ep, memory and emoti on. Prog on. Prog Brain Walk er MP, & Stick gol d R. Overnight alchemy: alchemy: sl ee p-depend p-dependent ent memory evol ution. Nat ution. Nat Rev Neurosci 11 (2010): 218; author author reply 218 . Walk er M P, & van der Hel m E. Overnight therap therapy? y? The role of sl ee p in emotio nal nal brain processing. Psychol Bull 135 (2009): 731-748. Young oung M E, & Bray MS. Potential role for peri pheral circadian clock dyssynch dyssynchrony rony in the pathogenesi pathogenesi s of cardiovascular cardiovascular dysfunc dysfunction. tion. Sleep Med 8 (2007): 656-667. Yu X, et al . TH17 cel l dif fe rentiation is regulate d by the circadian circadian clock. Science 342 (2031): 727-730. Z anqu anquetta M M , et al . Expressi on of clo ck g enes i n huma human n subc subcuta utaneous neous and and vi sceral adipose ti ssues. Chronobiol Int 29 (2012): 252-260. Z anqu anquetta MM , et al. Body weig ht, metaboli sm and clock genes. Diabetol Metab Syndr 2 (2010): 53. Z hang hang X, et al. Work ing around around the clock : circadian rhythms and andsk el etal muscle . J Appl Appl Physio l (198 5) 107 (2009): 1647-1654. Z isapel N. Sle ep and sle ep disturb disturban ances: ces: biol ogi cal basis basis and cli nical impli cations. Cell Mol Life Sci 64 (2007): 1174-1186.
PART III
BATTLE BA TTLE PLAN “The best defen defense se is a good goo d offense.” —Jack Dempsey
You now no w have have the t he lat lat est in intt ell elligence igence on the t he on the t he inner inner workings workings of o f the t he enemy enemy —and defensive tact t actics ics at your yo ur disposal to t o repel r epel the advances of o f the t he Pentaverate. It is time to put your training into action by formulating your indi in divid vidual ual batt batt le plan. plan. Befo Before re you move move your yo ur troo t roops ps to t o t he front li line, ne, we will will give you som so me trai t raini ning ng in battle batt le strategy. strat egy. In Part III you will develop a foundation in Strong Medicine physical training, learn lea rn the t he import importance ance of foo food d quality, quality, and strat egies for fo r the t he optim opt imum um feedin feedingg of t he flesh machine. machine. You You wi will ll put put t og oget ether her an individuali individualized zed plan for fo r lifestyle lifest yle change using your yo ur previous previous t rain rainin ingg and defensive defensive tactics, t actics, and finall finallyy track t rack your progress prog ress wit wit h analytics analytics (“stuff (“st uff you can measure”). measure”). Put your yo ur pieces pieces on the t he board and we will show you how to place the Pentaverate in checkmate with a devastat dev astatin ingg offensi offensive ve strategy. st rategy. I. St Stro rong ng Medi Medicine cine Physical Training II.. St II Stro rong ng Medi Medicine cine Nutrit Nutrition: ion: Indi Individual vidualized ized St Strat rateg egies ies III. II I. Put Puttt in ingg It It All All Tog Toget ether her IV.. Analyt IV Analytics: ics: “Stuff “St uff Yo Yo u Can Measure Measure””
BATT BATTLE LE PLAN PLA N I
PHYSICAL TRAINING: UNLOCKING UNLOCK ING YOUR BODY’S POTENTIAL
STRONG MEDICINE MEDICINE PHYSICAL PHYSICAL TRAINING Regular, mindful, intense physical training is central to the Strong Medicine transformational plan. The body and mind need physical stress to thrive, and the absence of regular exercise results in physical and mental deterioration over time. The necessity of physical stress through exercise is supported by the health benefits shown by scientific research. • Exercise Exercise slows the the aging process. pro cess. • Exercise Exercise pro pro tect tectss us from fr om bone bone and muscle wastin wasting g (osteopor (osteopor osis and and sarcopenia). • Exercise dramatically dram atically increases incr eases insulin sensitivity, sensitivity, pro tecting tecting us from fr om diabetes and obesity. • Exercise str str engthens the heart and prevents heart attacks attacks and stroke. stro ke. • Exercise Exercise rebuilds the the stressed brain, making us resilient resili ent against chronic chro nic stress. • Exercise Exercise pro pro tect tectss us from fr om neuro neurodegenerativ degenerativee diseases diseases such as Alzheimer Alzheimer ’s Dementia.
• Exercise Exercise helps helps us build a strong immune system system and r ecover from illness faster. • Exercise Exercise makes makes us mor e physically physically resilient resili ent,, preventing preventing injury injury and and allowing for faster recovery after injury. • Exercise Exercise helps r eset a broken bro ken circadian rhythm. Without exercise and its protective benefits in your daily life, the aging process is accelerated and you are vulnerable to disease and injury.
In the terms of hormesis, inactivity represents an inadequate “dose” of exercise and physical stress. We are going to show you how to train smartly and effectively to maximize your health benefits by staying in the “green zone” of the proper dose of exercise. We will also keep you out of the “overdose” zone that so many people fall victim to if they’re following a regular high volume “boot camp beat down” program. The Strong Medicine physical training program does not require gym memberships, huge time investments, or fancy equipment. We are going to strip things down to the basics and give you a foundation for a lifetime of health and fitness.
Inactivity Inactivity is the the fifth member of the “Pentav “Pentaver erate, ate,”” the cabal of chr onic preventable disease. Like the other four members, inactivity result r esultss in chro nic inflammation inflammation and
oxidative stress. We can break this link to chr onic disease di sease with a scientifical scientifically-based ly-based training traini ng progr pro gr am, informed by an elite-level elite-level coach’s coach’s years of o f experience. We will start with with a primer pr imer on pr ogr og r essive resistance resistance training—a true fo untain untain of youth—then present a scientific approach to cardiovascular training. These exercise defensive tactics are the equivalent of a tactical nuclear weapon against the Pentaverate. This is high-yield training for your war against chronic disease and a keystone keystone for achieving achieving your genetic potent potential. ial. We are only going to cover a few critical exercises to build a progressive resistance training foundation. You may add other exercises to create your own individualized program, but these core movements should be the pillars of your program: • • • • •
The Squat The Deadlift The Bench Press and Military ili tary Press The Row Abdomi Abdominal nal Training Trai ning
PHYSICAL TRA TRA INING I
STRONG MEDICINE RESISTANCE TRAINING: INTRODUCTION INTRODUCTION
USE IT OR LOSE IT In a fundamental sense, muscle and strength follow a “use it or lose it” scenario— but that would imply that the aging population (over 60) “had it” to begin with—yet flaccidity is epidemic in most of the Western population long before the sixth decade is reached. A cursory glance at traditional hunter-gatherer cultures (the few still in existence) reveals that their senior citizens are muscular, ripped and functional. They always had “it” and never lost “it.” They were lean with functional muscularity in their youth, maintained their physique through mid-life and retained it in late life. The elders in tribal cultures are active, fit, disease-free and exhibit the lean muscle mass that twenty twenty-year -year-ol -olds ds of moder n society would envy. envy. Their secret is simple; they maintained their primitive diets, eating the food-fuels they were designed to use. They inherited excellent genetics and attained a miraculous degree of functional fitness in their youth. They never stopped using their bodies in intense and prolonged ways, and as a result their flesh-and-blood machinery retained a magnificent readiness. Instead of driving carts around a golf course, these senior citizens lift, carry, run, jump, and hunt.
Compare this to the classical ‘civilized man’ born in a controlled environment, and who has never attained fitness. Fueled by artificial ‘foods’—just like running a race car on cheap kerosene instead of nitro-methane—this ‘civilized man’ has never exerted himself in the slightest. With no muscle tone or strength gained earlier in life, physical functionality continues to diminish from an ever-increasing lack of late life activity. The end result is a pathetic, weakened creature unwilling, unable and incapable of being functionally mobile. Weak flaccid muscles grow weaker, bones which have never been stressed become lighter than air. Further immobility is compounded with fragility. Next they might fall down—if they are lucky, they’ll avoid shattering a hip as fragile as a glass figurine on concrete—at best they will have fallen and are incapable of standing back up. We have all seen the commercial with the pathetic plaintive cries of the elderly person helpless on the floor after a fall. The advertisers are saying, if you are old you need their “alert system” so you can be safe and secure in your own home. The not-so-subtle underlying message is that this situation is inevitable for everyone in the last decades of life. l ife. But, But, this this could coul d be your fate if you succumb to sarcopenia and “experienced” years. years. osteoporosis in your “experienced” We are seeing sarcopenia at younger and younger ages in modern society. It’s caused by a lack of resistance-based activity in an increasingly sedentary population.
SARCOPENIA Sarcopenia literally means “loss “lo ss of o f skeletal skeletal muscle mass”—and the the result r esulting ing loss l oss of strength—as we age. You may think it is natural and expected for everyone to lose muscle as we age. Yet, we can do plenty to slow the decline of muscle-mass through the expert use of resistance training. Sadly, the majority of us are needlessly sarcopenic. • • • •
The r ate of muscle loss lo ss in adults is 1-2% every year year after age 50. 50. Strength loss lo ss after age 60 is 3% every year. The healthcare healthcare cost of sarco sarcopenia penia is 18 billion dollar dollar s every year. Sarcopenia Sarco penia has been associated associ ated with increased incr eased r isk of death. death.
MUSCLE MASS MAINTENANCE IS CRUCIAL FOR HEALTH. • Retaining muscle mass and strength keeps a person biologically young, regardless of their chronological age. Many adherents to resistance training are able to retain lean muscle mass and tremendous strength late into their 70s and 80s. Many 50 year olds o lds have a body sig nificantly mor mo r e capable and functio functional nal than sedentary 25 year o ld men and women.
• Maint Maintaini aining ng muscle muscle mass mass is the best defense against ag ainst insulin insulin resistance and diabetes. Muscle is the largest insulin sensitive organ in the body. The loss of muscle mass (sarcopenia) disrupts the body’s ability to handle glucose effectively. effectively. Loss of o f muscle mass has been shown to to be an extremely extremel y strong stro ng predictor of the development of insulin resistance and diabetes.
• Progressive Pro gressive resistance training training is hugely benefic beneficial ial in t reatment reatment and prevent prevent ion of sarcopeni sarco penia. a. Clinical studies r epeatedly epeatedly show the benefit of progr pro gr essive resistance resistance training in treatment and prevention prevention of sarcopenia. Impressive impro vements vements in strength strength are r outine; power power is i s gained from fr om specific workout pro tocols. Strong Strong Medicine protocols protocol s can increase powe po wer, r, strength, and and can stop sarcopenia in its tracks.
OSTEOPOROSIS Our bones are the body’s central support structures which allow us to function upright against gravity. Our muscles can only exert force when they are attached to our bones, so maintaining a robust skeletal system is of upmost importance— particularly as we age. Osteoporosis is the thinning of bone tissue as mineral content decreases. The body constantly builds new bone while reabsorbing old bone. Osteoporosis and osteopenia (the early stages of osteoporosis), occur when bone break-down exceeds bone construction.
Osteoporosis is rampant in women after menopause. One out of five women over 50 have have some degree degr ee of oste o steopor opor osis. Half Half of women over the age age of o f 50 will will suffer a hip, wri wrist, st, or spine fracture in their lifetime. Men get osteoporosis osteopor osis later later in life than women, but are still at risk. There are many contributors to the development of specifically lack of resistance training—is the osteoporosis, but inactivity— specifically
prim primary facto factorr that enabl enables es osteoporosis ost eoporosis to t o t ake roo root. t. If we view osteoporosis through our “first principles” lens, bone physiology is
simple—bones respond favorably to systemic, prolonged and consistent resistance training by becoming thicker, denser, and more resistant to breaking, chipping or cracking. Bone subjected to weight training grows dense and strong. The age-defying benefits of resistance training do not require a complicated approach. The Strong Medicine approach uses simple stripped-down strength training pro tocols accessible accessible to everyone.
KEY POINT: If you want to age successfully, prevent life altering fractures, and stave off insulin resistance and diabetes, then resistance training is not optional.
DOING FEWER FEW ER THINGS BETTER BETTER Long before the current economic crisis forced fitness-minded individuals to reexamine and reduce their fitness spending, barebones approaches were prophetically championed by retro experts. These men insisted that modern fitness —fancy health clubs, ineffectual inef fectual perso per sonal nal trainer trai ners, s, expensive exercise exer cise machines, machi nes, elaborate supplements and miracle fat burners—was bogus, false and not nearly as productive as the old-school methods first used in the 1950s. This back to basics approach is always a tough sell, especially during good economic times. But now, people are taking a second look at minimalistic training methods. • The most result-producing methods methods of pr pr ogressive og ressive resistance training use freeweights—barbells, dumbbells, and kettlebells. The goal of resistance training is to build and strengthen streng then the the 600-plus muscles in the human body. Compound Compo und multi-joi multi-joint nt exercises exercises using barbells and dumbbells dumbbells cause gr oups of muscles to to work together in synchrony to stimulate muscle fibers in a way unobtainable using resistance machines. • Exercise machines that mimic free-weight fr ee-weight movements are ar e demonstrably demonstr ably inferior since they eliminate the “third dimension of tension.” Free-weight exercises requ r equir iree activat activation ion o f the muscle muscle stabilizer stabilizerss to contro l side-to-side movement. Free-weight exercises always result in more muscle fiber stimulation
(the (the goal g oal of r esistance esistance training) training) than than resist r esistance ance machines machines mimicking fr ee-weight ee-weight exercises. Free-weight exercises also translate better to real-life movements such as lifting, carr ying, pushing pushing and pulling.
MAKING MAKIN G LIGHT WEIGHTS HEA H EAVY VY Although one of us is a top powerlifting coach, we are not here to make you a powerlifter. You do not need to fear getting crushed under a heavy barbell or otherwise injuring yourself with heavy weights with the Strong Medicine approach. Our techniques use relatively light weights to maximum benefit by “making light weights heavy.” This will protect you from injury while you make transformative gains in strength and function. There is no need to fear free-weights. The Strong Medicine program is truly strength training for anyone. It doesn’t matte matterr if you ar e very experienced or have never never perfo rmed a squat in your lif e. We will build you from the ground up with technique, strength, and confidence. You will learn free-weight lifting techniques step-by-step from a master coach with 50 years of experience. The squat, deadlift, bench press, overhead press, and the “statue row” will be the pillars of the program. Even if you are experienced with the lifts, you will improve your technique and maximize your strength gains. We will also show you how to maximally train the abdominal muscles without ever doing a sit-up or cr unch. unch.
PHYSICAL TRA TRA INING II
KING KIN G SQUAT SQUAT
“KING “KING SQUAT” SQUAT”
Friends don’t let friends squat high. Why is the squat the king of all progressive resistance exercises? When it comes to building leg power, proper upright squats performed with a perpendicular torso and significant weight is unsurpassable. Properly performed, full, deep squats stimulat stimulatee mor e muscles than than any other other single sing le prog pr ogrr essive resistance resistance exercise. No one does proper full squats anymore for numerous reasons. “Experts’’ of every kind have either condemned full squats as dangerous—or worse, they teach some perverse technical abomination instead of the productive classic deep squat.
Our core technique for all squat variations—front squats, back squats, kettlebell squats, or squats with no weight—is identical. The hardcore squatter’s motto is, “Shallow squats are wor thless squats. squats. Fr Fr iends don’t let fr iends squat hig high. h.””
SOME TRAINERS AND AN D MEDICAL ME DICAL PROFESSIONA PROFE SSIONALS LS WILL SAY SAY, “DEE “D EEP P SQUA SQUATS TS ARE BAD BA D FOR F OR THE KNEES. KN EES.””
My response—after r esponse—after watching watching them demonstrate a squat—is, “The way YOU squat is bad for the knees.” A deep squat with the correct biomechanics (body positioning) is far from “bad for the knees.” The forces on the knee joint in a proper deep squat are sig nificantly nificantly less than than in partial or o r parallel squats. squats. The damaging damaging for ces in quest question ion are ar e joint shear s hear and compression compres sion stress. str ess. Compression stress is the stress on the knee from force pushing the knee cap backwar backwar ds onto o nto the knee joint. jo int. Joint shear is is a force attempting to move the the upper upper leg l eg bone (femur) either backwards backwards or o r for wards wards over o ver the tibia tibia (a lowe lo werr leg bone). Many trainers will tell you not to squat below parallel. This is bad advice since the greatest compression stress on the knee occurs at parallel (90 degrees). These trainer trainerss want want you to stop your squat squat then then exert exert more mo re for ce to stand stand up fro m the point of maximum compressive force fo rce o n the the knee joint. jo int. This Thi s makes NO sense. s ense.
Also, most people squat by initiating the movement from the knees first, shooting the shins way out in front of the feet. This knee poison puts huge joint jo int shear ing for fo r ces on o n the knees. Force measurements measure ments of the deep squat with wit h vertical verti cal shin position posi tion show less compression stress and less joint shear than the “safe” parallel or partial squat.
The deep squat is not only safe for knees, but may actually help strengthen the knee joint and make it more resilient in daily physical activities and sports. Olympic weightlifters routinely go into ultra-deep squat positions with heavy loads and have one of o f the lowest rat es of o f knee injuri injuries es in any sport . This is a proven fact. We have taken countless clients who pr eviously eviousl y avoided avoi ded squats because because they “hurt their knees” and have helped them perform full depth, pain-free squats in a matter of minutes.
MAKING MA KING LIGHT SQUATS SQUATS HEA HE AVY No other progressive resistance exercise triggers the primal “fight or flight” psychological response to the same degree as limit squats. Limit squatting unleashes tremendous hormonal benefits. We seek ways in which to increase squatting’s degree of difficulty. Why would we want to exponentially increase the difficulty of the world’s most excruciating exercise? Why are we requiring butt-to-heels depth on every rep of every set—with a purposeful pause at the bottom of each super-deep rep? Because this will strengthen the squatter over the entire range of motion (ROM). This will simultaneously maximize muscle growth and exponentially increase our brute power. Strict attention to technique will limit the amount of
weight we’re able to handle—we will reap maximum physiological results by lifting a minimum amount of weight. The Strong Medicine squat technique makes light weights heavy by achieving an ultra-deep squat depth depth and pausing at the the bottom of o f the rep befor befo r e ascending. • The ultra-deep squat involves invol ves starting the upwar upward d movement from fr om a leve r age ag e allows all ows and the optimum o ptimum leng l ength th the the compromised position —as far as lever muscle will stretch. str etch. There Ther e is no need to load lo ad up on the weig weight. ht. The ability abili ty to to g et a potent potent neuro neurolog logical ical stimulus stimulus (our goal go al with with strength training) training) fro m relat r elatively ively light lig ht weig weight, ht, has has many advantages. You can g enerate much mo r e strength streng th (technically, torque) in a curl when your elbow is flexed to 90 degrees than when it is fully full y extended. extended. The ultra-deep ultr a-deep squat puts puts you at a lever age and muscle length leng th
disadvant disadvantage, age, requiring requir ing much mor e effor t from fro m the the nervous system system to drive dr ive you out of the bottom. This allows us to use light weights and still trigger the adaptive response. Light weight also decreases load on the spine, making our squat safer for those those with a history history of o f back injuries. • The pause pause at the bottom of the the squat makes light lig ht weights heavy by taking away ( SSC). This Thi s a refl r eflex ex an important advantage —the stretch sho r tening cycle (SSC). similar to the one produc pro duced ed when when a doctor hits your patellar tendon tendon with a reflex hammer. The SSC is most active in plyometric exercises, but research has shown that that it is also sig nificant in nor mal-speed squat squats. s. The lowe lo weri ring ng por tion of a normal speed squat increasingly stretches the leg muscles. This stretch primes them for greater activation, and adds to the force used when ascending from the squat. squat. Think of o f it as a “turbo boost” boo st” fro m the bottom bottom of the squat. squat. But, But, ther theree is only a very short window for taking advantage of this SSC reflex. Our insistence on a one second pause at the bottom of the squat takes away this “turbo boost” reflex.
COACH’S CORNER: When we champion maximum range-of-motion squats, we are accused of r esistance tr tr aining malpractice. malpr actice. Delicate people claim squatting that deep will blo w out knees and cause the the deep squatter squatter to become becom e permanent per manently ly confined confi ned to a wheelchair. Despite Despite being called call ed out on o n it, and despite the the lack of deep-squat cripples or blown knee victims, the seriousness of the accusation has gained traction in the wider athletic training community who who larg ely believe super super deep squats squats are ar e dangerous. dangero us. Meanwhile, eanwhile, trainees tr ainees who squat super deep using pr ecise techniques develop injury-proof knees and astounding muscle and strength results.
BASIC SQUAT MECHANICS DESCENT
BASIC SQUAT MECHANICS ASCENT
SQUAT PROGRESSION 1: THE BODYWEIGHT SQUAT 1. The bodyweig bodyweight ht squat is the the key squat pro gr ession, essio n, the foundation on which all subsequent squat squat variations variatio ns are ar e built. Lear Learn n it, master it. i t.
2. Star Startt with with a shoulder -width stance, and toes toes slig htly turned outwar outwards. ds. 3. Sit back and and down while keeping keeping your yo ur shins vertical. ver tical. Do not let the knees knees shoot for war war d. 4. Keep your weight balanced mid-foot; mid-fo ot; do do not shift for ward or backwards. 5. Imagine a stake driven dri ven through thro ugh the the mid-fo ot to to keep you rooted ro oted into the the floor. floo r. 6. On ALL ALL squat variatio vari ations, ns, the the knees are ar e FORCED FORCED o ut to the sides (laterally) during descent and ascent. 7. Inhale Inhale into into the the lower lo wer belly as you you descend. 8. Knees Knees should stay stay over the ankles as much as as possible, and not shoot out in front of the toes. 9. Sink all the way to the the bottom, bottom, go ing as far as you can while maintaining correct form. 10. In the bottom position, exhale; exhale; relax rel ax and sink further, losing lo sing all tension. (Only (Only do t his his wit wit h bodyweight bodyweight or light light loads). 11. After a one second diaphrag m breat br eathing, hing, inhale to seco nd pause pause, using diaphragm ascend while pushing your gut out against your thighs. 12. For heavier loads, use this alternate alter nate technique: technique: inhale, sink to the bottom, maintain tension and pause for one second. seco nd. Exhale at the top top o f the ascent. 13. When ascending DO NOT let the tailbone shoot shoo t up fir st! The tailbo tailbone ne and upper body should move as one unit during ascent. “Grind” out of the bottom bottom position. 14. Perfor m three three sets sets of 10 reps before moving up to to loaded squat squat variations. Stop immediately if your technique breaks down.
“GRIND” THE SQUAT After After sinking as low lo w as possible while while maintaining maintaining a bolt-u bo lt-uprig prig ht tor tor so, the squatter pauses a beat before ascending. How someone rises from a paused, upr upr ight, ig ht, ultraultra-deep deep squat determines the amount of benefit he or she will derive. Never let the tailbo tailbone ne “shoot “shoo t upwar upward” d” when when the ascent ascent begins fr om the
bottom of o f the squat. squat. Fight this natur natural al inclination incli nation to “make the move easier” on the legs. When the tailbone shoots upward, allowing the legs to extend, extend, they’r they’ree put in a much mor e favor able position posi tion to push. But, But, it’s it’s a devil’s bargain—allowing the tailbone to shoot up causes your weight (or bodyweight) to shift forward, in front of the feet. Now the spinal column must be hoisted erect, using the hip-hinge and a few tortured vertebra on the the verge verg e of r uptuing. uptuing. Instead, we should “grind” out of the bottom, embracing the sticking point and slowly pushing through thro ugh it with perfect technique, technique, the the tailbone and upper upper body rising as one unit. unit. A purposefully slowe slo wed d “gr ind” speed speed is an expression o f lo w-end w-end torque. The actual speed of the grind rep is not—and should never be—radically slowed slo wed down. Slow rep r ep pro ponents continually make this fatal mistake. Grind Gr ind speed is purposely slo w, just barely slow slo w enough. We “make lig ht weig weights hts heavy” heavy” by adding “inten “i ntensity sity boosters” boo sters” to full range-of-motion squats. We add pauses at grind rep speed to create the ultimate excruciating exercise. Repeatedly grinding full ROM paused squats optimally trains proper technique.
THE TH E BODYWEIGHT BODYWEIGHT SQUAT SQUAT
Side view of squat descending descending sequence s equence
Fro nt view of squat ascending ascending sequence
SQUAT PROGRESSION 2: THE GOBLET GOB LET SQUAT SQUAT The second squat progression, uses added weight held with both hands out front like a goblet. Otherwise, it is performed exactly like the bodyweight squat. The added weight in front fr ont acts as a counterbalance to make sitt si tting ing backwar backward d in the squat feel mor mo r e stable. 1. Hold a single singl e appro priately-sized pr iately-sized kettlebell kettlebell or dumbbell at chest height with both hands. 2. Star Startt with with a shoulder width width stance, stance, toes slightly slig htly turned outwar outwards. ds. 3. Sit back and and down while keeping keeping your yo ur shins vertical. ver tical. Do not let the knees knees shoot for war war d. 4. Keep your weight balanced mid-foot; mid-fo ot; do do not shift for ward or backwards. 5. Inhale Inhale into your your lower lo wer belly belly as you descend. 6. For ce your your knees out to the the sides (laterally) (laterall y) dur during ing descent and ascent. 7. Knees Knees should stay stay over ankles as much as possible, they they should not shoot out in fr ont of the the toes. 8. Sink all the the way way to to the bottom, bottom, or as far as you can descend descend while while maintaining correct form. 9. In the bottom position, exhale then r elax and sink further, losing lo sing all tension. Only Only perform t his his step st ep wit wit h bodyweight bodyweight or light light loads. 10. After a one second breathing inhale to to seco nd pause pause, using diaphragm breathing
ascend while pushing your gut out against your thighs. 11. For heavier loads, loads, use thi t hiss alternate alternat e techni t echnique: que: inhale then sink to bottom while maintaining tension. tensio n. Pause for one second. seco nd. Exhale at the top top of the ascent. ascent. 12. When ascending, DO DO NOT NOT let the the tailbo tailbone ne shoot up fir st! The tailbone and upper body should move as one unit during ascent. “Grind” out of the bottom position. 13. Follow Foll ow the sets and r eps of your curr ent pro gr am. Stop Stop immediately if your technique breaks down.
THE GOBLET SQUAT
Goblet Gobl et squat descending sequence: note that the knees knees are ar e for fo r ced out to the sides as
he initiates the the movement mo vement from fro m the hips, sinking back and down. The spine stays s tays straight into the bottom position. He will pause for one second at the bottom position and then ascend with his tailbone and upper body moving together.
SQUAT SQUAT PROGRESSION PROGRESSION 3: THE TH E FRONT FRON T SQUAT The third squat progression, uses added weight in each hand, held at shoulder level. Otherwise, it is performed exactly like the bodyweight squat. The added weight held at shoulder level makes the abdominal muscles work hard to maintain a stable upright posture. 1. Hold a single singl e appro priately-sized pr iately-sized kettlebell kettlebell or dumbbell in each hand at shoulder level. Arms are kept tight against your ribs. 2. Star Startt with with a shoulder width width stance, stance, and your toes to es slightly tur tur ned outwards. 3. Sit back and down while while keeping your shins vertical. ver tical. Do not let your your knees knees shoot for war war d. 4. Keep your weight balanced mid-foot; mid-fo ot; do do not shift for ward or backwards. 5. Inhale Inhale into your your lower lo wer belly belly as you descend. 6. FORCE FORCE your knees out to the the sides (laterally) (laterall y) dur during ing descent and ascent. 7. Your knees should stay over yo ur ankles as much as possible, they they should not shoo shoott out in fro nt of your yo ur toes. 8. Sink all the the way way to to the bottom, bottom, or as far as you can descend descend while while maintaining correct form. 9. In the bottom position, exhale then r elax and sink further, losing lo sing all tension. Only perform this step with bodyweight or light loads. 10. After After a one second pause, pause, using diaphrag m breathing inhale to ascend, pushing your gut out against your thighs. 11. For heavier lo ads use this alter alternate nate technique: technique: inhale then then sink to to the bottom while maintaining tension. tensio n. Pause for one second. seco nd. Exhale at the top top of the ascent. ascent. 12. When ascending, DO DO NOT NOT let the the tailbo tailbone ne shoot up fir st! The
tailbone and upper body should move as one unit during the ascent. “Grind” out o ut of the bottom bottom position while keeping keeping an upright uprig ht posture. posture. 13. Follow Foll ow the sets and r eps of your curr ent pro gr am. Stop Stop immediately if your technique breaks down.
THE TH E FRO FRON T SQUAT SQUAT
Front Fro nt squat squat:: the the higher center center of gr avity avity of the the weight makes makes for a increased challenge challenge for the the cor e to maintain a straight spine during the the movemen mo vement. t.
HE LP FOR BEGINNE HELP BEGIN NERS RS WITH KNEES KNE ES THAT SHOOT FORWARD Newcomers to the squat often struggle to start their descent with a hip hinge. Instead, they will immediately shoot their knees forward to squat, putting significant shearing forces on the knees. People with this motor pattern avoid squatting because it hurts their knees—and no doubt do ubt it does! The most direct way to stop the “shooting knee” pattern is to position the lower body so that shooting the knees forward is almost impossible. This will force the correct pattern of beginning a squat with a hip hinge. Simply place the forefoot on a 1-2 inch board as shown below.
Practice with the board until the hip hinge feels natural, then remove the board and start training.
Knees Knees shooting for war war d is poor poo r squat squat form for m and bad bad for the the knees. knees.
Placing the board under the feet does not allow for the knees to come forward, and helps train starting the squat movement from the hips.
KNEE COLL COLLAPSE? APSE?
Knees collapsing inward (called “valgus collapse” in medical terminology) during the squat is the most common fault seen in those who include the squat in their training. It is an easy trap to fall into, especially as loads increase, but it is relatively easy to fix. We will provide a minimal force to push the knees inward, using physiotherapist Gray Cook’s idea of “feeding the mistake.” We can use a simple Theraband to provide the force. The nervous system will respond to the inward inward fo rce by reacting reacting against it with with the the natural natural r eflexive response of for cing the knees outward—which is what we want. This technique is good for correcting beginners, and also useful for priming the nervous system of experienced trainees for corr cor r ect movement before befor e a squat squat workout worko ut..
The arro ar ro ws show the the valgus (inward) coll apse of the knees. knees.
Adding the band cues the nervous system to resist the inward collapse, correcting the knee knee positio n.
THE ASSIS ASSISTED TED SQUA SQUAT T If you have not squatted deeply since childhood, and are having difficulty getting started with the bodyweight squat, begin with our multi-phase assisted squat progression.
PHASE I: THE SHORTENED REP-STROKE SQUAT We will use proper technique for partial squats. Establish an initial rep stroke depth that is comfortable, and adjust a seat to this level. Work up to one set of 10 perfect reps, lightly touching the seat, not bouncing, and standing back up. Sit back and down, inhaling on the descent, exhaling on the ascent. When you can perform a perfect set of 10 reps, add a second set. Finally, in a few sessions or few weeks, add a third set. When you are capable of three sets of ten reps, lower the seat FOUR inches. Start from the beginning with one set of 10 reps and repeat the process above until you can perform 3x10 at this height. After you have lowered the seat height over time and are now capable of squatting squatting 3x10 to parallel, par allel, we will begi n squat schoo schoo l, phase II. II.
PHASE II: THE DOORWAY/POLE SQUAT Stand facing a doorjamb or pole and grab the support at waist height. Now squat
down and back, allowing your arms to pull on the doorway/pole as you descend. Inhale until you reach parallel. Now exhale, relax any leg tension, and allow the weight of your torso to push your hips to the lowest possible position. Use your arms to offset your bodyweight and to keep your torso upright (critically important). Inhale and stand up, using only your legs to lift your torso. Pull upward with with your arms ar ms as necessary necessar y to stand up while while maintaining perfect perf ect technique. technique. Pulling with your arms will take weight off of the torso as needed, helping you to push though the squat sticking point. You are self-assisting a forced rep.
Using a pole for assisted squatting instead of a door jam (phase II). Anything stable you can gr g r ab with your hands will do. The phase III III assisted squat will use a towel to wel or rope to increase instability and thus difficulty.
PHASE III: TOWEL OR ROPE SQUAT Loop a rope or towel over the top of a chin-up bar or other sturdy overhead anchor-point. Grab one end of the rope or towel in each hand, then lower yourself down into a perfectly ultra-deep full squat. Pull on the rope or towel to lighten the load as you descend, then pull on the rope or towel as much as needed when standing standing back up. We can learn perfect squatting by self-assisting—reducing the amount of weight lifted—with lifted—with the rope ro pe or towel. When we we learn lear n squatting squatting fr om abso lute weakness, weakness, we we will develop a series of bad habits when “sneaking” through sticking points. Gains in strength and hypertrophy lie in battling through sticking points—not developing
questio questionable nable techniques that that allow us to avoid them.
GRADUATION Once you have increased your basic leg strength and are able to perform three sets of ten reps of ultra-deep bodyweight squats with correct technique, you are ready to work with dumbbells or kettlebells for the weighted squat.
STRONG MEDICINE TACTICS: Use the squat as one of the foundations of your resistance training program.
PHYSICAL TRA TRA INING III
THE DEADLIFT DEA DLIFT = THE HEAL HEA LTHLIFT THL IFT
THE CROWN PRINCE PRINCE OF THE THE POSTERIOR The squat is the undisputed king of resistance exercises, but the deadlift certainly has a place in the royal family. Many would argue that the deadlift is a stiff competitor with the squat for the overall title of the “king of exercises.” That is debatable, debatable, but the “Cr “Cr own Prince” Pri nce” is surely sur ely eyeing Dad’s thro thro ne. The proper deadlift is the undisputed prince of the posterior chain—the back and gluteal muscles. No other progressive resistance exercise adds strength and muscle to the back (traps, upper upper lat l ats, s, lower lats, lats, erectors, erector s, rhomboids, rho mboids, ter ter es, and rear deltoids) deltoids) and your gluteal gl uteal muscles than a perfectly executed deadlift. Like Bubba Gump’s endless shrimp possibilities, there are a seemingly infinite number of deadlift variations. Deadlifts can be performed while standing on a plate or box of varying heights for different results. Box deadlifts are also much more difficult at the start. Stiff-leg deadlifts can be done “Chaillet Style”, the lifter drags a
super heavy barbell up the thighs. A lighter and more precise “bodybuilder stiffleg” deadlift requires that the lifter purposefully allows the barbell to swing away from their body, this subtly shifts the muscular stress from the erectors to the hamstrings. You can do speed deadlifts or halting deadlifts. You can even incorpor incor porat atee partial rep deadlifts deadlifts using using a power r ack. Other options include ultra-wide-stance sumo deadlifts, and various “double overhand” deadlifts to build an eagle talon grip. You can also use straps to allow for overloading the back muscles. There are enough legitimate deadlift variations to keep a serio serio us trainee trainee very o ccupied ccupied for the the rest of his natural natural life. li fe.
THE HEAL HE ALTH TH LIFT From a medical perspective, no other exercise translates better to protecting the back and preventing injuries during daily activities than the deadlift. Regular deadlifters are never in the doctor’s office with back pain complaints; compl aints; the deadlift deadlift has made their backs vir tually indestructible when faced with the physical trials of work and home. This may sound contrary to the idea many people have of the deadlift being “bad for fo r the back.” back.” With With a properly executed deadlift, nothing could be further from the truth. The deadlift deadlift can even even be restorativ restor ativee for a previously previo usly injured back. back.
WH Y THE WHY THE SU SUMO MO DEA D EADLIFT DLIFT IS ALL WE NEED For our purposes, the only deadlift variation we need is the “sumo-style” deadlift. It is the easiest to teach, to perform, best translates to daily activities. It is also safer for the the beginner while still pro viding plenty plenty of challenge challenge fo r the the experienced lifter. lifter.
“One “One technique, deep dee ply ingrained, is ten times time s better than ten sup s uperficial erficial techniques. techniques .” —Bruce Lee In a perfect world, we could effortlessly teach athletes the sumo and conventional-style deadlift with equal ease and effect. 50 years of experimentation tells us something quite different. If an individual takes the time and effort to learn
our particular upright posture squat technique, learning the sumo deadlift will be as easy and natur natur al as taking a walk. The conventional deadlift is a sophisticated exercise that requires accurate positioning and the discipline to maintain the strict, straight, upward pull. The conventional deadlift has many more opportunities for breaking form. Repeatedly breaking technique to skirt a sticking point is shortsighted—both immediately and ultimately detrimental. Over time, bad habits become ingrained and almost impossible to break or correct. The conventional conventional deadlifter deadlifter can find a lot of ways ways to work around aro und or completely completely avoid sticking points. Resorting to these shortcuts is not clever or advisable. Elite trainers and master deadlifters understand that the essence of deadlifting (and of resistance training) is to find and embrace the resistance. These elite purposefully power through the sticking point, pushing or pulling with all their might straight ahead with no variation—and fail wherever they may fail. The maximum muscle and strength gains are born from the struggle of these barely completed reps. We should live to struggle through the sticking point instead of trying to find clever—and ultimately shortsighted—ways to slip by the resistance. Those who truly understand seek muscular conflict will regularly and routinely push up to (and past) mo mentary capacity. capacity. How a trainee deals with the sticking points and the struggle associated with effective resistance training will ultimately determine the degree of his success. We define successfu successfull pr ogressive og ressive r esistance esistance training training in two two ways—a ways—a radical increase incr ease in raw strength with a radical increase in lean muscle mass. Nothing more, nothing less. Acquiring these two attributes is profound.
WHY THE SUMO DEADLIFT? Experience has repeatedly shown that teaching proper sumo deadlift is far easier than teaching the conventional deadlift. First, there is a lot of technical similarity between a correct squat and a proper sumo deadlift. Think of the sumo sumo deadlift as a “reverse squat” squat” as there there ar e far mor e similarities similar ities than than differ ences. ences. The perfect sumo deadlift is similar to a partial r ep squat— squat—only only instead instead of the the weight being on your clavicles (as in a front squat) squat) or on your back (back squat) the weight is in front, hanging down from your hands.
Using an upright torso style for a sumo deadlift puts the emphasis on leg power. Those with weak legs will try to neutralize their relative lack of leg strength streng th by compensating compensating with high hips hi ps to start the lift. The lifter li fter will invariably end up strug struggling gling to for ce their their out o ut-of-po -of-position sition tor tor so into the final lockout lo ckout..
THE SUMO DEADLIFT 1. Grip a barbell, kettlebell(s), or dumbbell (around one end) and assume the start position. 2. Feet should be wider than shoulder width, width, with with the tor tor so as vertical as possible. 3. Tense the the upper back, attempting attempting to pull the shoulder blades together. tog ether. Tense the the gluteal gl uteal muscles, lower lo wer back, and thighs, then take take a big breath into the bottom of o f the belly. 4. Smoothly bring the weight off the floor with your legs. Do not jerk the weight. 5. The tailbone and upper body rise together, initially maintaining an upright torso. Do not let the tailbone shoot up first! 6. The reverse hip hinge powered by the gluteal muscles finishes the lift. The lower back and torso must be locked into one unit. 7. Maintain muscle tension at the top (the standing standing por tion of o f the lift) during exhalation. exhalation. 8. Inhale Inhale into the belly and start to lower lo wer the weight using the rever se squat technique—squat technique—squatting ting down do wn and and back while while maintaining mai ntaining an upright upri ght torso. tor so. 9. Lower the weight in a controlled grind speed and gently place it on the gr ound with with minimal noise. This controlled controll ed lowering techniqu techniquee is an exercise unto itself with profound benefits. 10. If you ar e performi perfo rming ng multiple reps, do no t lose tension as the the weight touches the floor. Break the weight off the floor (#4) and start another rep.
The Strong Medicine Robots demonstrate optimal sumo start position. Now, simply push your thighs downward. Your leg and torso length will determine how vertical your torso will be at the start. The robots have long legs which necessitate a more inclined torso. Try to achieve a spine position positio n as vertical ver tical as your anatomy will allo w. A wider stance will enable a mor e vertical vertical tor tor so.
Sumo Deadlift starting position.
DEADLIFT TACTICS EMBRACE THE HARD START.
Our deadlifts have a signature technique rooted in structural architecture, physics and safety. safety. The idea is to never lose lo se tension once o nce the deadlift deadlift set starts. Do Do not let the weig weight ht “settle” “settle” on the flo or between between reps, r eps, this this prevents a loss lo ss of body tension. We We want to create cr eate maximum body tension at the start of the first rep of the first deadlift set, and never lose that tension for fo r an instant. instant. Optimally, the the weight will will lightly lig htly touch touch the floor flo or between between r eps.
BRAKING THE “NEGA “NEGATI TIVE”. VE”. As the barbell approaches the floor between reps, the muscular brakes are applied with with increasing tension, like a car approaching a brick wall. Slowing the weight down causes a new level of muscle fiber stimulation, maximally stimulating the back, back, glutes, upper thighs, and hamstrings. hamstri ngs. The braking effect enables the lifter to exert maximum control at the “turnaround” ar ound” where descent becomes ascent. Slow, slower, slowest slo west—lig —lightly htly touch the weig weight ht to to the platfo platforr m and begin begi n the next r ep.
NO SHORTCUTS. If the the legs are ar e not stro stro ng enough to br eak the the weight weight from fro m the floor while while maintaining the proper start position, then go back and work on squats until until your yo ur legs ar e strong enough to deadlift. deadlift. Stop Stop playing playing to your biases and strengths—correct your weaknesses. Those who think the hip-hinge trumps the legs ar e missing missi ng the point. The question is not whether whether the hiphinge trumps leg power o r if the legs are better better than than strength strength from fr om the hiphinge. The Taoist Taois t answer answer is, ‘Not one, o ne, not the other, both!’ both!’ The optimal deadlift technique technique uses both bo th the the legs leg s and hip-hinge. hip-hing e.
EMBRA EM BRACE CE THE TH E STICKING POINT POIN T...
In the sumo deadlift, as long as the torso is held erect and only leg power is used to to br eak the the bar from fr om the floor, floo r, there there is no opportunit o pportunity y to avoid a sumo sticking point. Bouncing reps are not allowed. To reduce momentu mom entum, m, we use heavy heavy breaking on the eccentr eccentr ic movement mo vement and and acceler acceler ate ate during duri ng the concentr concentr ic pull. In the sumo, the sticking point occurs when breaking the barbell from the floor. The first six inches of a sumo pull is 100% leg power. To keep the sumo deadlift simple, and to increase the amount of weight you’re able to lift, increase your squat and leg power. Once the bar approaches the knees, the lift is as good as done. The upright torso allows for a perfect, str str aight-line pull. pull. The pull pull becomes easier the the closer you are to the lockout. A limit set of deadlifts activates every muscle on the human body to some degree.
EDDIE PENGELLY: SUBLIME SUMO
Note the wide stance allowing a near vertical torso. The vertical torso requires requir es almost 100% leg power to break the weight weight from fro m the floor. Once off the floor, floo r, the hips and back back can finish the lift.
SINGLE DUMBELL/KETTLEBELL DUMBELL/KETT LEBELL SUMO DEADLIFT
Sumo Deadlift side view with with single singl e kettlebell: kettlebell: fr om the star starting ting position, pos ition, the tailbone tailbone and upper upper body ascend tog toget ether her (arr ( arr ows) as the legs br eak the the weight weight from fr om the floor floo r at grind gr ind speed. As the the weight passes the the knees the the hips extend to an uprig upr ight ht position positio n to finish the lift. Revers Reversee the sequence sequence to bring bri ng the weight down slowly enough so there is minimal sound when the weight touches the floor.
DOUBLE DOUBLE KETT KET T LEBELL SUMO DEADLIFT DEA DLIFT
Sumo Deadlift fr ont view with with double kettlebells: The technique is identical to the single kettlebell lift except for a wider stance. Double kettlebells allows for heavier loads as you get stro stro nger.
Star Startt position for f or the Sumo Sumo Deadlift with a bar bar bell: the stance stance width width is wide enough enoug h so that your arms can be positioned inside of you knees. You can alternate grip position with your hands (shown here) or put both hands in a pronated (palm down grip).
Sumo Deadlift with a barbell: bar bell: the technique technique remains r emains the same with the tailbone and upper upper body bo dy ascendin ascending g toget tog ether her as the legs break the weight weight from fro m the floor at grind gri nd speed. As the the weight passes the knees the the hips extend in a revers r eversee hip hinge hing e to an upright upri ght position posi tion to finish fi nish the lift. Reverse the sequence to to br ing the weig weight ht down slowly enough so there is minimal sound when the weight touches the floor. To the trained eye, a perfect deadlift—sumo or conventional—is every bit as beautiful and technically intricate as a golf swing, a tennis serve, or a baseball pitcher’s windup. Careers are built on coaching the raw mechanics of athletic swings and throws. Every pro baseball team has a batting coach; every NFL team has a quarterback coach who drills quarterbacks on an ideal technical template for throwing and releasing a football. Definable coaching specialists and technical experts exist for improving raw athletic mechanics in every sport—a quicker release for a young NFL quarterback, a faster bat speed for a pro baseball power hitter, a more refined power serve for a grand prix tennis player, or a better golf swing swing for fo r a PGA circuit pro. pro . Sadly, in the deadlift, there’s no equivalent—anybody can claim to be a deadlift expert and “teach” deadlift technique. It seems every self-proclaimed deadlift expert is blissfully ignorant of deadlift technique, and prefers to lecture about sets, reps and frequency. Or, worse yet, they will teach some sort of “spinal cracker” deadlift technique that works well initially, quickly plateaus, and ultimately runs a high risk of spinal column injury. Bad deadlift technique forces a poorly positioned spinal column to straighten for the lock out on a limit deadlift rep. Proper deadlift technique technique keeps the spinal discs stacked as the lifter pulls the bar straig ht up.
BUILT-IN SUMO SAFETY” We insist on breaking the weight from the floor with leg power first then
finishing with the hip hinge not just for strength, but for safety. Breaking the weight from the floor with the hip hinge with high hips and an inclined torso at the starting position, puts significant shearing stresses on the lower back. The upright uprig ht,, mor e vertical tor tor so position posi tion we we require r equire stacks the vertebrae of the back, and minimizes stress on your spine. It’s It’s less likely likely with with our mor e vertical tor tor so position fo r the the lower back to “round “ro und”” (a commo n cause of back injury) when fatigued fatigued under under load. l oad.
COMMON FLA FLAWS WS IN FORM 1. THE HYPEREXTENDED SPINE This back position is called “hyper-lordosis” in medical terminology. It happens when when the the upper upper torso becomes unlocked from the the lower body during the initial part of the lift. This occurs o ccurs when the the legs ar e not strong enough to break br eak the the weigh weigh fr om the floor. The upper part of the torso will change position to become more upright without the legs moving. This puts the entire initial load on the back, and places the spine in a bad position.
Reduce the amount of weight and concentrate on keeping the lower back and upper upper torso locked together. The r ule—if the the legs do not no t move, the the upper upper body does not move. Use a weight that will allow you to break the weight off the floor using only your legs.
Here the trainee’s upper body rises before her tailbone at the start of the lift causing hyperextension (backward bend) of the spine. This form error usually means the weight is too heavy and the legs are not strong enough to break the weight from the floor. flo or. Lighten the the load lo ad in this case so that the the tailbone and upper body bo dy can rise ri se in unison, maintaining a straight spine during the lift.
2. ROUNDING THE BACK DURING DESCENT Avoid the temptation to bend forward while descending with the barbell. Using a precise and slow lowering technique will maximize the strength and muscle building attributes associated with the heavy eccentric/negative phase of the deadlift rep.
Maintain an upright posture during descent, similar to a reverse squat. Rounding the back during the descent of a deadlift is asking for a ruptured disc. The deadlift should look exactly the same during the ascent and descent. If we took pictures of a lifter during the upwards and downwards parts of the lift, they should be identical. Poor Poo r descending technique with with the Sumo Sumo Deadlift: the tr tr ainee lets her back bend for war war d (flexion) inst i nstead ead of maintaining maintaining the neutral neutral spine position as she lowers the the weight. This is usually a sign of fatigue and is a sure way to injure your back. The sumo deadlift is a required part of your resistance training program. It will protect your back from injury and forestall the hands of time by potently preventing sarcopenia and osteoporosis.
STRONG MEDICINE TACTICS: Implement the Sumo Deadlift as part of the foundation of your resistance training progr am.
PHYSICAL TRA TRA INING IV
BENCH PRESS PRESS AND OVERHEAD OVERHEA D PRESS
When it comes to building front torso muscles, no other progressive resistance exercise comes close to duplicating the results from proper, repeated and intense flat bench pressing. You might think lying flat on a bench and pressing a barbell or pair of dumbbells to ar ms’ length would be the the simplest task imaginable. imagi nable. But, But, we are confronted by a myriad of choices... What technical pathway will we use for the lowering phase? Where will we touch on the chest? Will we pause the rep, or touch-and-go? If we pause, for how long? Will we push on a straight or curved arc path? The trajector trajector y and speed speed of the bar ’s path path during during the the lowering and raising phases phases dramatically affects muscular targeting, and overall effectiveness of the exercise. We need to consider these things before every set. Become conscious and attuned to what what you you are ar e doing during dur ing every r ep of every set.
BENCH PRESS PRESS TECHNIQU TECHN IQUES, ES, TACTICS AND AN D TOOLS
We want to make the bench press maximally difficult, while the rest of the fitness world wants to make their bench presses easier with half-reps, machine pressing, reps bounced off the chest, or raising the butt off the bench at the sticking point. These are ego-inflating techniques that degrade strength and hinder results. Anyone who consciously or unconsciously makes their bench presses easier is defeating the purpose of resistance training. They don’t understand why they are lifting weights! Our mission is to resurrect the ancient tactics used by champion bench pressers, men who sought ways to increase the difficulty when they benched. Difficultly in resistance training is the pathway of progress. Making resistance training easier makes resistance resistance training less effective. effective.
Our goal is not to present a comprehensive set of bench press techniques and variations. We will provide our strategy on sets, reps, frequency and workout duration. The go al is to produce pro duce dramatic dramatic increases in lean muscle mass and equally dramatic increases in pure pushing power. A universe of pushing possibilities exist within the tight confines of flat benching. But, But, we we will fo cus on a single si ngle variation, vari ation, and hone the dumbbell dumbbell bench press to perfection.
LEARN TO LOVE DUMBBELLS Elite trainers love the cumbersome and awkward nature of the unwieldy dumbbell. In the right hands and used the right way, dumbbells are unrivaled for stimulating the pecs, shoulders and triceps. Dumbbells cause muscle stabilizers to fire to a higher degree than two-handed barbell work, or any of the resistance machines that mimic the bench press. We will pair the dumbbell’s inherent instability (an advantage) with our intensity-
enhancing techniques. In our first dumbbell variation, pause with the dumbbells at the bottom of the rep, then actually release the tension in the chest and arm muscles with an exhalation. This relaxation tactic is considered heretical by the resistancetraining mainstream. After the pause, re-engage the stretched, relaxed pecs, inhale and use a purposefully slow speed on the concentric (push) phase to increase the difficulty of the rep. All of our subsequent bench press variations are constructed based on our ultra-basic dumbbell techniques.
DUMB BELL DUMBBE LL BE BENCH NCH PRES PRESS S TECHN TECHNIQUE: IQUE: RELAX, RELA X, PAUSE, PAUSE, GRIND The most difficult bench press technique you will probably encounter is a limit set of ultra-deep, relaxed, paused, dumbbell bench presses performed with a purposeful “grind” (slightly slowed) rep speed. Mastery of the paused dumbbell bench using grind speed is our very own version of bench press boot camp—a bench press version of SEAL BUDs Hell Week. Once you have paid your dues with long and prolonged prol onged bout bo utss of o f paused dumbbell dumbbell bench bench presses, everything everything else seems like a walk in the park.
DUMBBE DUMB BELL LL BE BENCH NCH PRESS TECHNIQUE 1. Select two two dumbbells and sit on the the end of the exercise bench with with both dumbbells. The handles should sho uld be vertical with the the plates in your lap. 2. Lie back and simultaneously tur turn n the the handles handles outwar outwar d. You are ar e now lying on the bench with with the the dumbbells in the bench press start position. po sition. 3. Exhale and allow the the dumbbells dumbbells to sink. Maintain Maintain control, contro l, even though the pecs and shoulders are relaxed, the grip stays tight. The dumbbells are now in push position. 4. Relax, feel the the dumbbells dumbbells stretch the the pecs pecs and shoulder s downwar downward. d. Perfor m this “pre-stretch” “pre-stretch” at the the start start of o f every single singl e rep. r ep. 5. We have maximally maximall y inhaled and are full of air at the same instant the dumbbells touch the chest at the bottom of the descent. Then, we exhale, relax, and stretch. 6. After After allowing allo wing the bells to to str str etch downward, conscio usly r e-engage e-engag e the pecs, pecs, delts, and triceps. Shift from fro m stretching and relaxation rel axation into pushing and contracting.
7. When it is time to to push, inhale mightily mig htily and push upward. upward. The rep speed is not fast or super super slow—but slow—but it is consciously slo wed. wed. 8. This consciously-slo conscio usly-slowed wed r ep speed is called “gr ind.” ind.” We gr ind the dumbbells to a “hard” (full-and-complete) lockout. We synchronize our exhalation to end at lockout. locko ut. 9. This unor unor thodox str str ategy accomplishes accompli shes two two monumental tasks: it ingrains perfect technique and isolates/stimulates the maximum number of muscle fibers. 10. This fundamental fundamental bench bench press technique technique succeeds in making light weights heavy, and stays stays true to our overall over all philoso phy. phy. 11. All subsequent bench press pr ess variations vari ations spring spr ing fro m this pause-relaxpause-r elaxand-grind technique. After practicing this technique, all other forms of benching are easy.
Dumbbell Dumbbell Bench Press set up position. posi tion.
Dumbbell Bench Press start position (top view and floor level).
Dumbbell Bench Press: start from relaxed bottom position, produce tension, press at gr ind speed to top lockout, lo ckout, descend slowly, slowly, pause at the the bottom, repeat r epeat… …
DUMBBE LL BEN DUMBBELL BENCH CH PHASE II: BEYOND BE YOND PAUSE, RELAX, RELA X, GRIND Our bench press theme is the pause-relax-and-grind dumbbell technique. As we introduce each subsequent new bench press variation, it will be easier than its predecessor. This the natural order of proper progressive resistance training. Human nature is to jump ahead to the sexier bench press variations without mastering the basic basic theme. This is a big mistake. How can we develop a deep understanding of any variations without without fir st mastering the theme? theme? The first step—which includes all the physiological benefits of bench press expertise—is to master m aster the dumbbell bench press with the the pause-stretch-relax-in-thepause-stretch-rel ax-in-the-
bottom-position technique, then using the grind speed to push the dumbbells to lockout. All subsequent bench press and barbell variations are built on this core technique. Do not skip ahead before mastering the “pause-relax-and-grind” style. Without mastering this technique, the trainee cannot appreciate the “easing effect” as they master each subsequent bench press variation. We adhere to an overarching over arching philosophy of using ultra-strict, ultr ultr a-simplistic, a-simplistic, but sophisticated techniques to make light weights heavy. By design, any bench press techniques after the pause-relax-and-grind approach with dumbbells will seem light and easy by by comparison. compar ison.
ADVAN ADVANCING CING THE DUMBBELL DUMBBE LL BENCH BEN CH PRESS PRESS After After mastering masteri ng the cor co r e technique, we we can proceed pr oceed with the next next two two dumbbell dumbbell variations: 1. Pause at the the bottom like li ke befor e, but instead instead of pushing with a slow slo w “grind” “gr ind” speed, push the dumbbells up explosively. Compared to the excruciatingly slow pause-relax-and-grind technique, dumbbell bench presses with an explosive push seem easy by comparison. 2. The second seco nd variation vari ation eliminates eli minates the pause. pause. Lower Lower the dumbbells dumbbells to the bottom position, po sition, then immediately push them up explosively explosivel y. This is the “touch “touch and go” go ” variation. The second variation (touch-and-go) (touch-and-go) allows for maximal loads. Strong Strong Medicine trainees trainees coming fro m the hell hell of o f pause-and-relax pause-and-relax gr ind benching to touch-and-go explosive dumbbell bench press technique will feel as though they are cheating. Now we can choose to use a barbell—or not.
THE OVERHEA OV ERHEAD D DUMBBELL DUMBBELL PRESS PRESS The ability to push in the vertical plane is important in daily life. The overhead dumbbell press will train this ability, giving you specific strength that not many
people possess. While big bench press numbers are impressive, overhead pressing arguably translates better to real-life applied strength. In our opinion, “How much can you press?” should be the benchmark question for upper body strength, not, “How much can you bench?”.
COILED EN ENERGY ERGY:: FROM BOTTOM TO TO TOP The perfect press starts with the lower body, not the upper body. You must have a strong, steady foundation. A flaccid lower body during the press is a very serious “energy leak”. Energy which could help push the weight overhead is lost to an unstable lower body if improper technique is used. Your press should start by tensing tensing the ent entir iree lower body, body, as if you are ar e compressing compr essing a coiled spring. spr ing.
COACH’S CORNER: A successful standing overhead dumbbell press depends on a super stable push platform. The thighs and legs are maximally contracted, glutes are clenched, and there there is i s tremendous tremendo us tension in the mid and upper back.
THE OVERHEAD OVERHE AD PRESS PRESS Dumbbells and kettlebells are the ultimate tools for overhead pressing. You can pr ess one o ne are ar e at a time, or both at once. We We will be using usi ng two dumbbells dumbbells or kettleb kettlebells ells for fo r the the double arm press. 1. Grab Gr ab a set of appropri appro priately ately sized dumbbells dumbbells or kettlebells. kettlebells. Be conservative and and err on side of “too “too light” if you are ar e in doubt. doubt. 2. Position Positio n the bells in the clean position at shoulder height. 3. Clench your calves, thighs, thighs, glutes, and abdominal muscles maximally maximall y before pr essing. T his his is the start position. 4. Press the the bells explo explosively sively over head to full elbow lockout. lo ckout. 5. Pause with the bells overhead over head while maintaining maximal tension tension thr thr oughout ougho ut your your body. body.
6. As you lower the bells slowly, build even mor e tension tension in your body. You ar e compressing compr essing the coiled spring. Do not let gr avity avity take take control of the bells in an uncontrolled drop. The negative (lowering) part of this exercise is just as important as the push upwards. 7. The coiled spring tension tension generated will prepar preparee you you for the the next next r ep. Pause briefly brief ly at the the bottom then explo explosively sively push the bells upwar upward d again to lockout. 8. Repeat until until the the desired desir ed number of repetitions are completed.
Dumbbell Overhead Press: start the press from a strong base with legs and glutes contracted. Build tension (coiled spring) during the descent to power the explosive push on the next repetition. The dumbbell bench press and overhead press are the pinnacle of upper body pushing movements. After you have developed good technique in both, you can move forward in your training. With every push, we need a pull to maintain balance. For our purposes, the the ro w is the the best best option option for fo r an upper upper body pulling exercise.
STRONG MEDICINE TACTICS: Use the dumbbell bench press as one of the foundations of your resistance training progr am.
STRONG MEDICINE TACTICS: Implement the overhead press as one of the foundations of your resistance training progr am.
PHYSICAL TRA TRA INING V
THE ROW
When selecting an appropriate pulling exercise, the choices are extremely limited. The elite choose from chin-ups and pull-ups done with various set and rep combinations. For those able to perform them, proper chin-ups or pull-ups from a dead-hang stretch to chin-over-bar is unparalleled for activating, building, and strengthening every muscle of the back. But, few have the requisite strength-tobodyweight bodyweight rat r atio io needed needed to perfo r m this difficult exercise. exercise. Chin-ups and pull-ups are difficult because we are forced to handle 100% of our bodyweight—and most people are not that strong. There are clever gym machines for assisted chin-ups and pull-ups with counterweighted knee platforms that push upwards—but how many of us have access to such a marvelous device? We are for ced to to look lo ok aro und for exercise alternative alternatives. s. After experimenting with different back exercises, one that seems to fit all the criteria as a successful chin-up/pull-up replacement is the “frozen statue row.” But, before we can do the “frozen statue row” (FSR), we will start with the single arm ro w to build a founda fo undation tion of perfect techniq technique ue before befor e advancing. advancing.
The Chin-up: wor wor ks the back back like nothing no thing else.
COACH’S CORNER: We realize that a row pulls in the horizontal plane while a chin-up pulls in a vertical plane. While the row is not a true substitute, it works for us because it is the direct opposite of a dumbbell bench press. The row will help us build symmetry by offsetting the horizontal push of the bench press with a horizont horizo ntal al pull.
PHASE I: THE SINGLE ARM SUPPORTED ROW 1. Use a dumbbell that is lighter than you think you need, and put it next to the bench. 2. Grab Gr ab one end of the the bench bench with with your left l eft hand and place your left knee and shin on the bench. The left side of your body is now supported on the bench.
3. Bring your r ight leg dir direct ectly ly out from fr om the the bench bench and plant your r ight foo t with with a stance wider than shoulder width. width. You You now have 3 points po ints of suppor suppor t—your t—your left hand, hand, left knee/shin, knee/shin, and and your right ri ght foot. foo t. 4. Keep this position. posi tion. Reach down and and grab gr ab the the dumbbell dumbbell with with your r ight ig ht hand. hand. Now raise your r ight shoulder (keeping (keeping your arm hanging straight down) until it is level l evel with your left shoulder. Let the the weight of the dumbbell stretch your back muscles but do not let your shoulder drop. Your spine should be straig str aight ht (do not “hunch” your back). This is the
starti start ing position. 5. First, Fir st, r etracting shoul shoulder der blade (scapula) towards your your spine. Your dumbbell will start to r ise as you elbow should not bend at this point. The dumbbell move your shoulder blade towards towards the spine (imagine trying to pinch something between your shoulder blade and your spine). Do not jerk the weight up from the starting position, move at a slow “grind” speed. 6. Direct your elbow elbo w up towards the ceiling . It will natural naturally ly bend when you do this, but we are not no t curling curli ng the dumbbell. Bring Bri ng the elbow up as high as possible but do not let the the front fro nt of your r ight shoulder r ise much above the level of your left shoulder. This mistake results in twisting the spine and poor technique. 7. Briefly Brief ly pause at the top position and lower the dumbbell with with a slow “grind” speed back to the start position. 8. After After completing co mpleting your r eps, switch to the the other side and r epeat the above steps.
Single Arm Supported Row: the shoulders stay level and the forearm pulling the weight stays vertical. The elbow is directed toward the ceiling in a vertical line.
THE “FROZ “FROZEN EN ST STA ATUE” ROW
The single ar m dumbbell dumbbell r ow perfor perfo r med at grind gri nd speed speed with with a pause truly truly makes light weights heavy. You can build incredibly strong and dense lats, rhomboids, lower trapezius, and posterior deltoids with this technique while using minimal weight. After several months of training, you can progress to the double dumbbell row, the “frozen “fro zen statue” statue” row r ow (FSR).
EXERCISE SAFETY Do not attempt the “frozen “fro zen statue” statue” row r ow until you have developed the requisite posterior chain (back, (back, glut gl utes, es, hamstr hamstr ing) strength and postural postural stability fro m training trai ning the sumo deadlift deadli ft and squat squat with with perfect technique technique for several months. The postur postur al demands demands fro m this exercise exercise could co uld result in back injury if yo u are insufficiently insufficiently prepared. The FSR involves holding your body in a static position “like a statue.” Instead of using a bench for suppor suppor t as in the the single ar m r ow, ow, the the “fro zen” position position is the the base of support for the double dumbbell row. Holding this base of support adds a significant level of difficulty and a much higher stimulation of the central nervous system. Stabilizing this position while just holding dumbbells is a workout in itself. Rowing the dumbbells from this position is maximally stimulating for the adaptive response we want want fro m our r esistance esistance training. training.
WHY WH Y MOST MOST FREE-WEIGHT FREE-WE IGHT ROWS ARE WORTHLESS WORTHLESS The classical barbell ro w and all its variations are ar e ofte o ften n fundament fundamentally ally
flawed in their execution. The problems are numerous: • Stances Stances tend tend to to be too nar r ow—widen your stance to at least shoulder width. • The spine is often bent, bent, make sure to maintain a neutr neutr al spine position without bending the back. • Most rower r owerss jolt jol t the the weig weight ht upwar upward d to to start star t the the movement. The latissimus (lats) muscles are not engaged (and not exercised) by jerking the weig weight ht at the star start. t. This is i s also very bad fo r the spine, and places significant, significant, abrupt shear shear ing forces fo rces on o n your verteb ver tebrae. rae. • Lifters make most of these these “mistakes” “mistakes” on pur pur pose and are ar e driven by ego. These techn technical ical err or s allow for heavier heavier weights weights to to be “r owed.” owed.” Moving the weig weight ht in this this manner is not no t a row ro w and misses the muscles we we want to exercise. exer cise. These attempt attemptss to impr ess others o thers ar e just a setup setup for injury. Heavy Heavy weight weight is not needed needed for maximum benefit benefitss fr om a cor r ectly ectly performed r ow. ow.
PHASE II: THE “FROZEN “FROZE N STA STATUE” ROW 1. Grab Gr ab a pair of dumbbells dumbbells that are ar e lighter than you think you need and hold them at your sides while standing erect.
2. Move your feet at least shoulder width apart. 3. While maintaining a flat, flat, neutral neutral spine, hinge hinge at the hips and lower lo wer the angle of your torso until until it is almost parallel to the the floo r. We We avoided this this high hip po sition with the the deadlift, but the lighter weights used for the FSR, FSR, ensures that the the stress on o n the spine is safe and manageable as lo ng as the spine remains locked in to a neutral position. The dumbbells will hang relatively close to the floor at this point. T his his is the starting st arting “frozen
statue” stat ue” position. position. 4. Hold this this position as you begin the the r ow. If initiat ini tiating ing the row causes you to break the “frozen statue” position, the weight is too heavy. 5. The first movement movement is retracting your your shoulder blades (scapu (scapula) la) towards your spine. Your elbows should not bend at this point. The dumbbells dumbbells will will start to rise r ise just from moving your yo ur shoulder blades blades towards the spine (imagine trying to pinch something between your shoulder blades and your spine). Do not jerk the weights up from the star star ting ting position, move at a slo w “grind” “gr ind” speed. speed. 6. Point your your elbows up towards the the ceiling. They will will naturally bend when you do this, but do not no t curl the dumbbell. Br Br ing the elbows up as high as possible while keeping yourself locked in the “frozen statue” position with a flat, neutral spine. Keep squeezing your shoulder blades together. 7. Pause at the top position briefly br iefly and lower lo wer the dumbbells with with a slow “grind” speed back to the start position. 8. Star Startt another repetition and r epeat until your set is complete. compl ete.
Frozen Statue Row: the spine remains flat (almost parallel to the floor) during the lift. The elbows are directed in a vertical line toward the ceiling with the forearms remaining perpendicular to the floor. (Note that the trainee has a hyperextended (bent back) back) neck in the star startt position but fixes it during dur ing the lift itself).
SIMPLE IS AS SIMPLE SIMPLE DOES D OES Many people have a hard har d time making the mind/muscle co nnectio nnection n with with the main muscles we’re trying to target—the lats. Here is a bit of muscle trivia I heard eons ag o: the lats are the least used muscles on the human body. Because of this, they they are the easiest muscles to str engthen and grow gr ow —assuming —assumi ng the smar sm artt trainee trai nee uses techniques techni ques that actually stimulate stimul ate the lats to to a significant sig nificant degree. degr ee. The muscle elite el ite had a saying, “Show me a man with gr eat lats, lats, and I’ll I’ll show you a man with sub-par sub-par biceps; show sho w me a man with outstanding outstanding biceps and I’ll show you a man with terrible lats.” In other words, if you can “arm pull” your r ows by activat activating ing the biceps, biceps, you are not using your lats. We must concentrate on pulling pulli ng our o ur r ows with the the muscles of o f the back. Become a dumbbell row technician and really learn, hone and develop develop your techniqu techniquee over o ver time. You have now learned the five core exercises which form the Strong Medicine resistance training foundation. But no resistance training program is complete without mentioning abdominal training. We will show you how to develop rock hard abdominal muscles without ever doing a sit-up or crunches. Before you think this sounds like a television infomercial, read on.
STRONG MEDICINE TACTICS: Incorpor Incor porat atee the the row r ow as one of th thee foundations foundations of o f your r esist esistance ance training training program.
PHYSICAL TRAINING VI
STRONG MEDICINE MEDICINE ABS A BS
We all want a hard, chiseled abdominal region—a “six-pack” to show off. There are literally hundreds of abdominal training videos that promise to give you the coveted six-pack. The truth is, only proper proper nutrition and lifestyle manageme management nt (good sleep, stress control) will give you six-pack abs, not endless crunches and sit-up variations.
SIT-UP SIT-UPS S ARE A RE A BAD IDEA... IDEA. .. Not only will you fail to achieve the “six-pack” look from sit-ups, they may lead to injury. Most sit-up variations involve anchoring the feet and significantly engaging your hip flexors (psoas) to achieve the sit-up movement. This is a problem pro blem for a couple of r easons.. easons... • The abdominal muscles are ar e not optimally optimall y activated activated or strengthen streng thened ed since the hip flexor flexor s are doing mo st of the wor wor k. • High activat activation ion of the the psoas (a major hip flexor) flexor ) puts puts major compressive compr essive for ces on o n the spine. A look lo ok at the psoas anatomy explains why. why. According Accor ding to Dr. Stuart McGill, a leading spine biomechanics expert, the average sit-up generates about 730 lbs. of compression on the spine with every repetition. This amount of compression compressio n is known to to lead to to disc injuries o ver time. Doing Doing hundreds hundreds of sit-
ups will will not do your yo ur back any favor favor s.
SIT-UPS ARE LOW BACK “POISON” As Dr. Dr. McGill McGill has studied studied in his spine spi ne biomechanics labor l abor atory ator y, sit-ups put a huge compressive load on the spine. To make matters worse, this large compressive force is applied when the lower back is in a flexed position. According to Dr. Dr. McGill’s McGill’s research, the best way to herniate herniat e a disc is with high compressive forces and repeated flexion, which exactly describes a sit-up!
Many clinicians ar e still telling their back pain patients patients to do sit-ups to strengthen their abdominals. But, But, situps situps are the exact o pposite pposite of o f what what
you shoul sho uld d do for fo r a healthy back. The abdominal muscles’ function is to stabilize the spine during activities such as lifting, carrying, pushing, and pulling. We need to train them as they were meant to function, instead of iso lating them with exercises exerci ses such as sit-ups and crunches.
If you have progressed to the dumbbell front squat, you will recognize the inherent difficulty in maintaining a neutral spine position while holding the weig weights hts at shoul shoulder der level during dur ing the squat. squat. You sho uld feel yo ur abdominal muscles str str uggling uggli ng to maintain maintain an uprig ht spine spine position while you are squatting. The abdominal abdomi nal muscles ar e meant to to stabilize stabili ze the spine dur dur ing activity. activity. So, this is how we will will train the abdominals.
ABDOMINAL TRAINING PHASE I: THE BASIC B ASIC PLANK PLANK A properly pro perly perfo r med plank plank fits the the bill for a gr eat abdominal exercise exercise that works wor ks the abs with with the rest of o f the body and strengthens str engthens their their function as a spine stabilizer. stabilizer . The Strong Medicine plank can seriously test your resolve. reso lve. There will be no doubt that that your your abdominal muscles muscles are ar e working. 1. Find a r elatively level space on the gr ound; use a mat if needed. Put your for earms on o n the the gr ound with with your your elbows directly directly underneath underneath your your shoulders. Your Your for earms should be shoulder width width apart apart on o n the the gr ound. You ar e in a kneeling position posi tion at this point. 2. Keeping Keeping your your forear fo rear ms in place, come off of your knees knees and straighten your your legs. Now Now,, only your for earms and the the balls of your yo ur feet are touching the ground. Your feet are positioned next to each other. 3. Flatten Flatten your your back (no sag in the middle), then then tig tighten hten your glutes gl utes and your thigh muscles. Do not look up; keep your eyes and head downward. 4. Push your heels away away from fr om you while while keeping the balls of your feet
planted (you will feel a stretch in your calf muscles). T his his is the startin st artingg position. 5. To begin begin your repet r epetition, ition, push your forear fo rear ms and and elbows elbows down into the ground gr ound while simultaneously simultaneousl y “pulling” “pulling ” them towar toward d your feet. Your for earms and elbows will will not move mo ve from fro m their their position. This “down and and backwa backwarr ds” force for ce is isometric, like pushing against a wall. 6. At fir st, try to hold this posi position tion with with the the “down and back back force” for ce” on the the for earms and elbows for 10 seconds per per repetition. repetition. Wor Wor k your way way up to sustained 30-second holds.
The Plank (phase 1): the the spine remains r emains neutral and the entir entiree body is under tension. Push the heels backwards while you press your forearms down and back.
ABDOMINAL TRAINING PHASE II: THE HIGH PLANK Once you can hold the basic plank for several sets of 30-second holds, move up to the high plank. pl ank. This var iation is i s exactly like the basic basic plank except except that that you are on your hands hands instead instead of your for earms. 1. Find a r elatively level space on the gr ound; use a mat if needed. Put your hands hands on the the gr ound directly underneath underneath your your shoulders with your your fingers finger s facing fo rewor d. Your hands hands should be shoulder width apart apart on the ground. gr ound. You You ar e in a kneeling position posi tion at this this point. po int. 2. Keeping Keeping your hands in place, come off of your knees and and straig hten your legs. Now, only your hands and the balls of your feet are touching the ground. gr ound. Your Your feet are positioned po sitioned next to to each other. o ther. 3. Flatten Flatten your your back (no sag in the middle), then then tig tighten hten your glutes gl utes and your thigh muscles. Do not look up; keep your eyes and head downward. 4. Push your heels away away from fr om you while while keeping the balls of your feet
planted (you will feel a stretch in your calf muscles). This is the starting position. 5. To begin your your r epetitio epetition, n, push your hands down down into the the gr ound while while simultaneously “pulling” your hands toward your feet. Your hands will not move from fr om their their position. The “down and and backwa backwards” rds” fo rce you yo u are using is isometric, i sometric, like pushing against a wall. wall. 6. At fir st, try to hold this posi position tion with with the the “down and back back force” for ce” on the the hands for 10 seconds per repetition. Work your way up to sustained 30second holds.
The High Hig h Plank (phase II): this this var iation uses the same technique as the plank but from the hands instead of the forearms. Push the heels backwards while you press your hands down and back. The One-hand O ne-hand Plank (phase III) III) will use the same technique but holding one hand out in front of your body reaching toward the wall in front fro nt of you.
ABDOMINAL TRAINING PHASE III: THE ONE HAND PLANK PLANK Once you can hold the high high plank for several sets of 30-second holds, move up to the one hand plank. This var iation is i s exactly like the high plank except you use only one hand for support. This adds an extra layer of challenging instability. 1. Find a r elatively level space on the gr ound; use a mat if needed. Put your hands hands on the the gr ound directly underneath underneath your your shoulders with your your fingers finger s facing fo rewor d. Your hands hands should be shoulder width apart apart on the ground. gr ound. You You ar e in a kneeling position posi tion at this this point. po int. 2. Keeping Keeping your hands in place, come off of your knees and and straig hten your legs. Now, only your hands and the balls of your feet are touching the ground. Your feet are positioned about shoulder wid Yo u widtt h apart. Yo
will need a wider wider base of support from fr om your yo ur feet f eet at first. 3. Flatten Flatten your your back (no sag in the middle), then then tig tighten hten your glutes gl utes and your thigh muscles. Do not look up; keep your eyes and head downward. 4. Push your heels away away from fr om you while while keeping the balls of your feet planted (you will feel a stretch in your calf muscles). T his his is the startin st artingg
position. 5. To begin your your r epetition, epetition, lift one hand hand off of the the ground gr ound and and hold it out in front of you. Generate the same isometric “down and back” force with with the hand hand on the gr ound. Tr Tr y to hold hol d this position positio n for 5 seconds. Keep Keep your shoulders level with each other with no twisting of the spine. 6. After After holding ho lding the one hand position positio n for 5 seconds, switch hands and lift the opposite opposi te hand up up in front fr ont of you. Continue Continue to switch hands hands every 5 seconds for the duration of the repetition (10-30 seconds).
“ANTI-ROTATION” The one hand plank is more difficult since the abdominals not only stabilize the spine from flexing or extending (in the sagittal plane), but also must stabilize the spine against rotation (in the transverse plane). This stabilization against rotation (Dr. McGill calls it “anti-rotation”) is an extr extr emely impor tant tant funct function ion of our abdominal muscles. Anti-ro Anti-rota tation tion is trained with the the one hand plank by keeping the shoulders shoulder s level during dur ing the hand switch.
ABDOMIN AB DOMINAL AL TRAINING PHASE PH ASE IV: IV: THE PLANK PLAN K ROW Once you have worked up to several sets of 30-second sustained one hand planks, planks, you are ar e ready r eady for the the plank row ro w. This This exercise is a huge challenge to the stabilizi stabilizing ng function o f the abdominal muscles. You You will definitely feel it. 1. Find a relatively level space on the gr ound; use a mat if needed. Grab Gr ab two light dumbbells and place them in front of you, parallel to the long
axis of your body (see photo). Instead of placing your hands on the gr ound, you you will grab g rab the dumbbells dumbbells firmly and use them them as your fr ont base of support. Be sure that the dumbbells are directly below your shoulders. 2. Keeping Keeping your hands in place on the the dumbbells, come off of your knees and straighten straig hten your your legs. legs . At this point only the dumbbells and the balls balls o f your feet are touching touching the the gr ound. Your feet are positioned about
shoulder wid widtt h apart (or (o r greater great er if needed). needed). 3. Flatten Flatten your your back (no sag in the middle), then then tig tighten hten your glutes gl utes and your thigh muscles. Do not look up; keep your eyes and head downward. 4. Push your heels away away from fr om you while while keeping the balls of your feet planted. T his his is the startin st artingg position. 5. To begin your your r epetitio epetition, n, lift one dumbbell off of the the gr ound with with the identical technique used in the previous section for the single arm row. Lift the the dumbbell at gr ind speed and pause at the the top. While one o ne arm ar m is rowing, generate the isometric “down and back” force with the hand grasping the dumbbell on the ground. Keep your shoulders level with each other and do not twist your spine during the row. Do not allow your back to bow or sag. 6. Row on alter alter nate sides for up 2-10 r epetitio epetitions ns per side.
The Plank Row (phase IV): the starting position (not shown) is a plank position on top of dumbbells or kettlebells. Shoulders remain level and the supporting hand pushes the the dumbbell or kettlebell kettlebell into i nto the floo r keeping the wrist straig ht. Use the the same rowing technique you learned previously leading with the elbow directed toward the ceiling. Notice that he has a wider foot position for stability.
SAFETY TIP: Make sure you use hexagonal style dumbbells or kettlebells with a large flat bottom for this exercise. A rounded bottom surface on dumbbells or kettlebells will not work, and will put you at risk for injury. Phases I-IV of Strong Medicine abdominal training will progressively work the abdominals as they are meant to work in daily life. This progr pro gr ession will also help your deadlift deadlift and squat squat since both both lifts require significant stabilization of the spine. The deadlift and squat by themselves are already training the stabilizing function of the abdominal muscles.
There are many excellent ways to train the abdominals as stabilizers (including (including the “anti-r “anti-rotat otation” ion” function). function). The prog ression ressio n covered here her e only scratches the surface. Stop training the abdominals in isolation with back-busting sit-ups and crunches. cr unches. The Strong Medicine abdominal training program will give you a six-pack (if your nutri nutrition tion and lifestyle lifestyle are locked on) and a bullet-pro bullet-proof of back.
STRONG MEDICINE TACTICS: Use Strong Medicine abdominal training to build an iro n core cor e and prevent prevent back injuries.
The last six sections have been a primer on Strong Medicine resistance training. These exercises should form the foundation of your weight training. Feel free to add exercises to this foundation to suit your individual needs and goals. We will now transition transition to cardiovascular training fo r both the the beginner and the experienced experienced trainee.
PHYSICAL TRAINING VII
STRONG MEDICINE MEDICINE BASIC CARDI CA RDIO O
High Intensity Interval Training (HIIT) is the preferred way to maximize the adaptive response of the body and lose fat in the shortest amount of time exercising. But, not everyone is ready for HIIT from both a fitness and psychological perspective. The effort and high target heart rates of HIIT can be overwhelming and intimidating to the new trainee. For an obese or diabetic trainee, making monumental changes in nutrition while starting an intensive exercise program at the same time is often too much to handle at once. We have created a Basic Cardio “ramp-up” for those in the above categories, or who are new to training and are substantially deconditioned. The Basic Cardio progr pro gr am can be progr pro gr essed to to subsequen subsequentt advance advanced d training using Strong Medicine tactics.
PREPARATION All you need to start is a basic heart rate monitor and your calculated theoretical maximum heart rate (HRmax). You will use your HRmax to plan your basic cardio training “ramp-up.”
MAXIMUM HEART RATE CALCULATION REVIEW For men: 208 - (0.7 X Age) = HRmax For women: 206 - (0.88 X Age) = HR max Example 1: Chr Chris is is 43 and wants wants to calculate his maximum heart r ate. He will multiply his age (43) by 0.7, which equals 30.1. He will then subtract 30.1 30.1 from fr om 208 to get 177.9 177.9 (we’ll r ound to 178). Chr Chr is’s HRmax HRmax is about abo ut 178 beats beats per minute. Example 2: Carr ie is 46 year s old. ol d. To calculate her HRmax, HRmax, we would would multiply her age (46) by 0.88 to get 40.5. We then subtract 40.5 from 206 to get g et 165. 165.5 (we’ll r ound up to 166). Car Car r ie’s HRmax HRmax is 166 beats per minute.
At this stage, our preferred cardio method is outdoor “power walking.” This is purposeful walking at a pace that will bring your heart rate up to a predetermined level. It is not a leisurely stroll chatting with friends. Train outdoors exclusively as long as your envir environment onment is safe. Outdoor Outdoor training has added benefit benefitss (stress r elief, etc.) that slogging away on a treadmill will not provide. The following is a sample 10-week basic cardio “ramp-up” using the heart rate monitor and a waist waist to to height rat r atio io to track your pr ogress. og ress. (Find (Find directions for calculating yo ur waist-heig waist-height ht ratio in the “Stuff “Stuff You You Can Measure” section at the the end of the book.) Carrie, a 46 year old female, is our example. Her HRmax was previously previ ously calculated to be 166 beats beats per minute (bpm). We will calculate calcul ate her
weekly target heart rate as a percentage of her HRmax of 166 (bpm).
The goal of Strong Medicine Basic Cardio Cardio training is to help someone start an exercise progr pro gr am from fr om the beginning beginning very ver y slowly at a low intensit intensity y and volume. volume. They will steadily incr ease both volume and intensity over 10 weeks weeks and will be well well prepared pr epared for the the full Strong Medicine physical training program.
Carrie calculat calculated ed her week week 1 target targ et By week 5, Carrie is is heart heart rate rat e of 91 power walking walking 5 tim t imes es a bpm by taking week for 20 minutes per her HRmax of session. She is keeping By the tenth week, Carrie’s waist 166 and her target heart rate as size has decreased significantly. She multiplying it by close to 112 bpm as is wearing wearing clothes clot hes 2 sizes s izes small smaller er 0.55 (55%). possible possibl e during the entire e ntire t han when when she start ed. She is is session. 166 X 0.55 = 91 exercisin exercisingg at a relative high high bpm. She will intensity (80% of HRmax) every We have steadil st eadilyy keep her heart day of t he week for 35 min minutes utes per increased both the rate at this level volume and intensity of session. for the duration of her workouts workouts over the t he She is is ready to move on o n to Strong her session.
She will do 3 sessions during week 1 for 8 minutes per session.
Medicine Medici ne High Intensity Cardio. past 5 weeks. She has already already seen the t he benefit benefit s with a decreasing waistheight height ratio.
Use Strong Medicine Basic Cardio Cardio as an “on-ramp” to your fitness fitness progr pro gr am. You You can also use power-walking power-walking as an active active r ecovery exercise instead of a complete co mplete rest day. day. Basic cardio cardi o can also als o be used any time you feel your stress cup is near o verflowin verflo wing g and high intensit intensity y exercise may be too much that day.
STRONG MEDICINE TACTICS: Build your cardiovascular training fo und Build undat ation ion wit with h Strong Medicine Basic Ba sic Cardio. Cardio . Now that you have a cardio training foundation, we will progress to the more advanced high intensity interval training to work the cardiovascular system to its fullest capacity. This will provide increased health benefits and accelerated fat burning.
PHYSICAL TRAINING VIII
STRONG MEDICINE MEDICINE HIGH INTENSITY IN TENSITY CARDIO
Most official physical activity guidelines from exercise and public health authorities recommend “at least 150 minutes per week of moderate to vigorous aerobic exercise.” For many people, fitting this much exercise into their hectic schedules means at least 30 minutes of mind-numbing monotony on a treadmill, bike, or elliptical elli ptical machine 5 days each week. week. It is no wonder that over 50% of those those who start a new exercise exercise prog pr ogram ram will not continue with it for even 6 months. The most common excuse for not exercising is a lack of time. Also, a half hour of moderate-intensity exercise on a machine is just plain boring. The boredom factor is a big part of exercise exer cise non-adherence. non-adherence. Strong Medicine addresses the time and boredom problems with our advanced cardio pro gram gr am cent centered on High Intensity Interval Training (HIIT). This type of exercise uses very brief periods of very high effort/intensity separated by periods of rest/recovery. HIIT protocols allow you to get all of health and fitness benefits of sustained moderate exercise (though HIIT is superior is some aspects) in a short amount of time. HIIT not only cuts down on the time needed for an effective exercise session, but it also also only r equires you to do cardio car dio 3 days per per week, week, instead instead
of 5 days or mor e with with traditional traditional mo derate intensit intensity y cardio. cardio . Recent Recent medical research supports suppor ts the the use of HIIT HIIT as a superior for m of of exercise for people with heart disease, diabetes, high blood pressure, and obesity. • A single session of HIIT HIIT improves blood glucose g lucose contro contro l in diabet diabetics ics and non-diabetic non-diabeticss for fo r 1-3 days after the exercise session. • For people with heart disease, HII HIIT T results r esults in bett better er hear t health health improvements as compared to moderate intensity exercise, even when the
amount of calories burned are the same. • HIIT HIIT was was superio superio r to moderate mo derate intensit intensity y exercise exercise for impro ving heart and blood vessel function in heart failure patients. • HIIT HIIT is mor e effective than moder ate intensity exercise exerci se for fo r control contr olling ling and pr pr eventin eventing g hig h blood pr essure. • HIIT HIIT is far superior to moderat moder atee intensit intensity y exercise for r educing educing body fat, especially around ar ound the belly. belly. The secret to the effectiveness of HIIT is the high intensity. HIIT protocols require you to push your heart rate up to 90% (or more) of your maximum heart rate for brief periods of time. The small amount of time spent at these high heart rates produces incredible beneficial adaptations in the body that moderate intensity exercise cannot touch.
MAXIMUM MAX IMUM HEA H EAR RT RATE RATE CALCULA CALCULATION REVIEW REVIE W For men: 208 - (0.7 X Age) = HRmax For women: 206 - (0.88 X Age) = HR max Example 1: Chr Chris is is 43 and wants wants to calculate his maximum heart r ate. He will multiply his age (43) by 0.7, which equals 30.1. He will then subtract 30.1 30.1 from fr om 208 to get 177.9 177.9 (we’ll r ound to 178). Chr Chr is’s HRmax HRmax is about abo ut 178 beats beats per minute. Example 2: Carr ie is 46 year s old. ol d. To calculate her HRmax, HRmax, we would would multiply her age (46) by 0.88 to get 40.5. We then subtract 40.5 from 206
to get g et 165. 165.5 (we’ll r ound up to 166). Car Car r ie’s HRmax HRmax is 166 beats per minute.
KEY POINT: High Intensity Interval Training (HIIT) involves periods of high intensity exercise separated separated by rest and recover y periods. perio ds.
HIGH INTENSITY INTE NSITY INTER INTE RVAL TRAINING TRAIN ING PROTOCOL PROTOCOL The HIIT HIIT protocol pro tocol involves pushing your heart rate to approximately 90% of your maximum heart rate for short shor t perio perio ds of time with with rest breaks in between. between. Let’s Let’s use Carrie Carr ie as an example: Carr ie has alr al r eady calculated her HRmax at 166 166 beats per minute. mi nute. She will multiply her HRmax HRmax by 0.9 0.9 (90%) to g et about 149 beats beats per minute.
166 X 0.9 = 149 beats beats per minute. This is i s her he r target heart rate. 1. She will put put on her heart rate monitor and choose a cardio cardio machine (a bike, elliptical, treadmill, stair climber, etc.). 2. She will war warm m up her muscles at a slow pace for fo r 2-3 minutes. minutes. 3. She will then then exercise exerci se har hard d enough enoug h to get her heart rate up up to to her 149bpm target, for a total exercise time of 60 seconds. 4. After After the 60-second exer exer cise inter interval, val, she will rest for 60 seconds (or pedal/walk very slowly). 5. After After the 60-second rest period, peri od, she will star startt another 60-second exercise interval at the target heart rate of 149 beats per minute. 6. Car Car rie ri e will will repea r epeatt this this for a total total of 10 60-second 60-second exercise exercise inter inter vals, then then cool down for 2-3 minutes minutes after after finishing.
7. The basic HIIT HIIT protoco pr otoco l has been used in many r esearch esear ch studies and works gr eat for weight weight loss and reversing diabetes diabetes..
IMPORTANT MEDICAL REMINDER: As we discussed in the obesity obesi ty chapter, chapter, it is extrem ext remely ely import import ant that you speak with with your your doctor first fir st befor befor e starting a pro tocol like li ke HII HIIT. T. This is especially true if you have previously had a heart attack or chest pain with physical exertion. If you fall into these categories, you MUST get approval from fr om your physician physician first for safety safety reasons. There ar e plenty plenty of other exercise routines that you can do safely and will still be beneficial. HIIT is highly beneficial, but make sure your heart can tolerate high intensit intensity y exercise befor e you begin. begi n. You can use the HIIT protocol with a variety of different exercises. You can even set up your HIIT session with alternating exercise types after every 60-second interval. For example, rowing for the first interval, cycling on the second interval, elliptical on the third. There is something very primal about pushing your cardiovascular system to 90% (or higher) hig her) of o f your maximum heart heart rate. It is hard to get bored bor ed or preoccupied with with worr y or rumination when when you are ar e exercising at this this level. The stress relieving r elieving effects and endorphin (feel-good brain chemicals) rush are second to none with these these protocols. pro tocols.
HOW MUCH IS TOO TOO MUCH? MUCH ? There are circumstances when the basic HIIT protocol is too much of a good thing. A night of bad sleep or an exceedingly stressful day at work may not leave room in your stress cup for the demands of the basic HIIT protocol. How can we make sure to get g et the the optimum optimum (hor metic) metic) dose of o f exercise o n any given day?
We want to to be in the “gr “g r een zone” with exercise intensity, intensity, the “hor metic dose.” We do not want to under-train and miss the benefits of the adaptive response to exercise, and we certainly do not want to overtrain and overfill the stress cup. To address this problem we have devised an alternate HIIT protocol that automatically takes into account the “fullness” of your stress cup on any given day, and ensures that you get the right “dose” of exercise. It also automatically adjusts for fitness levels, and will not overtrain the novice while still giving the veteran trainee all al l that he or she can handle. We We call it the “Burst “Burst Cardio” Cardio” protocol.
BURST CARDIO—INDIVIDUALIZE CARDIO—INDIV IDUALIZED D HIIT “Burst “Burst Cardio” is a 20 minute pro pro tocol for fo r getting getting the most out of your workout without without overfilling your stress cup.
A 20 minute Bur Burst st Car Cardio dio session: sessio n: • Burst up to 90-95% of your predicted predi cted max heart rate (HRmax), (HRmax), then then stop
as soon as you reach it.
• 90% HRmax is the requirement, 95% is the goal. • Recover until your heart hear t r ate slows slo ws to 70% of HRmax. • Burst again up to 90-95% 90-95% of your HRmax. • Repeat the burst bur st cycle until 20 minutes have elapsed. Using Using a heart rate monitor with with Stro Stro ng Medicine Medicine “Burst “Burst Cardio” will ensure ensure you don’t overfill your stress cup. cup. On a day when stress is low and you feel rested, you will have a relatively low sympathetic (flight or fight) nervous system drive. Once you “burst” up to 90-95% of HRmax you will recover to 70% of HRmax relatively quickly. This quick recovery will allow you to do more cycles up to your 90-95% HRmax in the 20 minute time period.
There is i s plenty plenty of ro om in the str str ess cup for high intensity intensity exercise exercise when overall stress is low. The sympathetic (flight or fight) nervous system will have relatively relatively low lo w overall sensitivity sensitivity,, allowing for quick heart heart r ate ate r ecover y. Mor e “burst cycles” can be completed compl eted in that that 20 minute session.
You will be able to do more work in the session without overflowing
the st ress cup. cup. On a day when your overall stress is high, your sympathetic nervous system will be sensitive to further “threats,” including exercise. Once you burst up to 90-95% of heart rate max, it will take longer for you to recover to 70% HRmax because the nervous system is overactive from work stress, poor sleep, etc. Longer recovery
t imes imes mean mean you will will not be able able to t o do as many cycles cycles of o f the t he burst prot pro t ocol oco l in in the t he 20 min minute ute workout. workout . More time will be spent in the the recovery recover y period. perio d.
High stress at work, a bad diet, and poor sleep have filled most of your stress cup today. Using the Burst Protocol with a heart rate monitor will prote pro tect ct you from fro m overfilli o verfilling ng the cup. cup. You You will need longer recovery reco very times for your heart rate to drop back down to 70% HRmax, which will ensure that your body is g ets the the rest r est it needs needs between between “bursts” on a str essful day.
THE BUI BUIL LT-IN SAF SAFETY ETY SYSTEM Using the heart rate monitor allows you to plug into the state of your nervous system, and ensure you get adequate rest between bursts. On low stress days, your fast heart rate recovery may allow you to get 10 burst cycles in 20 minutes. On high str str ess days, days, your slo wer wer heart rate recovery recover y may only allow for 4-5 bur bur st cycles. cycles.
Getting only 4-5 burst cycles on a high stress day is a good thing. You are listening to your nervous system by monitoring recovery and not overtraining (overfilling the stress cup). Remember that consistently overfilling the stress cup leads to chronic inflammation, oxidative stress, and chronic disease.
KEY POINT: Using the heart rate monitor with the burst protocol is a built in safety system that allows you to get the most out of your workout on any given day. It automatically adjusts the protocol to the other stresses in your life and your fitness level. Individual heart rate recovery also allows a very fit person to train with a beginner. The person with a high fitness level will be able to do more intervals because their recovery time will be much shorter than the beginner’s. Their wellconditioned heart and nervous system will require a higher relative intensity to reach their target heart rate. The beginner will shoot up to their target heart rate relatively quickly, but will take considerably more time to recover than the fit person. The beginner will do fewer total intervals in during the 20 minute session by design. Monitoring heart rate will ensure both get exactly the right amount of exercise to trigger beneficial adaptations without overtraining. As the beginner becomes more fit, they will recover faster and be able to increase their number of intervals in i n 20 minutes. You can use any any modality modality or tool for fo r your burst bur st cardio cardio protocol: pro tocol: • Running • Elliptical Elli ptical or stair stepper stepper • Biking • Cross countr countr y skiing (or simulation) simulation) • Burpees, medicine ball slams, kettlebell kettlebell swings, or any other bodyweight bodyweight circuit training exercise.
We prefer “4-limb” cardio that activates arms and legs at the same time. Cross country skiing, rowing, and many bodyweight circuits work well. Be creative with your choice choi ce of exercises for your int i ntervals ervals and mix it up. We will lo ok a little l ittle deeper into the Burst Cardio protoco pr otoco l, and see it in action. We We will also show you how use it to fine-tune your nervous system, and as a potent tool for stress stress relief r elief.. Take a look at the graphic on the next page. There are some important things to note on the two profiled workouts.
• The recovery reco very periods perio ds get longer as the the workout progr pro gr esses. The recovery recover y interval needed between exercise periods automatically adjusts itself as as you become more fatigued during the workout. Your nervous system is dictating how much reco very time you yo u need, instead instead of using usi ng a set interval as in the basic HIIT HIIT protocol. • When your “stress “stress cup level” is low (as in workout #1), you you can can spend spend mor e time in the the higher intensit intensity y heart rate zones because because you can perfo rm mor e exercise intervals in the 20 minutes. Although workout #1 and #2 were performed by the same person in the same week, you could easily imagine the data data fro m workout worko ut #2 being generated from fro m a beginner or deconditioned deconditioned trainee. • It is easy to see how much a night of bad bad sleep—or anything else that fills fill s the the stress cup—has an impact on your nervo us system. You would never know this this unless you were monitoring your heart rate. This is the built in safety system that prevents prevents overtraining over training and allostatic allostatic overload over load (an overflowing over flowing stress cup).
moderatee • Duri During ng the the recovery reco very periods, perio ds, you never drop below the 70% moderat intensity level. You You are ar e still burning significant sig nificant calories calor ies during the the recovery reco very
intervals.
BURST CARD CARDIO: IO: FURTHER FURTHE R ANA A NAL LYSIS Chris uses the Polar® Beat application for iPhone or Android, and the Polar® Flow website to track workout data. Both are free and highly recommended. All you need is a Bluetooth heart rate monitor. The following graphics have been taken fro m actual actual workout worko ut data data from his Polar® Po lar® Flow account. account.
The follo wing wing ar e examples examples of the Bur Bur st Cardio Cardio protocol pro tocol in action with with data data from fr om Chris’s actual workouts. At the time, Chris was 43 years old. His HRmax was calculated at 178 bpm, putting his 90-95% target heart rate range between approximately 160 and 169 bpm (0.95 X 178 = 169 and 0.90 X 178 = 160). His 70% HRmax is about 125 bpm (0.70 X 178 = 124.6).
WORKOUT #1: Chris was able to do 6 total intervals in 20 minutes, with relatively quick recovery times between between intervals. Notice Notice the pro por tion of o f time spent in the the higher intensity “zones” (zones 4 and 5) is relatively high in this workout.
WORKOUT #2: This workout was 5 days after the first workout above and took place after a night of bad sleep. Notice that that Chr Chris is was only able to do 4 intervals inter vals in the 20 minute minute workout with long recovery periods needed to get back down to 70%. Also notice the time spent in zones 4 and 5 is relatively low compared to workout #1.
TRAINING THE TH E RECOVERY RE COVERY,, BALANCING BALA NCING YOUR FITNESS The Burst Burst Cardio protocol pro tocol also allows us to do something almost never never discussed discussed in modern moder n fitness— fitness— using using the recovery period as a trainable event . Moder n society is hyper-competitive, always looking to achieve higher levels of performance in the speed of our cars, our computers, and certainly our workouts. This is why “boot camp beat-down” fitness programs are really popular. In Chinese philosophy, we are ar e too much in the “yang” “yang” dir ection without the the balance of “yin.” The time it takes to recover from the “burst” up to 90-95% of max heart rate down to the 70% level will vary depending on your fitness and stress levels. We can actively train during the recovery time with the mindfulness breathing techniques and biofeedback we learned in the chronic stress chapter. • Once you have have hit 90-95% of your maximum heart r ate with the fir st interval, stand in a relaxed posture po sture and start the breathing exer cises. We We are ar e calming the sympath sympathet etic ic (flig ht or fight) nervous system system in a mindful manner manner to r educe educe our heart rate. • Watch your heart hear t r ate monitor moni tor display as you br br eathe, using it as a biofeedback biof eedback device. device. Follow Follo w your heart hear t rate as it slows, slowing slowing your breathing breathing and r eleasing muscle tension. Follow your heart rate down to 70% then start your next interval. Using this technique for training your recovery, you will be able to bring your heart rate down faster between intervals and ultimately complete more total intervals in your 20-minute burst protocol. Referring again to Chinese philosophy, we are balancing the interval training (yang) by actively enhancing the recovery (yin). In Western scientific terms, we are balancing the sympathetic nervous system stimulus of the exercise interval by training the parasympathetic nervous system during the recovery period. Training the recovery recover y has carryover carr yover effects effects into our daily life. Being Being able to quiet your mind and focus your breathing during recovery from a high intensity exercise interval (often in the midst of the noise and distraction of a busy gym) is a very
valuable health-enhancing skill.
Imagine the benefits of training to be calm in the middle of the “storms” of your daily life. This is another another approach—built approach—built in to your yo ur workout worko ut—t —to o help master master your stress/threat system and reduce the effects of chronic stress.
AN AD ADAPT APTAB ABLE LE SYST SYSTEM EM The burst cardio system also takes into account the type of exercise you are performing in your interval. Heavy kettlebell swings will take more of a toll on your nervous system than the elliptical machine. It will take longer to recover from the kettlebell swing interval than the elliptical machine interval. It is no problem to mix different exercises as your nervous system will adjust automatically for the proper recovery time between exercises. This is important since most injuries happen when the nervous system is fatigued and exercise form breaks down. The rotocol will help prevent injury from poor form due to nervous system fatigue.
KEY POINT: Most injuries happen in a state of nervous system fatigue. The Burst Car Car dio pr otocol will help prevent injury by monit mo nitor or ing the stat statee of the the nervous nervo us system with with the the heart rate. r ate. The total time of the burst cardio protocol can be adjusted if you are really feeling run down, have limited time, or have performed intense strength training directly before your cardio session. Burst cardio sessions of 10 minutes are still highly effective in the right circumstances. You can use this protocol in your home, the the gym, or o r ideally immersed in a natural setting. setting.
TRAINING TIP: If you are having difficulty achieving at least 90% HRmax during your intervals, find fi nd another exer cise. You You may have become becom e too efficient at a single singl e exercise exerci se (i.e. elliptical) and your nervous ner vous system has adapted. adapted. Mix up your your exercises!
TRAINING TIP: HIIT has been shown to significantly improve performance capacity in endurance athletes like marathon runners, cyclists, and triathletes. Research has sho wn that that endur endurance ance athletes athletes were able abl e to cut as much as 25% of their r egular training and replace r eplace it with with HII HIIT T pr otocols without without losing any per per for mance capabilit capability y during competition. competition. This is a gr eat way way to cut down on training volume and potentially prevent overuse injuries for competitor competitorss in endurance-based endurance-based sports.
A trail run in the woods is an ideal way to do the Strong Medicine burst cardio cardio protocol.
o f HRmax. Burst int int erval: erval: pushing up to 90-95% of
Burst recovery: mindful breathing and biofeedback down to 70% of HRmax. The Strong Medicine burst cardio protocol will give you the health benefits of
HIIT with an extra built in safety system to prevent overtraining and injury. We are now going to show you how to program your exercise sessions weekly, combining strength training and cardio for an individualized template of physical transformation.
STRONG MEDICINE TACTICS: Implement Strong Medicine “Burst Cardio” to supercharge your metabolism, enhance fat burning, sensitize insulin, and train your recovery reco very without without overfilling your stress cup.
PHYSICAL TRA TRA INING IX
EXERCISE PROGRAMMING ROGRAMMING
TRANSFORMA TRAN SFORMATIO TIONA NAL L FITNESS “Eventually, “Eventually, after all the books are read and all the thoughts are thought, it becomes becomes time to actually train— what to do: how to do it.” —Marty Gallagher We need a transformational template and we need to structure our lives to “make room” for fitness. Once we have the game plan and have set aside training time, it is time for the rubber to meet the road for some actual training. Training is split into two generalized disciplines: resistance training and cardiovascular training. The idea is to mix and meld these two training disciplines to elicit specific physiological effects. There are enumerable variations within each discipline. We won’t throw you into the deep end of the pool—most professional fitness trainers require new trainees to engage in drills past the limits of their capacity. It is cruel and counterproductive to make an untrained person—who has done nothing
more strenuous than walk to the refrigerator for decades—suddenly and immediately begin high-impact jogging at a pace past their capacity on day one. Our approach eases the trainee into our methodology: we establish initial performance benchmarks and improve upon the previous week’s performance, in some way each week. By asking slightly more of ourselves each week we continually trigger the adaptive response and the extremely beneficial hormonal tsunami that accompanies it. We want to safely and consistently exceed our best efforts— effor ts—th that at is where where the pro gr ess lies.
DAY DA Y ONE ONE,, WEEK WEE K ONE, ONE , SESS SESSION ION ONE ON E We will assume you have spent the time to develop your technique for the five core exercises—the squat, deadlift, bench press, overhead press, and the row— before launching into a formal program. Once you have done your homework with the lifts, you can start training.
TAC ACTI TICA CAL L TEMPLATE: TEMPLATE: WEEKL W EEKLY Y TRAINI TRA INING NG REGIMEN REGIMEN DAY RESISTANCE TRAINING CARDIO Superset of Squat with overhead Power Po wer-walk -walk or Rest press Burst Cardio Cardio session 10-20 Tuesda sday None one minutes Superset of Dumbbell Dumbbell Bench Press Pre ss Wednesday Power Po wer-walk -walk or Rest wit wit h Row T hursday No ne P o wer-walk o r Burst Cardio Friday No ne No ne Sat urday Sumo Deadlift P o wer-walk o r Rest Burst Cardio Cardio session 10-20 Sunday none one minutes Monday
Using the Tactical Template as a guide, the following is a six-week plan for progr pro gr essing the exercises exercises from fr om week to to week. Use the Tactical Template to determine what exercises you will do on specific days of the week, and use the weekly progression charts to determine how you are doing the specific specific exer cise as it r elates to sets, reps, time, and intensity intensity..
WHAT WH AT IS A SUPERSE SUPERSET? T? A super super set consists consists of o f two two exercises perfo r med one after another without without pause. For example, on Monday we will alternate or ‘superset’ ultra-deep squats with overhead dumbbell presses. First perform a technically perfect set of ultra-deep ul tra-deep paused squats. Upon completion compl etion of o f the squats, squats, walk to the dumbbell station, pull the dumbbells to your shoulders and complete the press reps, then rest. The athlete will perform the pattern three times in succession—squat, press, rest, squat, press, rest, squat, rest, press. This strategy is used again on Wednesday alternating the dumbbell flat fl at bench press with the the statue statue r ow—bench, row ro w, rest, r est, bench, bench, row ro w, rest, bench, row ro w, rest. r est. The superset alternating alternating exercise strategy is a major time saver. saver. The tr tr ick is to pair up “non-conflicting” “non-conflicting” exercises. exer cises. For example, example, you would never pair up, or superset overhead presses with bench presses because these two two exer cises use many of o f the same muscles. We We would never superset or or alternate deadlifts and squats squats as they also use many of o f the same muscles. How long should you yo u rest r est between between super supersets? sets? Wait Wait until until your yo ur breathing br eathing normalizes then hit it again.
WEEK 1
Exercise
Sets/Reps/time/intensity
Squat Bodyweight, 3 sets, 8 reps Overhead Press 3 sets, 8 reps (enough weight so 8 reps is hard) Dumbbell Bench Press 3 sets, 8 reps (enough weight so 8 reps is hard) Row 3 sets, 8 reps (enough weight so 8 reps is hard) Sumo Deadlift 3 sets, 6 reps (enough weight so 6 reps is hard) Power Walk 15 minutes at 60% HRmax Burst Cardio 10 minutes with exercise(s) of choice Example: Using the Tactical Tactical Template, our workout wor kout on Monday of Week Week 1 would be: supersets of bodyweight squat and overhead presses, for 3 supersets of 8 reps per exercise. You could power walk for 15 minutes (60% HRmax) after lifting or skip the power walk and rest.after lifting or skip the power walk and rest.
WEEK 2 Exercise
Sets/Reps/time/intensity
Squat Bodyweight, 3 sets, 10 reps Overhead Press 3 sets, set s, 10 reps (main (maintt ain poundage poundage from f rom last last week) week) Dumbbell Bench Press 3 sets, 10 reps (maintain poundage from las week) Row 3 sets, set s, 10 reps (main (maintt ain poundage poundage from f rom last last week) week) Sumo Deadlift 3 sets, set s, 10 reps (main (maintt ain poundage poundage from f rom last last week) week) Power Walk 25 minutes at 65% HRmax Burst Cardio 11 minutes with exercise(s) of choice Example: Using the Tactical Tactical Template, our workout wor kout on Tuesday of Week Week 2 would t raini ning ng t oday, perform perfo rm an 11 min minute ute Burst Cardio Cardio session. be: no resistance trai
WEEK 3 Exercise Squat Overhead Press Dumbbell BenchPress Row
Sets/Reps/time/intensity Goblet Squat, 3 sets, 6 reps (enough weight that 6 reps is hard) 3 sets, 6 reps (use 5 lbs heavier dumbbells than last week) 3 sets, 6 reps (use 5 lbs heavier dumbbells than last week) 3 sets, 6 reps (use 5 lbs heavier dumbbells than last week)
Sumo Deadlift 3 sets, set s, 6 reps (use 10 lbs heavi heavier er than t han last last week) week) Power Walk 30 minutes at 68% HRmax Burst Cardio 12 minutes with exercise(s) of choice exerci se on o n Wednesday Wednesday of Week Week 3 Example: Using the Tactical Template, our exercise would be: supersets of dumbbell bench presses and rows for 3 supersets of 6 reps per exercise, using dumbbells 5 lbs. heavier than last week. After lifting, you could power walk for 30 minutes (at 68% HRmax) or rest.
WEEK 4 Exercise Squat
Sets/Reps/time/intensity Front Squat, 3 sets, 10 reps reps (enough weight weight that 10 reps reps is hard) 3 sets, set s, 8 reps (mai (maintain ntain poundage fro m last week)
Overhead Press Dumbbell Bench 3 sets, set s, 8 reps (mai (maintain ntain poundage fro m last week) Press Row 3 sets, set s, 8 reps (mai (maintain ntain poundage fro m last week) Sumo Deadlift 3 sets, set s, 8 reps (mai (maintain ntain poundage fro m last week) Power Walk 30 minutes at 70% HRmax Burst Cardio 13 minutes with exercise(s) of choice Example: Using the Tactical Template, our workout on Thursday of Week 4 would be: no resistance trai t raini ning ng t oday, power walk walk for fo r 30 min minutes utes (at 70% HRm HRmax) or or choose choo se a 13 minute minute Burst Cardio Cardio session.
WEEK 5 Exercise
Sets/Reps/time/intensity
Squat Front Squat Squat , 3 sets, set s, 6 reps (use dumbbel dumbbells ls 5lbs 5lbs heavier) heavier) Overhead Press 3 sets, set s, 10 reps (main (maintt ain poundage poundage from f rom last last week) week) Dumbbell Bench Press 3 sets, set s, 10 reps (main (maintt ain poundage poundage from f rom last last week) week) Row 3 sets, set s, 10 reps (main (maintt ain poundage poundage from f rom last last week) week) Sumo Deadlift 3 sets, set s, 10 reps (main (maintt ain poundage poundage from f rom last last week) week) Power Walk 30 minutes at 73% HRmax Burst Cardio 14 minutes with exercise(s) of choice Tactical Template, our workout wor kout on Friday Fr iday of Week 5 would would be: Example: Using the Tactical No training. A complete rest day.
WEEK 6 Exercise Squat
Sets/Reps/time/intensity Front Squat, 3 sets, 8 reps (maintain poundage from last week) 3 sets, 6 reps (use dumbbells 5 lbs heavier than last week)
Overhead Press Dumbbell Bench 3 sets, 6 reps (use dumbbells 5 lbs heavier than last week) Press Row 3 sets, 6 reps (use dumbbells 5 lbs heavier than last week) Sumo Deadlift 3 sets, set s, 6 reps (use 10 lbs heavi heavier er than t han last last week) week) Power Walk 30 minutes at 73% HRmax Burst Cardio 14 min minutes utes wit wit h exercise(s) of o f choice cho ice Tactical Template, our workout wor kout on Saturday of o f Week Week 6 would Example: Using the Tactical be: sumo deadlift, 3 sets of 6 reps using weights 10 lbs. heavier than in week 5. After t he weight weight t raini raining, ng, power walk walk for 30 min minutes utes (at 73% HRm HRmax) ax) or rest. rest .
ADV AD VAN ANCED CED PRO PROGRAMMIN GRAMMING: G: SEASONAL “PRIMORDIAL CYCLING” Elite athletes know that the optimal length of time to peak the human body for athletic competition is twelve weeks. This is empirically-based experiential knowledge based on 70 years of observation and preparation. Elite athletes and coaches at the highest levels try to avoid preconceptions. Preconceptions interfere with with the per per ception of r eality. eality. • The fundamentalist fundamentalist has a set of frozen, fro zen, fossili fo ssilized zed beliefs and will r everse evers e engineer an elaborate rationale to justify their belief system. The fundamentalist rejects new input and knowledge as it could potentially threaten or undermine their their beliefs. • The scientist scientist continually expands expands his knowledge, knowledge, and seeks new data. Without Without clinging to beliefs, the human performance scientist has loyalty to one master— tangible, tangible, measurable, physiolo physiolo gical results. Empirical science has formulated a loose consensus for the optimal time period of a serious fitness effort. All this assumes the athlete has a goal—by definition, all athletes have a goal—to improve performance within their sport. We have learned through hard-earned gym wisdom that twelve weeks (84 days, three months) is an
optimal length of time for building muscle mass, power, strength, conditioning, leanness, stamina and endurance.
PRIMAL CORRELATIONS We think it is no accident that the optimal length of time to peaking human performance is three months is one season. Summer, winter, spring and fall are three month chunks. Primal hunter-gatherers migrated with animal herds for hundreds of thousands of years. Widespread agriculture was only implemented about 10,000 years ago, a mere blip compared to the total time we have been on this planet. Prior to agriculture, we spent our time foraging and following migrating herds of animals for protein sources. Walking, moving, running, chasing, being chased, living on pristine animals, supplemented with whatever wild fruits, roots, and vegetables could be found. Humans were parasites living off of massive migrating herds of animals.
In temperate regions to a great degree, and all geographic regions to a lesser degree, each passing season caused humans to adjust to nature’s whims. Even in a desert, a summer drought can wreak havoc on all living things. By all accounts, these primal hunter-gatherers, would physically wipe the floor with modern man. The primal ancients were far leaner, more muscular, had greater endurance, no cardiovascular or insulin-related maladies, and no cancer or obesity. These people continually adjusted their lives, based on nature, the seasons, and their impact on the herd. The animal herd sustained them. In a time of drought, if the herd suffered, then humans suffered. Optimally, the herd moved south as cold weather set in. The migration reached the southernmost point as spring gave way to summer. With the onset of the warm months, the herd moved north until fall gave way to winter and the cycle repeated. Indigenous tribes worldwide were synced up to the weatherinduced induced migr ator ator y habits habits of animals. Flashing forward to the present day, is it any surprise that modern elite strength
athletes have discovered that a three-month training cycle is optimal? Once we understand and embrace this idea, the next logical step is to sync a transformational goal with the seasonal cycle of 12 weeks. It would make sense to meld seasonally appropriate training and eating in an attempt to reconnect with our primal encoding.
Winter: the best time for goals of gaining muscle mass and strength. What better time than the dead of winter for hardcore, barebones, ultra-heavy strength training when the thick soups, root vegetables, and heavy rich foods taste better. Add some muscle mass and add 20% to your strength during winter’s 12-weeks.
Spring: when the magnificence of the true spring arrives, shift physiological gears. After a winter strength training cycle, shift to more volume, more sessions, less weight, and more cardio. Shift to seasonally appropriate lighter meals with more carbohydrates.
Summer: as the deep summer takes root, we want to become maximally lean. During the summer heat, our activities peak, our appetite is low and we want the lightest proteins, more salads, fruits, vegetables and less food volume. Weight training becomes high-rep, high-volume, and high-frequency. We will do a lot of cardio with plenty of moving and sweating.
Fall: with the onset of true fall, we will add more substance to our weight training. Richer, more savory foods suddenly taste delicious as the weather becomes colder. The fall phase peaks over the holidays—we want to be maximally large and lean heading into the almost hibernation-like strength-training winter phase. Give seasonal training a try to see how it works for you. It makes sense from a “first principles” perspective and also aligns with our “feed your activity” concept.
CONCLUSION
We have presented a template for training that incorporates foundational resistance training with proper doses of cardiovascular training. This is a template that may be especially especiall y useful to the beginner but it remains only a template. Use it as a starting point. Entire books have been written on exercise modes and periodized training, and deeper coverage of these topics is well beyond the scope of Strong Medicine . We have given you a foundation of ideal techniques and tactics for resistance training that can be progressed as you advance. This is a rock solid program to begin your yo ur fight fig ht against inactivity inactivity, the the fifth member of the Pentav Pentaver erate. ate. Inactivity is no match for Strong Medicine physical training.
“MILITARY INTELLIGENCE” INT ELLIGENCE” (REFERENCES): Adams OP. The impact of brief high-intensity exercise on blood glucose levels. Diabetes Metab Syndr Obes 6 (2013): 113-122. Maturitas 72 (2012): 311-316. Bird SR, & Hawl ey J A. Exe rcise and type 2 diabetes: new pr prescription escription for an old problem. problem. Maturitas Burd Burd NA, et al. M uscle uscle time under tension dur during ing resi stance stance exe rcise sti mulates diff erential muscle muscle protei protei n sub-fractional syntheti c responses responses in men. J Physiol 590 (2012): 351-362. Cardiovasc Dis 2 (2012): 102-110. Ciolac EG. High-intensity interval training and hypertension: maximizing the benefits of exercise? Am J Cardiovasc Gi bala bala M J, e t al. Physi ol ogi cal adap adaptations tations to low- vol ume, hig hig h-intensity i nterval training training in heal heal th and and disease. J Physiol 590 (2012): 1077-1084. Gi ll en JB, et al . Acute Acute high-i ntensity interval e xercise reduces the postpr postpran andial dial gl ucose ucose response and and preval preval ence of hypergly- caemia in patie patie nts wi th type 2 diabetes. diabetes. Diabetes Obes Metab 14 (2012): 575-577. Med 43 (2013): 993-1008. Hartmann Hartmann H, e t al. Analysi s of the lo ad on the the k nee j oi nt and vertebral vertebral column with changes changes i n squa squatting tting depth and and wei ght load. Sports Med 43 Hawley JA, & Gibala MJ. What’s new since Hippocrates? Preventing type 2 diabetes by physical exercise and diet. Diabetologia 55 (2012): 535-539. Sports (2013). Larsen I, et al. H ig h- and moderate-i ntensity ntensity aerobic exe rcise and exce ss post-exe rcise ox yge n consu consumption mption in men with metabol metabol ic syndrome. syndrome. Scand J Med Sci Sports (2013). Li G, & He H . Hormesi s, all ostatic buffe ring capa capacity city andphysi ol ogi cal mechanism mechanism of physi cal activ activ ity : a new theoreti theoreti c framewo framewo rk. Med Hypotheses 72 (2009): 527-532. Physiol (1985) 111 (2011): 1554-1560. Li ttle JP, et al. Lo w-v ol ume hig hig h-intensity i nterval training reduc reduces es hyperglycemi a and increases increases muscle mi tochondrial drial capacity i n patie nts with type type 2 diabetes. J Appl Physiol (1985) McGi ll S. U lti mate mate Back Back Fi tness tness andPerforman Performance. Stuar Stuartt M cGil l, PhD PhD (2007). Kinetics (2004). McGi ll S. Low Back Di sorders, Second Second Editi Editi on. Human on. Human Kinetics (2004). Meyer P, et al. High-intensity aerobic interval exercise in chronic heart failure. Curr Heart Fail Rep 10 (2013): 130-138. Mo lme n-Hansen HE, e t al. A erobic i nterval training reduces reduces blood pressure pressure andimproves my ocardial ocardial f unction in hypertensiv hypertensiv e patie nts. Eur nts. Eur J Prev Cardiol 19 (2012): 151-160. Physiol (1985) 98 (2005): 1619-1625. O’Donovan, O’Donovan, G, et al. Changes Changes i n cardiorespiratory cardiorespiratory fitness and coronary coronary heart dise dise ase risk factors foll owi ng 24 wk of moderate- or hig hig h-intensity e xercise of e qual energy cost. J Appl Physiol (1985) Re hnTA, et al . Increasing physi cal activi ty of high intensity to re duce the prevalence of chronic chronic dise dise ases andimprove publi c health. Open Cardiovasc Med J 7 (2013): 1-8. Rognmo O, et al. High intensity aerobic interval exercise is superior to moderate intensity exercise for increasing aerobic capacity in patients with coronary artery disease. Eur J Cardiovasc Prev Rehabil 11 (2004): 216222. Database Sy st Rev CD003817 (2006). Shaw Shaw K, et al. Exe rcise rcise for overwei ght or obesity. Cochrane Database Tj onna onna AE, e t al. A erobic i nterval training versus continuou continuouss moderate exe rcise as a treatment for the metaboli c syndrome: a pil ot study. study. Circulation 118 (2008): 346-354. Sci (Lond) 116 (2009): 317-326. Tj onna onna AE, e t al. Aerobic i nterval training reduces reduces cardio vascular vascular risk factors more thana multitre atment approach proach in ove rwei ght adol escents. Clin Sci (Lond) Obes (Lond) 32 (2008): 684-691. Trapp EG, et al. The effects of high-intensity intermittent exercise training on fat loss and fasting insulin levels of young women. Int J Obes (Lond) Whyte LJ, et al. Effe cts of single bout of very high-intensity high-intensity e xercise on metaboli metaboli c health health biomark ers in overwei ght/ob ght/obese ese sedentar sedentary y men. Metabolism 62 (2013): 212-219. Wi slo ff U , et al . Superi or cardiovascular cardiovascular effe ct of aerobic i nterval training versus moderate moderate continuous continuous traini traini ng in heart heart fai lure patients: a rand randomi ze d study. Circulation 115 (2007): 3086-3094.
BATT BATTLE LE PLAN PLA N II
STRONG MEDICINE MEDICINE NUTRI N UTRITION: TION: INDIVIDUALIZED STRATEGIES
I. FOOD: SOURCES AND QUALITY II. CARBOHYDRA CARBOHYDRAT T E T OLERANCE III. III. FEED YOUR ACTIVIT ACT IVITY Y IV. IV. ONE WEEK OF FOOD
INDIVIDUALIZED STRATEGIES I
FOOD: SOURCES AND QUALITY QUA LITY
CULINARY CONSENSUS The world’s best chefs insist on seasonally appropriate, locally grown, natural, fresh, organic fruits, vegetables and proteins. They want the freshest local ingredients, and the less time between harvest and consumption the better. Flavor intensity (for any fruit, vegetable or protein) is at its peak the instant it is picked or caught. Every minute after the food was gathered adds another degree of flavordegradation. But, flavor is not the only thing that degrades as the time from harvest passes. The nutrient density of produce significantly and rapidly degrades in fruits and vegetables soon after picking. It is convenient to get out of season fruit from New Zealand, but it has a long journey from the grove to your home, and will sacrifice nutr nutr itional potency along the way way.. The world class chef and the Strong Medicine trainee want the same foods for entirely different reasons. Above all else, the chef wants potent flavor and vibrancy. Trainees intent on triggering transformation understand that nutrition can be an art and a science—optimally fueling fuel ing the body to provide pr ovide exactly what it needs at exactly exactly the right time, in direct proportion to the duration and intensity of the exercise session and the the sever sever ity of the training training protocols. pro tocols.
To grow muscle mass requires that we stress the body—then feed it what it wants in the proper amounts; then we rest the body and muscle grows. We can also set up physiological situations which cause the body to use its stored body fat to power activity. Taste goes hand in hand with potency. With nutritional potency, you also find the most intense taste and flavor. This is a divine coincidence—the smartest “dieter” eats potent gourmet meals made from the finest, freshest, most flavorful seasonally appropriate local ingredients. Organic, locally-produced food is suited for both the flavor-crazed chef and the athlete seeking nutrientdense food/fuel. Amongst the world’s finest chefs there is surprising unanimity regarding the best way to prepare fresh food—make the ingredients the star of the dish, not the chef. We should learn how to amplify, not smother or overwhelm the perfection of nature’s bounty, eaten at its finest, freshest and most potent state.
“ORGANIC” To earn the US Department of Agriculture “organic” label, fruits and vegetables must be grown and processed within strict guidelines. • Most synthetic synthetic pesticide chemicals chemicals are ar e not allowed. • Synthetic Synthetic fertilizer fer tilizerss or sewage sludge cannot be used. • No genetica genetically lly modified or ganisms (GMOs). (GMOs). Livestock must meet the follo wing guidelines g uidelines to be USDA USDA certified cer tified “organic”. • No antibiotics antibiotics or gr owth hormones hor mones used with with the the animals. animals. • Livestock must be fed 100% or ganic feed containing no animal byproducts. • Animals must have access to to the outdoor outdoo r s.
30% of the animals’ animals’ food foo d must come from fr om g razing. 70% 70% may come from fr om or ganically produced dry dry feed. The Strong Medicine trainee needs potency. Most of the foods purchased at the local chain grocery store are nutritionally impotent compared to locally grown foods from the farmer’s market. One trip to the Farmer’s Market dispels the misconception that quality food is expensive. At the Farmer’s Market the prices are equal equal or o r bette betterr to the mega-chain mega-chain gr ocery ocer y store and significantly significantly cheaper cheaper than than most upscale upscale organic or ganic food foo d markets. Plus, you are supportin suppor ting g your local farmers. far mers.
DON ’T BE FOOLED BY APPEARANCES. DON’T APPEARAN CES.... LOCAL IS BEST Local food is simply more nutrient dense. It may not look as pretty as the waxed and polished fruit and vegetables in most supermarkets trucked in from thousands of miles away (or from fr om across acr oss the globe). But But local food foo d makes makes up good lo oks with with more health benefits. The longer fruit and vegetables have been stored after harvesting, the more nutrients they lose. The buffed and shined supermarket food has often lost over half of its beneficial natural minerals, vitamins, and cancer fighting chemicals by the time they reach the dinner table. Most supermarket produce is all show and no go. We want nutrient-dense fruits and vegetables harvested by your local farmer, eaten only days after harvesting. This local produce may not look as polished, but it retains most of its health-promoting vitamins and minerals beneath a humble outward appearance.
FOOD QUALITY FOR THE OMNIVORE Homo sapiens developed as omnivores. Good foundational science shows that the introduction of nutrient dense animal-based food—especially marine animals—into our diet allowed for both the expansion of our relatively large brains, and the shrinking of o f our digestive tract tract as compared to our nearest hominid relatives. relatives. Humans especially need the polyunsaturated omega-3 fat DHA DHA (see Nutrition 101) for proper brain function. Provocative new research theorizes that we were able to develop our large brains by obtaining DHA from marine animal food sources (fish and other seafood). Recall that we can convert very little alpha linoleic acid (18 carbon omega-3) to the “big brother” omega-3, EPA and DHA. This is why it is important to get some pre-formed EPA and DHA from our diets. Fortunately
larg e amounts are naturally naturally fo und in animal-based animal-based foods. As discussed previously, adequate DHA is critical for the early brain development period from infancy through adolescence. Plant-based omega-3 (such as ALA in flax seed) is not converted to DHA in high enough quantities to support healthy brain development. For this reason, incorporating high quality animal-based foods in the diet is important from a health perspective, especially for children. Animalbased based foods are ar e also— calorie o f pr o tein to suppor sup por t the calorie for calorie —the best sour ces of flesh machine’s need for essential amino acids.
T he conversion co nversion from fro m ALA t o EPA and DHA is very ineffici ineff icient ent It is estimated that only 5% of dietary ALA is converted to EPA and DHA. High ALA bypass the t he poor poo r foo ds like flax f lax seed ar e a poor po or way to to get EPA EPA and DHA. DHA. You can bypass
conversion by eating EPA and DHA directly from fatty fish and grass fed animals. For animal food sources, quality is paramount. Unhealthy animals raised in confinement, pumped full of antibiotics and growth hormones, then fed processed pesticide-laden feed are poor nutrient sources for omnivores. There are significant ethical and humane issues with animals r aised in co nfinement as well. A template template for fo r an optimum high-quality high-quality omnivoro o mnivoro us diet:
• Locally Locally produced produced fruit fruit s, veget ables, ables, and tubers grown with with organi org anicc to pay for o fficial farming principles. (Some small farms are not larg e enough to “organic” “or ganic” certification. certification.)) This categor categor y should comprise compr ise the the largest proportion propo rtion of of your meals by weight. The fermentable fiber, minerals, and disease-fighting phytonutrients in these foods should form the foundation of your nutrition plan.
• 25-30 grams of prot pro t ein per meal meal from fro m a hig hig h quali qualitt y source: — Beef Beef fro m 100% grass-fed cows or bison.
— — — — — —
Wild game (deer, elk, boar, turkey, etc.). etc.). Poultry (chicken/turkey) should be “pastur “pastur e-raised” e-r aised” with with or ganic feed. oily fish such as salmon, tuna, sardines, mackerel, and trout. Wild-caught oily Crab, oysters, oyster s, lobster, lo bster, mussels. Eggs from fr om pasture-r pasture-r aised chickens. chickens. Pork Por k from fr om pastured pastured pigs.
PRISTINE PRISTINE PROTEIN
The quality of animal foods is directly related to the environment where they they are r aised. Animals Animals fr ee to roam r oam and eat natu naturr al foo ds are the most nutr nutr itious for the the omnivore. omnivor e. • Cows Cows eat gr ass; it is their their natural food! foo d! Grass-fed Gr ass-fed beef is leaner leaner overall over all and has significantly sig nificantly mor mo r e long lo ng chain o mega-3 (EPA (EPA and DHA)fats, DHA)fats, BBvitamins, Vitamin Vitamin E, Vitamin Vitamin K, and the anti-inflammator anti-inflammato r y fat conjugated co njugated linoleic acid (CLA), than beef from cows eating grain in the feedlot. Grain-fed cows confined to feedlots are awash in antibiotics and growth hormones. hor mones. Beef Beef from fr om gr ain-fed catt cattle le has almost no beneficial long chain omega-3 fats. fats. • Chickens and turkeys are omnivor omnivo r es, eating insects insects as well as gr ain. Poultry meat from pasture-r pasture-r aised organic or ganic chickens chickens and turkeys turkeys is hig her in EPA EPA and DHA DHA (omega(o mega-3) 3) and lower lo wer in omeg a-6 fats. Commer cially produc pro duced ed poultr poultr y are confined to to cages and crowd cro wded ed indoo indoorr poultry houses. These birds are sickly, require antibiotics, and have almost no omeg a-3 fats in their meat. Avoid this type of poultry poultr y. • Wild-caught ild-caug ht oily oi ly fish such as tuna, tuna, salmon, salmo n, sardines, mackerel, and trout tro ut are DHA superstars. Farmed fish fed a diet of fishmeal (often containing pesticide residues and antibiotics) have only trace amounts of the
beneficial long chain omega-3 fats. Stick with wild-caught fish and avoid farmed fish. • Pigs are omnivor es, and pork por k from pasture-r pasture-r aised pigs (allowed to gr aze and and forage) forag e) is leaner leaner and has mor e beneficial beneficial omega-3. Convent Conventionally ionally r aised pigs eat grain-based pig pig feed and and live in hor rific ri fic crowd cro wded ed conditions conditions r equiring antibiotic antibiotic use. Healthy Healthy animals which have eaten eaten their their natur natur al foods, fo ods, and are ar e pastureraised or wild caught, are the healthiest for us to eat.
GRASS GRASS-FED = EXPENSI EX PENSIVE? VE?
Grass-fed Gr ass-fed beef beef and wild wild game meat purchased from r etail etail stores stor es can be very pricy. But, you can find local sources of grass-fed beef, pastureraised poultry, eggs, and pork, and buy large quantities relatively cheaply. Many local farmers will sell grassfed beef in bulk in quantities such as a whole, half, or quarter cow. Even after processing and packaging fees, the price per pound is often comparable to conventional conventional feed-lot beef sold in stores. Buy in bulk and store in your freezer. The best best resource resour ce for finding fi nding a local farmer selling pastured pastured animal produc pro ducts ts in your ar ea is www.eatwild.com www.eatwild.com.. Go check it out! You will get a gr eat deal on a healthy healthy protein source and suppor suppor t your local lo cal farmer at the the same time. If you do not hunt wild game, talk to any hunters you know. You can probab pro bably ly work o ut a good deal on o n a portion por tion of the wild wild game they kill kill during hunting season. Elk, deer, and boar are fantastic protein sources.
DOC’S RANT: Many people who complain about the cost of food are the same ones who spare no expense on the latest big screen televisions, buy daily $5 coffees, and have the the most mo st up to date smart phones. Food quality is simply not not a prio r ity for most of us. People People in this country country are used to buying low lo w cost processed foo d and scoff at the the idea of having to spend more of our income on what we eat. Americans spend on average less than than 7% of their income on o n food, foo d, the the lowest propor pro portion tion in the the world. The U.S. is one of the most prosperous and productive nations on Earth but with one of the worst rates of chronic preventable diseases. There seems to be a connection between our poor health and the unwillingness to demand demand high quality quality food foo d and spend spend a higher propor pr opor tion of o ur income inco me to purchase purchase good food. Perhaps we we need to to r ethink ethink our prio rities… ri ties…
ANIMAL AN IMAL WELFARE WELFARE The Strong Medicine omnivor e should insist on pastu pasturr e-raised animals as prote pro tein in sources sour ces for mor e than than health health reasons. r easons. Convent Conventional ional feed-lot operations ar e equivalent equivalent to to concentration concentration camps fo r animals and depri deprive ve them of their health with crowded disease-promoting conditions. We understand these animals are raised as food sources, but we have an ethical obligation to ensure they are treated humanely. Find a local source so urce for your protein pro tein and visit visit the the farm yourself your self to observe the tr tr eatment of the animals you ar e eating. Reconnect Reconnect with with your foo d source.
WHA WH AT ABOUT AB OUT ME MERCUR RCURY Y IN IN FISH? F ISH?
Elementa Elementall mercury mer cury fr om the envir environment onment is converted converted to to “or “o r ganic mercury” (methylmercury) in fish. Methylmercury (MeHg) is extremely damaging to ner ve cells in the br br ain. Small fish contaminated with mercury are eaten by large predatory fish— tuna, king mackerel, tilefish, sharks—and marine mammals such as whales. Methylmer ethylmer cury (M ( MeHg) is co ncentr ncentr ated or bioaccumulated in the larger predat predator y fish. Methylmercury is especially damaging to the developing brains of fetuses, infants, and young children, prompting warnings to avoid the above fish as sources of pr otein and and omega-3, especia especially lly for pregnant or nursing mothers and young children. The advice advice to avoid these these specific specific fish for fo r this this gr oup of people is still prudent, but there is a litt l ittle le mor mo r e to the stor stor y. Methylmercury (MeHg) produces its toxic effects by directly stopping the action of many antioxidant defense enzymes, which are crucial for prote pro tect cting ing us fr om damaging fr ee radicals. Many Many of these enzymes enzymes are dependent on the nutrient selenium for fo r proper pro per function. MeHg eHg can dir ectly ectly inhibit the enzymes AND AND bind to selenium. seleni um. The binding of MeHg to selenium effectively r emoves selenium, sel enium, and stops stops the antioxidant defense system enzymes which are dependent on it. i t. Without Without the pro tectio tection n of o f the antioxidant defense enzymes, the nerve cells are damaged by free radicals. A key point is that an increase in dietary selenium can counteract the
damaging effects of methylmercury from these fish. As long as the fish have higher selenium levels than MeHg MeHg levels, the antioxidant defense enzymes are still able to function because they have
adequate selenium. The damaging effects of MeHg are greatly diminished in this case. Recent r esearch esear ch was conducted conducted on the Canadian Canadian Inuit population, populatio n, a gr oup whose diet consists largely of seafood with a relatively high MeHg content. It was was found fo und that the high selenium sel enium levels in the fish appeared to prote pro tect ct the the Inuit Inuit from fro m neurolog neuro logical ical oxidat o xidative ive damage fr om HeM HeMg. This research research implies implies that as long as selenium content in the fish is i s adequate, the effects of MeHg may be minimal. Most ocean fish have more selenium than mercury, making them theoretically safe to eat despite their mercury levels. Exceptions are sharks and pilot pilo t whales. whales. Meat Meat fro m these two two species s pecies has mo r e MeHg MeHg than selenium, selenium, making them them potentially potentially toxic for your brain.
QUICK QUICK MEDICAL MEDICA L NOTE: This r esearch is still preliminary, pr eliminary, so it is still wise to be cautious cautious by minimizing predatory fish consump co nsumption tion (tuna, (tuna, swordfish, swor dfish, tilefish, tilefish, king mackerel) mackerel) for pregnant and nursing nursing mothers, as well as infants infants and children until until mor e studies studies are perfor perfo r med.
KEY POINT: Most ocean o cean fish have higher selenium conten co ntentt than than methylmer methylmercury, cury, making them theoretically safe to eat for most adults. The high selenium content protects the brain from the effects of methylmercury.
QUICK QUICK MEDICAL MEDICA L NOTE: This r esearch is still preliminary, pr eliminary, so it is still wise to be cautious cautious by minimizing predatory fish consump co nsumption tion (tuna, (tuna, swordfish, swor dfish, tilefish, tilefish, king mackerel) mackerel) for pregnant and nursing nursing mothers, as well as infants infants and children until until mor e studies studies are perfor perfo r med.
KEY POINT: Most ocean o cean fish have higher selenium conten co ntentt than than methylmer methylmercury, cury, making them theoretically safe to eat for most adults. The high selenium content protects the brain from the effects of methylmercury
IS THE CHOLESTEROL CHOLE STEROL AND AN D FAT IN ANIMALANIMA L-BASED BASED FOODS CAUSE CAUSE FOR CONCERN?
We have all been warned war ned about eating too much saturated fat and cholestero cholestero l from fr om animal food foo d as it will surely lead to “clogged “clogg ed arter arter ies and heart disease”. Let us tackle tackle the issues one at a time. eating cholesterol fr om natur natur al food foo d sources such • Dietary cholesterol: eating
as eggs and animal meat has no impact on the health of your arteries. For most people, cholestero cholesteroll fr om the the diet has has a minute effect effect on their their blood bloo d cholestero cholestero l levels. Please Please see our extensive extensive discussion discussion of cholestero cholestero l in the Analytics section of this book. That section should ease your fears about the the “danger “danger s” of eating eating cholest chol estero erol-contain l-containing ing fo ods.
• Fat in animal animal foods fo ods:: after reading the Nutrition and Metabolism 101 section section in i n the the beginning of o f the book, we are now much mor e knowledgeable abo ut fat, fat, especially saturated satur ated fat. fat. i) Remember that mo most st types types of saturated satur ated fats fats are ar e beneficial the body. Pastured animals have higher amounts of beneficial saturated fats (such as stearic acid) and lower amounts of the potentially inflammatory palmitic acid. ii) Almost half of the fat in animal-based foods is monounsaturated fat. This is the same healt health-promo h-promo ting fat in olive oil (oleic acid). The idea that that high quality animal-based animal-based foods fr om pastured pastured sources so urces contribute to heart disease has no scientific foundation and is a very outdated way of thinking. This erroneous message really needs to be stopped stopped once and for all.
“DEADLY MEAT” There are countless news stories about recalls of meat contaminated with bacterial pathogens such as E. coli O157:H7, a potentially deadly strain of bacteria responsible for several deaths. Almost without fail, the contaminated ground beef and pork on the news is from “factory-farming” operations. The crowded conditions and improper feeding practices (using processed animal feed instead of the animal’s natural food) lead to overgrowth of deadly pathogens such as E. coli O157:H7. In the attempt to stop this type of contamination, factory-farms give the animals high doses of antibiotics which are still present in the meat when you bring it home from the grocery store. High levels of antibiotic use in factory-farms is also thought to greatly contribute to the development of antibiotic-resistant “super bugs.” These are additional additional r easons to to o btain btain your pr otein from fro m pastured pastured animals, living in un-cr un-cr owded conditions, conditions, eating their natural natural foods. foo ds. The massive amounts of animal waste (manure, etc.) from these operations have huge potential effects on our environment as well. Some factory-farms are ecological disasters waiting to happen.
Investigative journalist David Kirby has brilliantly illustrated the potential impacts to human health and the environment posed by factory farming in his recent book Animal Factory —highly —hig hly r ecommended eco mmended r eading .
INSIST ON FOOD F OOD QUALITY QUA LITY We are making a big case for pastured pastured animals and wild-caught wild-caught fish as omnivore omnivor e protein sources. As more people demand high quality, humanely raised pastured animals, more local farms will appear and increase the supply. As supply and competition increase for this type of food, prices will go down. This change must be driven from the ground up by the consumer, otherwise the food industry will continue to push factory-farmed animal products because of their high profitability. Even though factory-farms are profitable, it is at the expense of animal health, animal welfare, the environment, and your long-term health. The Strong Medicine omnivor e should demand demand high quality quality prote pro tein in from fr om pastur pastur ed animals animals or wild game.
FOOD QUALITY FOR THE VE VEGET GETARIAN ARIAN Given the current state of the animal-based food supply from factory farming, it is no wonder that an increasing number of people are becoming vegetarian. Vegetarianism can be a healthy way to eat if done correctly, but can be disastrous if done improper ly. ly. respects those who who turn turn to vegetarianism for strong Strong Medicine completely respects moral and ethical reasons. However, it is a fallacy to state that a vegetarian diet is healthier than an omnivorous diet based on wild/pastured animal protein and organically grown fruit, vegetables, and tubers. There are some potential issues
with the vegetarian (and especially vegan) dietary practices that need to be optimized.
• Deficiency Deficiency in essential essent ial amino amino acids- vegetarian vegetar ian and vegan diets can be relatively deficient in certain essential amino acids. Recall from Nutrition 101 that essential amino acids cannot be made by the the body and must be obtained fro m food. Most animal proteins have large amounts of essential amino acids, but vegetarians will need to make a little more effort to get adequate amounts during the day. The essential amino acid lysine is often deficient in vegetarians who base their diets on grains. Legumes such as lentils, black beans, garbanzo beans (chick peas), and pseudo-grains such as quinoa are relatively good sources of lysine and should be eaten daily to ensure an adequate supply of essential amino acids. Obtaining plant-based protein from a combination of sources is called eating complimentary roteins. Please note that plant-based protein is not as easily digested or utilized as well as animal protein. This means that a vegetarian will need to eat a larger amount of plant-based protein to get the same amount of useable (bioavailable) protein as an omnivore. Vitamin B-12 is a crucial cr ucial B-vitamin. Deficiency Deficiency in in • Inadequate Inadequat e Vitam it amin in B-12. Vitamin this this vitamin can lead lead to neurolog neuro logical ical pro blems, anemia anemia (low bloo d cell count), and may increase the risk for heart disease from inflammation. Vitamin B-12 is produced by bacteria in the soil and is concentrated in animal-based foods. It has often been erroneously thought that vegetarians can obtain B12 from plantbased sources such as mushrooms and nutritional yeast. Unfortunately the laws of biochemistry and several scientific studies refute these claims. Plant-based “vitamin B-12” analogs are not true vitamin B-12. They are also not biologically active in humans. In other words the analog B-12 found in some plants does not work for humans. Nutritional yeast does not naturally contain vitamin B-12 since yeast cannot make it. Nutritional yeast with vitamin B-12 has been fortified or supplement supplemented ed from fr om other so urces of o f vitamin B-12. B-12. Without a regular supply of vitamin B-12, vegetarians (and especially vegans) will become deficient. It is easy to correct this deficiency by using a vitamin B-12 supplement and working with your doctor to monitor the effects of supplementation. Vitamin B-12 supplements are made from bacteria sources, so vegans and vegetarians vegetari ans can supplement without without worr wor r y.
LEGUME PREPARATION IS KEY TO PREVENT TOXICITY
Legumes (beans) contain co ntain natural natural chemicals called call ed lectins that that can be toxic toxic to humans and o ther animals. anim als. It It is thought thoug ht that that plants plants have them in their seeds (legumes) to protect against predators. Legumes in particular can have a high amounts of a compound called phytohemagglutinin (PHA). PHA PHA can cause several toxic effects and can even be fatal in high hi gh enough eno ugh doses. Proper Pro per preparation pr eparation of leg umes is impor tant tant to to r educe educe levels of lectins and and prevent toxicity. Soak raw legumes for 24 hours before cooking. Rinse the legumes after soaking. Then boil the legumes for at least 30 minutes. These steps will reduce lectin levels to a safe range.
Never slow cook beans. Cooking them at temperatures below boiling can actual concentrat e lectin level levelss and lead lead to t o t oxicity.
QUICK QUICK MEDICAL MEDICA L NOTE: Vitamin B-12 deficiency can lead to neurological problems, anemia, and an increased risk for heart disease. Low vitamin B-12 leads to increases in an inflammator inflammator y marker mar ker called homocysteine. homocysteine. High High homocysteine homocysteine levels are a strong pr edictor edictor for developing developing heart disease. disease.
The best way way for a vegetarian vegetar ian to detect a vitamin B-12 deficiency is to have their their doctor test test their their blood and measure measure levels o f methylmalonic
acid (MMA). High MMA levels indicate a possible vitamin B12 deficiency. deficiency. Supplement Supplement wit wit h B-12 and monit monitor or MM MMA A levels levels with your doctor. • Inadequ Inadequate ate long chain omega-3 omega-3 fats. fat s. Animals concentr concentr ate ate long lo ng chain omega-3 o mega-3 (EPA (EPA and DHA) DHA) from fr om the food foo d they eat (gr asses, algae, alg ae, etc.). etc.). This makes animal sour ces (especially co ld water water fish) o ptimal for getting adequate EP EPA and DHA. DHA. Vegetarians egetar ians and vegans o ften think think they are g etting etting adequate adequate omegao mega-3 3 in their diets by eating short chain omega-3s such as alpha linolenic acid (ALA) from plant sources. sour ces. As As we have discussed extensively, extensively, ALA ALA is ver y poor poo r ly converted co nverted to the longer long er chain EPA EPA and DHA DHA in the human body. Also r ecall from fr om Nutr Nutr ition 101 that that omega-6 and omeg a-3 compete for the the same conversio n enzymes enzymes to turn them them from fr om shor sho r t chain chain to long lo ng chain. This means that that if a vegetar vegetar ian or vegan has a relatively larg e amount of omega-6 o mega-6 in their their diet from g rains or vegetable vegetable oils, the already poor po or conversio conver sion n of ALA ALA to EPA EPA and DHA DHA will be even wor se! Vegetarians and vegans can ensure they get adequate long chain omega-3 (EPA and DHA) by supplementing with preparations of EPA EPA and DHA from algae sources . These algae-based products and supplements are available at health food stores or online. It is also helpful to reduce the amount of omega-6 in the diet (from grains and vegetable oils) so that as much of the short chain omega-3 from plant-based sources like flax seed as possible is converted to the long chain forms of DHA and EPA in the body (this is not much, but every little bit helps).
Maintaining aintaining a balance of lo ng chain omega-3 omeg a-3 with with omega-6 is cr ucial to avoiding chronic inflammat i nflammation ion (and the chr chr onic diseases that that go with with it) fro m high levels o f omega-6. Getting adequate long chain omega-3 is especially important for the developing developing brains br ains of children.
• Inadequat Inadequatee iro iron n and zinc. Vegetarians and vegans are also at risk for
developing developing iron ir on and zinc deficiencies, deficiencies, especially especially if they ar ar e consuming lar ge amounts amounts of gr g r ain-based ain-based foods or raw vegetables. vegetables. Ir on from fr om animal foo ds is predominantly predominantly in the the for m of heme iron which is more easily absorbed in the body than the the non-heme ir on fo und in plant-based foods. But, But, vegetar vegetarians ians and vegans generally have diets high in vitamin C which helps absorption of nonheme iron. The real problem with vegetarian diets based on grains, nuts and legumes (soy is a good example) is a molecule called phytate. Phytate is present in the germinating portion of plants (seeds, legumes, etc.) and binds minerals such as calcium, magnesium, iron, and zinc . The plants use phytate to ensure the developing “baby plant” growing from the seed has enough minerals to support its growth. Plants are able to release the minerals bound by phytate using an enzyme called phytase which dismantles the phytate molecule, releasing the minerals to the developing plant. Humans do not have the phytase enzyme and are unable to absorb many plant-based sources of minerals (iron and zinc especially) because they are still bound to phytate. The best way to lower phytate in grains, nuts, and legumes is through proper preparation. Soaking nuts for 24 hours before eating them will reduce phytate considerably. Soaking legumes and then boiling them will also decrease phytate content content,, allowing the the absorpt absor ption ion of iron ir on and zinc.
SPROUTING SPROUTIN G IS IS THE TH E WAY TO TO GO.. GO.... Sprouting (ger minating) minating) seeds, legumes, nut nuts, s, or gr ains not only reduces phyat phyatee levels making ir on and zinc mor e absorbable absor bable,, but also g reatly increases the vitamin content of these foods. Sprouting makes use of the biochemical biochemi cal changes chang es that take take place when the plant begins to gr ow. It takes takes a couple days to sprout grains, legumes, nuts, or seeds, but it is well worth it fro m a nutritional perspect per spective. ive. There are plenty of guides to sprouting on the internet, but you can also find a good go od overview o verview in Sally Fallon’s Fallon’s excellent excellent cookbook, Nourishing
Traditions. Traditions.
Using the simple recommendations above, a vegetarian or vegan diet can be wellbalanced and healthy. The Strong Medicine vegetarian should stay away from processed grains and use properly prepared plant-based powerhouse foods such as legumes, tubers tubers and pseudogr ains such as quinoa quinoa fo r prote pro tein. in. They should also take take full advantage of the incredible health promoting “natural pharmacies” in or ganically gr own fruits and vegetab vegetables. les. The Strong Medicine omnivore and vegetarian should maximize their intake o locally-grown organic produce, and make them the cornerstone of a nutrition battle lan against chronic disease.
ORGANIC VERSUS CONVENTIONAL PRODUCE
There has been significant hand-wringing in the public health and scientific scientific r esearch communities on wheth whether er conventionally conventionally g r own or or ganic pro duce duce is the most nutr nutr itious. They are missing mi ssing the bigger picture. • The amount of time fro m picking picking to eating eating is the most important variable for nutri nutritional tional value. value. Produce Pro duce (conventional (conventional or o r or ganic) imported impor ted from across acro ss the the globe, gl obe, which which spends spends several weeks in transpor transpor t and stor stor age will lo se its nutri nutritional tional value in the the fro m of o f vitamins, vitamins, minerals and other health promoting plant chemicals. • We insist upon or ganic produce pr oduce not as much for nutritional nutri tional value but but to avoid the pesticides and antibio antibiotic tic contamination often o ften found in conventionally conventionally gro g ro wn pr pr oduce.
• Locally-grown Locally-gr own org anic pro pro duce has the the highest highest nut nutrr itional value value because it has been r ecently harvested and has not been transpor ted and stored for fo r weeks. weeks. Organic Or ganic farming far ming pr actices actices ensure ensure that that we we are ar e not subjected to to toxic contaminant co ntaminantss such as pesticides.
Insist Insist upon local lo cal and org anic produce. Your Your local farmer’ farmer’ss market market is your best source so urce..
SPICE UP YOUR HEA H EAL LTH Food tastes best when we add in herbs and spices. Variations in herbs and spices create a flavor profile for our meals. Most of the herbs and spices that we casually place in our food has a long history of medicinal uses. Research is beginning to catch up with what traditional healers have known for centuries—that these seemingly simple and tasty additions to our food are actually beneficial to our health. Let’s add another word of caution here. Science is an amazing tool and this book is based on the most current research and foundational science. Scientific research, especially as it pertains to food, can also be reductionist and lose sight of the big picture. Many of the “active constituents” found in modern spices and herbs are extracted from the whole portion of the plant (which would traditionally have been used). These medically active chemicals are studied in isolation by modern science. We must keep an open mind to the potential of these substances. But, before you run to the supplement store or dump an entire bottle of turmeric on your food, we need a little more understanding of herbs as medicine. Herbal medicine is an entire aspect of medicine that requires a thorough understanding of when to use each herb, the right time to harvest, the correct part of the herb to use, the proper method for obtaining the benefits, and correct dosing.
QUICK QUICK MEDICAL MEDICA L NOTE: Before you run to the supplement store and stock up on herb extracts and pills, keep in mind mi nd that some her bs can have unwanted unwanted side effects. ef fects. If taken in large enough quantities they can interfere with other pharmaceuticals.
Make sure that you consult your physician if you intend to use any product for medicinal medicinal purposes. purpo ses. This section is intended intended as informat infor mation ion about some of the potential health benefits of using spices in your cooking, not as a cur cur e for diseases. diseases. Below is a brief overview of some of our favorite herbs and spices along with their their potential potential suppor supportiv tivee role r ole in i n your health. health.
GARLIC (ALLIUM SATIVUM) Garlic doesn’t just keep vampires away, it is used both as a seasoning as well as in medicine. Recent research has revealed potential health benefits from this pungent beauty. • Aged gar lic may help prevent pr event development of Alzheimer ’s disease. • Garlic Gar lic stimulates stimulates the antioxidant defense system (ADS (ADS “bouncers”) “bouncer s”) to a high hig h degree. Sprouted garlic seems to maximize this stimulation. • Garlic Gar lic can help keep you insulin sensitive sensitive and also may help increase incr ease heart r ate variability and improve heart function.
GINGER (ZINGIBER OFFICINALE) Ginger is widely used in Asian cuisine. The ginger root has taste enhancing and health health pro moting characteristics. Traditional medical uses for ginger have included included relief for maladies such such as diarrhea diarr hea and and nausea. nausea. Modern science is showing that ginger can help reduce inflammation. As chronic inflammation drives most of the diseases we have discussed in this book, adding ginger to the diet may benefit those with diabetes, high blood pressure, and heart disease.
CINNAMO CINN AMON N (CINNAMOM (CIN NAMOMUM UM SPP) SPP) Cinnamon comes from the bark of several species of the cinnamon tree and can be used in both sweet and savory dishes. Recent research has shown that this tasty spice also also can be good go od for us. • Cinnamon has been shown to have significant sig nificant benefit for fo r diabetics, diabetics, sensitizing insulin funct function ion and decreasing blo od glucose g lucose levels. • Cinnamon Cinnamon may also help help control high blood pressur pressuree and improve impro ve insulin
function in the brain (remember that Alzheimer’s disease shows impaired insulin function in the nerve cells).
TURMERIC (CURCUM (C URCUMA A LONGA) Turmeric is widely used in Indian cuisine and has been prized as a medicinal compound in traditional cultures. The active ingredient in turmeric is curcumin. Curcumin from turmeric has been the focus of substantial research over the last few years. Curcumin has significant anti-inflammatory actions. • Curcumin was was found fo und to be as effective as ibuprofen ibupr ofen for symptoms in a study of people with osteoarthritis. • Curcumin was found fo und to be beneficial for the symptoms of inflammator y bowel diseases such as ulcerative colitis. • Curcumin Curcumin has been shown to help prevent prediabetics prediabetics fro m progr pro gr essing to diabetes. • Turmer ic extracts are ar e actively being studied as cancer therapy adjuncts.
CAYENNE CAYENNE (CAPSICUM ANNUM ANN UM)) Cayenne is a popular ingredient for those who like their meals on the “spicy” side. Capsaicinoids are a group of natural chemicals derived from cayenne (and other hot peppers) that has been used as a pain reliever when applied externally. Research has recently shown other beneficial effects of using capsaicin-containing cayenne. • Capsaicinoids may help decrease food intake intake by suppressing suppressi ng the drive dri ve to eat. • These compounds compo unds may also help increase incr ease fat burning activity in fat cells and the liver. • Capsaicinoids Capsaicinoids increase adiponectin, adiponectin, the the anti-inflammat anti-inflammator or y hormone hor mone produce pro duced d by fat cells. The five spices profiled in this section are only a small handful of the natural compounds available which will not only make your food taste better, but can support your healthy lifestyle change as part of the Strong Medicine program. A helpful link for exploring more natural herbs and spices is the excellent website built by the the University Universi ty of Maryland: https://umm.edu/health/medical/altmed/herb/ You should now understand the importance of food quality as the foundation of your nutrition. We will now show you how to individualize your plan with training
on carbohydrate tolerance and nutrient timing strategies to “feed your activity.”
Five health-promoting spices
INDIVIDUALIZED STRATEGIES II
“CARBOHYDRA “CARBOH YDRATE TE TOLERANCE” TOLERAN CE”
You now have an understanding of the importance of the quality of your food, whether you follow an omnivorous or vegetarian eating pattern. Although food quality is the rule, some trainees will need to adjust the amount of starch/sugar in their eating pattern depending on their current metabolic health. During Basic Training we showed you how glucose (one of the simplest carbohydrates and a primary fuel for the brain) can become toxic at high levels in the bloodstream. Many of the nasty effects from diabetes come from high blood glucose levels leading to chronic inflammation and oxidative stress. We showed you how to assess your Individual Glucose Tolerance (IGT) in the Obesity section. The IGT is crucial for ensuring that you do not eat more glucose—a product of starch and sugar digestion—than your body can tolerate at any given time. Organic oatmeal and sweet potatoes are examples of fantastic high quality foods that can become problematic for people with a poor capacity to tolerate high starch loads lo ads (i.e. trainees with insulin r esistance and outrig ht diabetes). diabetes).
THE CASE FOR “LOW CARB” EATING EATING The Strong Medicine trainee now understands there is more to carbohydrates than starch and sugar. Fiber is the forgotten carbohydrate. Most people associate a
“low carb diet” with an eating pattern containing very little starchy carbohydrates and sugar. These diets are often high in fiber so they are not technically “low carb.” In Strong Medicine, we will refer to this type of eating as a “low starch/sugar” pattern. n. (LSS) eating patter An LSS eating pattern can be an extremely powerful approach for repairing a diabetic’s broken metabolism. LSS diets can be very nutrient dense and healthful if done correctly for defined periods of time . In extreme cases—such as advanced diabetes with compromised pancreas function—LSS may be appropriate for the long-term. LSS works amazingly well (this is supported by an ever-expanding body of research) in the obese/diabetic/insulin resistant population to restore metabolic health, increase fat loss, and in some cases put type 2 diabetes into remission. LSS works because the low dietary glucose intake allows the body to sensitize itself to the effects of insulin.
FLASHBACK Go back to the “Diabesity” sectio section n in Par t II “Knowing the Enemy” and Metabolism Basics in Part I “Basic Training” for a review of insulin, glucose toxicity, and insulin resistance. The trainee with insulin resistance (especially diabetes) simply cannot tolerate the same amount of starch with their meals as the trainee with good insulin sensitivity. This is true no matter how “good for you” the starch-laden food is thought to be. We went on a bit of a rant about whole grains and diabetes in the Obesity chapter, and with good reason. Oatmeal, quinoa, fruit, and tubers (potatoes, etc.) can be highly nutritious but may not be tolerated well by the trainee with insulin resistance or diabetes. Dealing with the glucose load from digesting these foods may be too much for those those trainees. In our opinion, the toxic effects of high blood glucose insulin resistant trainees may experience from eating these foods certainly outweighs the potential benefits. If you are obese/insulin resistant/diabetic you would certainly benefit from an LSS approach to eating until your metabolism heals and you become insulin sensitive
again. We We do not no t need to to o vercompli ver complicate cate LSS. LSS. Some pr inciples o f LSS follo w.
LOW STARCH/SUGAR (LSS) EATING PATTERN • Make fibrous vegetables such as leafy greens, cucumbers, peppers, broccoli, bro ccoli, cauliflower, jicama, r adishes, adishes, carr ots, parsnips, onions, onio ns, etc. etc. the the foundation foundation o f your meals. Mushroo ms (obviously not a vegetable) are also good go od choices. choices.
• Limit tubers such as po tatoes tatoes and sweet potatoes and starches such s uch as rice. • Limit fruit to lower sugar varieties such such as blueberri blueberries, es, raspberries, raspberr ies, blackberr blackberr ies, and avocados avocados (yes they they are fruit fr uit). ). • Cut Cut out all processed foo ds made from gr ain-based ain-based flours flour s (bread, pasta, pasta, etc.). • Eat 25-30 grams gr ams of o f high hig h quality protein pro tein with with every meal. Vegetar Vegetarian ian diabetics diabetics should use pr pr operly operl y prepared leg umes. • Most Most fat should come naturally naturally fr om high quality quality pro tein tein sources sour ces (pastured animals and wild-caught fish). You You co uld consider co nsider supplement supplementing ing fat from fr om high medium chain tri triglyceri glyceride de (MCT) (MCT) sources sour ces such as coconut coco nut oil (co oking vegetables with it). it). MCTs MCTs can supply supply a quick source sour ce of energy energ y while while you are r educing educing starch/sugar. Adding Adding olive oli ve oil on on your salad is also a good way to supplement beneficial fats. • Use the Individual Glucose Tolerance (IGT) from the Obesity chapter to
periodically perio dically assess assess your tolerance for star star ch. After After several months of LSS eating, you will likely be able to add nutrient dense starchy/sugary foods such as sweet potatoes, apples, pears, and oranges. While LSS has been shown to be highly effective in improving metabolic health in obese, insulin resistant, and diabetic trainees, long-term use can cause problems for some people. LSS is not needed in trainees with good insulin sensitivity and can slow their metabolism over time. Conversely, trainees who have sustained damage to the pancreas from long-term diabetes may never again have normal tolerance to starch and sugar. They may need to stay on a relatively low starch/sugar eating pattern for life, and can use the IGT to determine their individual tolerances. Optimizing Optimizing bloo d sugar levels to within within a safe range is cr ucial for preventing preventing the ravages of a broken metabolism such as heart disease, accelerated aging, cancer, high blood blo od pressure, Alzheimer ’s dement dementia, ia, kidney failure, and stroke. Contro Controlling lling blood sugar levels with the sophisticated but simple approach of adjusting eating patte patterr ns to carbohydrate tolerance is the key restoring your metabolism. metabolism. We will move on to an individualized dietary pattern using nutrient timing around exercise that will keep your body fat low, performance levels high, and stoke your metabolic furnace to white-hot levels. This approach will greatly benefit the obese and diabetic trainee as well. You will master the concept of feeding your activity.
INDIVIDUALIZED STRATEGIES III
FEED YOUR ACTIVITY
We have given you a food quality template to follow whether you are an omnivore or vegetarian. We have also discussed the concept of carbohydrate tolerance for those with diabetes and insulin resistance. Now we will show you how to optimize your metabolic “blast furnace”, improve physical performance, keep body fat low, and prevent muscle wasting through strategies using nutrient timing to support your activity levels . During your Strong Medicine Basic Training, you learned some of the inner workings of the the flesh machine: • The brain brai n is an energ y hog and r equires equir es glucose. gl ucose. It is tr tr ue that much of the the brain can use ketones (the breakdown products of fats) for energy, but there is still a requirement for glucose. Without adequate glucose, the stress response (HPA axis) will be triggered to produce cortisol. If there are inadequate stores of glucose (fr om g lycogen in the liver) cor tisol will ensure that that adequ adequate ate glucose is available available by making it from fro m amino acids “stolen” from the the prote pro tein in in your muscles. Thus, depending on your activity, eating too little glucose (starch) can
result in muscle wastin wasting, g, and shrinking o f your hard-earned muscle mass. • Conversely, Convers ely, eating too much starch (chains of glucose) gluco se) will r esult in excess glucose co nver nver ted ted into trig lycerides (fat) by the the liver and adipose adipose cells which which will be stored as fat. Too much starch over the long term can make you fat. The excess excess glucose is also toxic to to the the body, body, for ming high hig h levels of advanced advanced glycation gl ycation endpro ducts ducts (AGE) which we discussed in the obesity chapter. chapter. How does a Strong Medicine Medici ne trainee, traine e, eating high quality qualit y foods and following a high intensity exercise program, ensure that they get enough glucose to the brain to avoid a stress response (and the high cortisol that goes with it) without consistently eating too much glucose (starch) and increasing their body fat?
The answer to this is a relatively simple strategy and eating pattern summed up by the phrase “feed your activi act ivitt y.”
FEEDING FEEDING YOUR ACTIVITY The high intensity resistance and cardiovascular training we prescribe needs proper post-exercise nutrition for optimal recovery of the body. This type of exercise is stressful to the flesh machine but will produce a beneficial adaptive response (through allostasis) if we give it the building blocks to recover successfully. It stands to reason that what and when you eat on your training days should be different than what you eat on your off days. Feeding the body for recovery when there is nothing to recover from makes no sense. You would not fill your car up with fuel if it already has a full gas tank, so do not do the same to your body. The following is a template for planning food (fuel) intake around your exercise program.
I. NON-TRAINING DAYS There is not a big need for glucose on low activity days. Your body needs protein for muscle growth during recovery and the majority of the body can run very efficiently on fat from the diet and stored body fat. Muscle is running on mostly fat during this time so the available glucose can be sent to the brain for use. The breakdown products of fat burning (ketones) can also be used by the brain to run efficiently. The muscles’ glucose storage (glycogen) is high so a relatively low intake of dietary glucose during this time will ensure that excess glucose will not be tur tur ned into into fat and and stored. Some Some general g eneral r ules on for fo r non-training days to ensure the
system works optimally during this time:
• Eat the t he majority majority of your yo ur carbohydrat carbohydrates es as fermentable fermentable fiber fiber from vegetables. Fermentable fiber will be converted by gut bacteria into antiinflammatory short chain fats such as butyrate which will help recovery. Vegetables also contain the “edible pharmacies” pharm acies” of o f phytonutrients, vitamins, and minerals to r eplenish eplenish the the body’s body’s machinery on r ecovery days.
• Reduce Reduce the amount amount of sugary sug ary fruit fruit intake and starchy foods foo ds such as tubers uits like berr ies on these days. days. (potatoes, (potato es, sweet sweet potatoes). potat oes). Eat low sugar fr uits Berr ies have co mpounds that will will stimulate the antio antioxidant xidant defense system (ADS) (ADS) to control the free radicals that were generated during the adaptive response to exercise. exerci se. We need some exer cise induced oxidative stress for fo r adaptation adaptation but do not want it to get out of control. The ADS “bouncers” ensure things go smoothly.
• Eat 25-30 gram g ramss of high quality quality prot pro t ein wit wit h every meal. meal. We want to ensure that the muscle has both the stimulus and the building blocks to recover reco ver after exercise. The essential amino acids in high quality protein will meet these requirement requir ementss for muscle rebuilding. rebuilding.
• Ensure adequat adequatee fat intake primaril primarilyy from your prot pro t ein sources so urces if you yo u are coo king your food foo d in medium chain chain saturated saturated fats fats an om o mnivore. Also consider cooking such as coconut coco nut oil. These medium chain saturated fats (also kno wn as medium chain tri triglyceri glycerides des or MCTs) CTs) will pr ovide an instantly instantly available available energy source sour ce to use while starch (glucose) from the diet is low. MCTs are also anti-inflammatory and provide the brain with with extra extra ketones ketones to use for fo r energy in i n place of g lucose. Metabolically, this will spare muscle mass by preventing high levels of cortisol from the stress response. MCTs are also much less likely to be stored as fat in adipose tissue.
II. TRAIN TRAINING ING DA DAYS YS Directly after high intensity resistance and cardio training there is an increased need for starch (glucose) in the diet to refill the glucose stored in muscle tissue, the “glycogen tanks”. It is important to remember that the brain considers intense exercise to be a potential “threat” and will activate the stress-threat system to ensure that the brain has adequate glucose, and that muscle glucose storage tanks are refilled. As far as your brain is concerned, your intense exercise could have been running away away from fro m a bear bear or o r o ther ther predat pr edator. or. The stress-threat system responds to ensure that you are prepared to flee a predator in the near future and will jumpstart the physiological processes to make
these preparations. The primal parts of the brain do not know that your exertion was a grueling set of squats and a burst cardio protocol of kettlebell swings. The brain will default to the predator scenario to ensure survival. Without adequate nutrition (especially (especially glucose) g lucose) after an intense wor wor kout, the the brain will g o into into alert mode mo de and start breaking down the body for energy while slowing the metabolism (and fat loss) to a crawl. After all, why would the brain speed up metabolism during an energy conservation mode induced by stress. You would not race around in your car, flooring the gas pedal if you were low on fuel. The brain acts the same way and will slow metabolism down. To prevent the stress-threat system from inducing a catabolic (breaking down the body) state, we need to feed the flesh machine post workout. This ensures the brain is happy and the adaptive recovery process will make us stronger instead of breaking us down to protect the brain. It will also prevent the slower metabolism that accompanies a low fuel state. The strategy for doing this is very simple and will vary subtly depending on o n the intensity intensity of the exercise. exercis e.
We need to refill the container after high intensity exercise to prevent a catabolic state. The higher the intensity of the exercise, the more glucose from muscle storage will be used. Review your Basic Training (Metabolism Basics, concepts #3 and #9) to recall that exercise of a high enough intensity that adequate oxygen cannot be supplied supplied for the the metabolic metabolic demand demand is called “anaerobic” “anaero bic” exercise. Exercise such as high intensity interval training (HIIT) is highly anaerobic and must use glucose as primary energy source. Anaerobic training burns through muscle glucose in very little time creating a large empty “storage tank” in the muscle to be filled with glucose from the diet post-workout.
Metabolically, after a high intensity workout you can (and should) replace the lost glucose with a relatively relatively larg e amount of starch fro m your post-wor post-wor kout meal. meal. This will ensure that the muscles’ “glucose tanks” are topped off and the brain has enough glucose to avoid a catabolic stress response. We also do not have to worry about a huge long-lasting insulin spike from the post-workout starch meal because high intensity intensity exercise exercise turns muscles into a “glucose “gl ucose sponges” which do not requ r equir iree insulin to to transfer glucose fr om the bloodstream to the muscles. muscles.
This relat r elatively ively high intake intake of starch does not r esult in high high amount amo untss of glucose in the bloodstream (it is absorbed quickly by the depleted muscle glucose “tanks”) and does not result r esult in fat produc pro duction tion from fr om excess excess glucose. gl ucose. This strategy also ensures that the the brain does not trig ger a catabolic catabolic state from the the stress r esponse, the the metabolism metabolism stays high and results in fat burning for days after the workout during the nontraining days. days. Summarizing the training day strategy for eating...
• Your post -workout meal should consist of o f 25-30 grams grams of high quality quality protein. This will ensure enough essential amino acids are present to stimulate and build new muscle through the adaptive process (allostasis) after being torn down by exercise.
• Eat Eat st arch from nutrient nutrient dense dense foods such as sweet sweet potato pot atoes, es, potato pot atoes, es, and sugary fruits. Gr ains and pseudogr pseudograins ains such as rice, gluten free oat o atmeal meal and quinoa quinoa will do the the trick as well. The glucose from fr om the starch starch will r apidly refill the muscles’ glucose “storage tanks” and keep the metabolism revved up. We are ar e stimulating a • Lim Limit extra ext ra sources of fat during during thi t hiss refueling refueling tim t ime. e. We building process, and extra fat in the diet will likely be stored as fat during this time. Fat naturally present in high quality protein sources is fine. • Ideally, Ideally, training traini ng would be perfor perf or med in the late afternoon afterno on with a pro tein/starch meal post po st wor wor kout at dinner time. This strategy s trategy will help yo u sleep better better preventing preventing high hig h cor tisol spikes at night. night. If you train tr ain in the morning, fi ll your yo ur muscles’ glucose storage tanks slowly throughout the day with smaller starch loads with each meal as you may have daytime activity to feed during your postworkout recover y. Plan your meals around your training schedule. If the planned training falls through, adjust your meals accordingly by lowering the starch and increasing the fat. It is r eally that simple. Just make sure your yo ur food fo od quality stays high. You will need to experiment with different amounts of starch with your postworkout meal, your needs will vary depending on workout intensity and your individual metabolism. If you are starting to gain fat around the midsection, cut back a little of the starch amount. If you are losing muscle mass, add some back in. Do not fool yourself into thinking that a couple sets of barbell curls are going to significantly deplete muscle glucose and require a large glucose replacement with starchy food. Activities like HIIT, mixed martial arts, mountain biking, sprinting, and intense ‘superset” resistance training will deplete your glucose stores. You will have to play with this for a while to dial in your own “sweet spot” for post workout meals. This is just a template.
CALORIC RESTRIC RESTRICTION TION AND A ND “LOW CARB” DIETS Diets that prescribe periods of caloric restriction such as intermittent fasting can be useful in some situations but have no place in a wellness plan that involves
regular intense exercise. Caloric restriction in general will generate a stress response and is hard on the flesh machine, significantly filling the daily “stress cup.” Getting any long-term benefit from diet strategies that involve significant calorie restriction require that you have everything else in your life optimized to reduce overall stress (minimal social/psychological stress, restful sleep, and low intensity intensity exer cise). For most of us, this thi s is not reality. realit y.
THE “CALORIE RESTRICTION CUP” Extreme Extreme calor ie-restricted diets diets cause high stress o n the body, body, filling your stress cup significantly. Calorie restriction with the other stresses of daily life leave little room in the stress cup and can quickly lead to allostatic overload overl oad and activat activation ion o f the stress stress r esponse. High levels of co rtisol fro m the stress stress r esponse associated associated with with extreme extreme calor ie rest r estri rict ction ion can lead to muscle wasting. There are better ways to improve body composition. Long-term diets that are very low in starchy carbohydrate (LSS) do not mix well with high intensity exercise programs. The mixture of the two creates stress in the body due to inadequate amounts of glucose in the diet to support anaerobic exercise. It is a set up for failure, and will consistently overflow the stress cup. If you are temporarily on a LSS diet to reverse a broken metabolism (diabetes) you have to be careful with high intensity exercise. Our recommendations are to still include some starch post-workout and monitor your response with the Individual Glucose Toler ance (IGT) test discussed discussed in the obesity section. If you want to stay on an LSS eating pattern and it is working well for you, we advise that you limit your exercise to lower intensity protocols such as light resistance resistance training and low intensit intensity y cardiovascu cardio vascular lar training to prevent your your “str “str ess cup” cup” from fro m overflowing overfl owing and reversing the progr pro gr ess you have have made. made.
QUICK QUICK MEDICAL MEDICA L NOTE: Extreme Extreme calor ic r estr estr iction diets diets (we’ve (we’ve seen some limiting calo ries ri es to 500 kcal per day!) are never a good idea. Yes, you will lose weight for sure, but a significant amount of it will be lost as muscle mass. This is terrible for your health. Diets like this also put the brain in starvation mode, slowing the metabolism and priming the body for fat storage the next chance it gets. This is why so many people who lose weight with extreme caloric restriction gain it all back (and often more) when they stop the restrictive diet. diet. The brain r emembers! emembers! The loss of muscle mass has consequences as well. Muscle is a metabolic engine and a big fat burner. Lost muscle mass can slow your metabolism to a snail’s snail ’s crawl. Remember Remember that adequate adequate muscle mass can pro tect against insulin resistance and diabetes.
STRONG MEDICINE TACTICS: Feed your your act activity ivity to to keep your your met metabolism abolism high hig h and minimize stor stor age of of excess body fat. Now that you know the strategies for feeding your activity, we will give you several example recipes for simple and great tasting meals made with high quality ingredients you can use to fuel your flesh machine.
INDIVIDUALIZED STRATEGIES IV
ONE WEEK W EEK OF FOOD
There are countless recipes available on the internet and in cookbooks. The purpose of this section is not to tell you what to eat, but to give examples of easy to prepare meals which emphasize food quality. As long as you have quality ingredient ingr edientss and stay stay away away fro m pro cessed foods foo ds you really r eally cannot cannot go wrong. wrong . Continue to use the principles covered in “Feed Your Activity” when planning meals that are optimum for training and non-training days. Examples of this will be given. The following is a sample five day menu with recipes to follow.
EGG SCRAMB SCRAMBLE LE Ingredients: The vegetables listed will change based on seasonal availability. Vegetables should be organic if possible.
• • • • • • • •
6 eggs fro m past pasture-r ure-r aised chickens chickens 3-4 tbs coconut coco nut milk 3 oz org anic frozen fr ozen spinach spinach 6-8 slices bacon bacon from pastured pastured pigs ¼ of small onion, onio n, chopped 1-2 cloves gar lic, chopped 1 small rutabagas/po tatoes/ tatoes/pars parsnips, nips, etc. (thinly sliced or gr g r ated) salt and and pepper pepper to taste taste
Directions: In a glass bowl, beat the the egg s with coconut milk. mil k. Add salt and pepper pepper to taste taste and set aside. In a sauté sauté pan, cook coo k onions oni ons and g arlic. ar lic. Add Add potatoes and cook coo k for 5 min. Add Add in the bacon. bacon. Once the the bacon is mo stly cooked, coo ked, add in the beaten egg mixture and cook until the eggs are set to your desired texture. This recipe r ecipe is designed designed for 2 servings. Refrig Refrig erate the the leftovers leftovers fo r tomorr tomor r ow’s ow’s r eheated eheated breakfa br eakfast. st.
Comments: This recipe r ecipe will will given g iven you plenty plenty of prote pro tein in to star star t your day and a good goo d balance of omega-3 and omega-6 polyunsaturated fats (make sure the eggs are fr om pasture raised r aised chicken chickens). s). The coconut milk will will also provide medium chain fats that can be immediately used for energy.
SPICY SPICY BURGER BURGE R WITH JICAMA CHIPS
Ingredients: Spicy Burger
• • • • • • • • • • • •
2lb ground gr ound beef (fr om pastured cows, bison, etc. etc.) 1 tbsp. cumin cumi n 1 tbsp. tbsp. smoked smo ked paprika papri ka 1 tbsp. powdered garlic gar lic 1 tbsp. powdered onion onio n 1 tbsp. dried dr ied or egano salt to taste pepper to to taste taste 1 tsp. cor iander ½ tsp. tsp. cayenne (less if you yo u like it less spicy) ¼ tsp. cinnamon cinnam on zest of 1 lime
Jicama Chips • jicama • juice of 1 lime • ancho chili powder powder
Directions: Combine all ingredients in a bowl and mix thoroughly. If you are using lean ground beef you may want to consider adding an egg to the mixture to help keep keep your burger bur ger s moist. Divide Divide the the gr ound beef into into 4 burg ers and cook to your desired temperature. temperature.
Jicama Chips: Peel and slice the fresh fr esh jicama. Squeeze Squeeze the the fresh fr esh lime (which ( which you used for the zest) over the jicama and sprinkle with ancho chili powder.
Comments: This is a good go od r ecovery day meal with with plenty plenty of prote pro tein in and fermentable fermentable
fiber fr om the jicama. jicama. Add Add an avocado avocado for fo r mor e fiber and a goo d dose of healthy monounsatu mono unsaturr ated fat.
CHIPOTLE BUTTERNUT B UTTERNUT SQUASH SQUASH SOUP Ingredients: • • • • • • • • • • • • •
2-3 lbs chicken thighs; boneless and skinless 1 butternut squash 2 medium apples 1 can chipotle peppers in adobo sauce 2 small onions 10 cloves of gar lic 2 tsp salt 2 tsp cor iander powder 2 tbs tbs dried or egano 2 tbs dried dr ied thyme thyme 1 can coconut coco nut milk 2 cups of chicken bro th juice of 2 limes
Directions: 1. Preheat Pr eheat the oven ove n to 375 2. Roast apples, apples, butternut butternut squash, squash, 1 onion onio n and 5 cloves of gar g arlic lic • Peel and cube the butter butternut nut squash (don’t for get to r emove the the seeds) • Peel, cor e and chunk the apples • Peel and chunk onio n • Remove the skin of the gar lic • Place all vegetables vegetables listed immediately above + the apples on a baking sheet lined with with parchment paper and roast r oast for fo r about 30-45 minutes minutes until the vegetable poke tender tender • While this this is ro asting asting start start on remainder of the the soupl 3. Prepare remainder remainder of soup • Cut the chicken into bit size chunks • Mince 6-8 chipotle peppers
• Mince 1 onion, 5 gloves glo ves of garlic gar lic • Place chicken, chicken, onion onio n and gar lic in a stock pot and and remainder of ingredients listed above. Cook for about 30 minutes over medium heat 4. Puree roasted ro asted vegetable. • Once vegetables vegetables are cooked, remove remo ve from fr om oven and puree in blender blender with a small quantity of liquid from soup. • BE CAREF CAREFUL UL…Hot …Hot liquids in a blender increase the pressur pr essuree inside and can cause harm. • Add pureed vegetables and apples back to soup 5. Heat for about 5 minutes and and serve This meal is excellent excellent post-workout post-workout with with a go od amount of starch to r efill muscle glycogen tanks.
MEXICAN CHICKEN CHICKEN WITH SAUTÉED SAUTÉED KALE Ingredients:
• • • • • • • • • • •
2lbs of pastured chicken thighs cut into bite sized pieces 1 small onion, chopped 1 jalapeno, chopped 3 cloves of garlic, gar lic, chopped 2 tbsp. tbsp. Mexican oregano or egano 2 tsp. cumin cumi n 1 tsp. gr ound cor iander 1 tbsp. tbsp. r ed pepper flakes 1 tbsp. tbsp. ancho chili powder 2 tsp. smoked smo ked paprika papri ka zest of 2 limes
• • • •
juice of 2 limes salt and and pepper pepper to taste taste r aw milk cheese (Monterey jack), grated gr ated 2 bunches bunches of kale cleaned and torn tor n
Directions: Sauté garlic, onion, jalapenos, and lime zest with salt and pepper in coconut oil until softened and slightly browned. Add in the remaining seasonings and cook for another 2 minutes. Add in the chicken and juice of 2 limes. Cook until the meat is done. During the last 10 10 minutes of the chicken cooking, in a separate pan, sauté the torn kale in coconut oil, salt, pepper and gar g arlic lic powder po wder until it is lightly li ghtly wilted. Place the kale in the the bottom of o f each serving ser ving bowl, bo wl, top top with chicken and cheese. cheese.
Comments: This dish is high hig h in protein pr otein with with a super super dose of o f fiber and antioxidan antioxidantt defense defense stimulation stimulation fro m kale.
SPICY SPICY CHICKEN SOUP Ingredients: • • • • • • • • • • • • • • •
2-3lbs of boneless, skinless chicken thighs, thighs, cut into bite sized pieces 1 bag bag of frozen fro zen sweet sweet cor n 2-3 jalapenos, chopped 2-3 medium sized sweet potatoes, cubed cubed 1 sweet onio n, chopped 3-4 cloves of garlic, gar lic, chopped 2 tbsp. or egano 1 tbsp. cumin cumi n 1 tsp. cayenne 1 tsp. Ancho chili powder 2-3 cups of chicken stock zest of 1 lime fresh fr esh cilantro cilantro (optional) salt and and pepper pepper to taste taste 1 tsp. tsp. coconut coco nut oil oi l for sauté
Directions: Sauté Sauté the the onion, garli g arlic, c, and jalapeno jalapeno in a small amount of coconut co conut oil (o r r endered duck fat) until softened. so ftened. Add in chicken, seasoning, and chicken stock. Cook on medium to low heat covered for 20 minutes. After chicken has cooked, add in sweet potatoes, lime zest, and corn and cook for an additional 20 minutes (or until the the potatoes ar e easily penetrated with with a for k). Garnish with fresh cilantr cilantr o and serve. ser ve.
Comments: This is a gr eat post post workout worko ut meal meal with a goo d dose of o f a nutrient dense dense star star ch from fr om the the sweet sweet potatoes. potatoes. This dish will r efill lost l ost muscle glycog en and stimulate muscle growth after a tough exercise session.
PASTURED PORK CHILI Ingredients: • • • • • • • • • • • •
3-4 lb. lb. boneless por por k shoulder shoulder r oast from a pastured pastured pig 2-3 jalapenos, seeded and diced 4-6 garlic gar lic cloves, minced 1 larg e onion, onio n, minced 1 large can of diced tomatoes tomatoes ¼ cup apple cider vinegar 1 cup vegetable bro th 1-2 tbsp. chili chil i powder po wder 1 tsp. cayenne 1 tbsp. cumin cumi n 2 tsp. cor iander 2 tbsp. or egano
• salt • pepper
Directions: Cut boneless pork shoulder roast into bite size chunks. Combine all ingredient ingredients into into a slow cooker and cook on low lo w for 8 hours or high for 4 hours.
Comments: This is another gr eat lunch lunch meal that that you can prepare ahead in a larg e quantit quantity y and have have several several por po r tions ready for r eheatin eheating g fo r a couple of days.
SALMON WITH CARROT CA RROT NOODLES Ingredients: • • • • •
1lb wild wild caught salmon (cut into 2 pieces) 1 tsp. coconut coco nut oil oi l ½ tsp. salt ½ tsp. pepper peppe r ½ tsp. dried dri ed dill
Season the salmon salmo n on bo th sides with with salt, pepper and dill. dil l. In In a sauté pan, melt coconut oil. Once the oil is warmed, add in the seasoned salmon. Sauté Sauté on both sides for approximately 4 minutes minutes over medium to hig h heat. If salmon has skin o n it, cook skin ski n side down fir st. If the the oil begins to smoke, turn tur n down the heat.
Carrot Noodle Ingredients Ingredients and Directions:
• • • • •
8 medium medium to large carr ots cut cut into carr carr ot noo noodles dles 1 tsp. coconut coco nut oil oi l 3 cloves gar lic, minced ½ ciopollini ciopoll ini onion, onio n, minced salt and and pepper pepper to taste taste
Once the carrots are cut into noodles, set them aside. Melt coconut oil in sauté pan and add add onion oni on and gar g arlic. lic. Season with salt and pepper pepper and sauté until until o nions and gar lic are ar e translucent. translucent. Add Add in carr ot noodles noo dles and cook to desired tenderness.
Comments: This meal is a delicious way to get plenty of long chain omega 3 fatty acids (DHA and EPA). EPA). The carr car r ot “noo dles” are ar e a gr eat way way to enjoy nutrient dense noodles and avoid the processed high-density carbohydrates found in traditional pasta.
MAKING “NOODLES” Making carrot noodles is simple. Use a peeler and strip the carrot until you hit the core. Turn the carrot over to the other side and continue the process. You can peel the carrot on four sides to make excellent tasting realistic noodles.
ROASTED ROASTED CHICKEN CH ICKEN WITH ROASTED CELERY ROOT
Ingredients Ingredients Roasted Roast ed Chicken: Chicken: • • • • • • •
3-4lb whole chicken 5-6 sun-dr sun-dr ied tomatoes tomatoes in olive oil 3 cloves gar lic 1 bunch bunch fresh fr esh thyme thyme (leaves only) 1-2 tbsp. tbsp. coco nut oil, oi l, melted 1 small onion, peeled and cut in quar quarters ters Salt and pepper
Directions: Preheat oven to 450 degrees. In a food foo d processor, pro cessor, combine garlic, garl ic, sundried sundried tomatoes with with their their o il, thyme, salt and pepper. Pulse until well combined. Add in 1-2 tbsp. of melted coconut coco nut oil until the mixture’s consistency is paste-like. Using your yo ur finger, gently lift the skin from breast meat on each side of the breast bone. Place 1 tbsp. of the mixture o ver each breast. br east. Place 1 tbsp. into the chest cavity and rub remaining over the outer surface of the chicken. Generousl Gener ously y salt and pepper the inside of o f the chicken cavity. cavity. Add Add in the quarter quarter ed onion. Bake at 450 degrees for 1 hour. Allow the chicken to rest for 15 minutes prior to carving. carving.
Ingredients Ingredients and Direct Directions ions Roasted Roast ed Celery Celery Root : • • • •
2 whole celery roots, ro ots, peeled and diced 2 tbsp. tbsp. coconut coco nut oil, oi l, melted 2 tbsp. tbsp. gar lic granules salt and pepper
Preheat oven to 450 degr ees (you can use the same oven as the chicken). Peel and dice dice celery r oot, oo t, place place it in a Ziploc bag and coat the the diced root ro ot with melted coconut oil. Spread coated root on a cookie sheet lined with parchment paper. Dust Dust the the coated roo r oo t with with gar lic, salt and pepper. Roast Roast celery root until done, approximately 45-60 minutes so it can be cooked in the same oven with the chicken.
Comments: Celery r oot oo t is low in starch and is a g r eat subst substitu itute te for potatoes for fo r those with diabetes/insulin diabetes/insulin r esistance. You can r oast them as above or make celer celer y ro ot mash (like mashed mashed potatoes). potatoes).
BEEF BE EF POT ROAST Ingredients: • • • •
3lb beef chuck chuck roast (grass-fed of course) 1 medium onion, oni on, peeled and cut in to to quarters quarter s 6 cloves of gar lic, peeled peeled and crushed ¼ cup r aw apple cider vinegar
• • • •
¼ cup tamari sauce (gluten free soy sauce) 2 cups vegetable broth br oth 3 tbsp. Italian seaso ning Generousl Gener ously y season season roast r oast with with salt and pepper
Directions: Place all all ingr edients edients in the the slow cooker and coo cook k on low for 8 hours or or on high hig h for 4 hours. *Puri *Purists sts will will want to to brown bro wn the the meat before befor e placing it in the slow cooker. If you are one of these, coat the chuck roast in oat flour with salt and pepper. Brown it in coconut oil for approximately 5 minutes per side. Serve with with a larg e salad for a gr eat tast tasting ing and simple to prepare meal.
Comments: This is an excellent choice if you know you will be having a busy evening. You can start the slow cooker in the morning, and dinner will be ready when when you get home home fr om wor k.
PULLED PORK WRAPS WRA PS WITH MANGO MAN GO JALAPEÑ JALAPEÑO O RELISH RELISH Pulled Pulled Pork P ork Ingredients Ingredients and Direct Directions: ions: • • • •
Pork Por k shoulder shoulder ro ast (boneless from fr om a past pastured ured pig) 1 can of diced pineapple and the juice 2 tbsp. gar lic powder 2 tbsp. ginger gi nger powder po wder
• • • •
2 tsp. cumin cumi n 2 tsp. cinnamo cinnam o n 2 tsp. cor iander salt and and pepper pepper to taste taste
Season your pork roast and place it in slow cooker. Add in pineapple and juice. juic e. Coo Coo k on low l ow for fo r 7 hour s. Shred the por po r k with for ks and coo co o k for fo r an additional additional hour ho ur on lo w. Serve Serve with a simple mango and jalapeno jalapeno r elish.
Mango Relish Ingredients and Directions: • • • • • •
1 ripe ri pe mango diced diced 2 cloves gar lic minced ½ red onion minced minced 1 jalapeno seeded seeded and minced 1 lime, juiced Salt and pepper pepper to taste taste
Combine all ingredien ingr edients ts and and allow to sit at ro om temperature temperature fo r 1 hour befor beforee serving. Place pulled pork into a lettuce or cabbage wrap. Savoy cabbage leaves make an excellent wrap. Add Add the mango r elish and enjo y.
Comments: This is a great tasting recipe with a healthy cabbage wrap substituted for a traditional flour tortilla.
STEAK AND A ND POTA POTATOES (OR KALE) KA LE) Steak Ingredient Ingredient s and Direct Directions: ions:
• • • • • •
2 boneless ribeye steaks steaks salt pepper smoked paprika garlic 1 tsp. tsp. coconut coco nut oil, oi l, divided in half
Allow the the steaks steaks to to come co me to ro om temper temper ature ature for fo r 1 hour prior pr ior to cooking. coo king. Dust steaks steaks with salt, pepper, pepper, gar g arlic, lic, smoked sm oked papr ika. We We use a cast iron skillet to cook our steaks, but you can also grill them. If using the oven for the the steaks, steaks, preheat the the bro iler to 500 degrees and move the rack to the top top position po sition in i n the oven. Once the oven has come to temperature, place the seasoned steaks into the skillet and add ½ tsp. of coconut coco nut on top of the steaks. steaks. Cook Coo k for 5-6 minutes and flip. Cook Coo k an additional 4-5 minutes. Allow steak to rest on the cutting board for 5 minutes prior to serving.
Potato Ingredients and Directions: • • • • • •
2 medium medium sweet sweet potatoes 2 tbsp. tbsp. melted coco nut oil oi l salt pepper garlic cayenne
Preheat oven to 375 degrees. degr ees. Peel Peel and dice the sweet potatoes potatoes and place in in a Ziploc Ziplo c bag. Coat the the potatoes with melted coconut oil. o il. Place the the coated co ated sweet potatoes potatoes on o n a cooki co okiee sheet lined with parchment paper. Dust Dust potatoes with with salt, pepper, pepper, gar lic and cayenne. Cook in i n the oven for 45 minutes (until potatoes are “fork tender”). Serve.
Comments: This is another gr eat post-w post-wor or kout meal high in protein pr otein and starch. starch. If If you
miss the workout, just replace potatoes with a less starchy choice such as kale (pictured).
PROTEIN BERRY BREAKFAST SHAKE Ingredients Ingredients and Direct Directions: ions:
• ½ can can full fat coconut coco nut milk (6-7 ounces) • 6-8 ounces of water water • 25-30 gr ams whey pro tein • ½ - 1 cup or ganic ber ber ries ri es (bluebe (blueberr ries, ri es, raspberr ies, blackberr blackberr ies, strawberries, etc.) • 1 tsp. of local lo cal honey (optional) (optio nal) Place all ingredients in a blender and blend to a smooth consistency.
Comments: This is a quick meal replacement shake to ensure you get adequate protein first thing in the morning. The medium chain fats in the coconut milk will provide pro vide a great source of i mmediate mmediate energy and the the berr berr ies are one o ne of the top foods for stimulating the antioxidant defense systems in your body.
COOKING STRA STRATEGY TEGY The “week of food” example was just to illustrate several possible meals. The preparation time necessary to stick to a schedule as outlined in the 5-day plan is not doable for most people with busy lives. Our suggestion is to take one day (usually on a weekend) and prepare lunches for the week. For us, this this involves making a big batch batch of o ne of the meals in a slow cooker coo ker and
portioning it out for lunches for the week. The drawback is that you will be eating the same thing thing for f or lunch every day, but it is much healthier than eating out o ut for lunch. It is also very convenient to grab a pre-made lunch in the morning and heat it up at work. Try to also loosely plan your meals around your workouts. On days when you have an intensive exercise session planned, make sure you have enough starch in your post-workout meal to replenish your muscles’ glycogen. If life gets in the way and you miss your workout, you can make minor changes on the fly; instead of having steak and potat po tatoes, oes, make steak and kale. The recipes here are only given as examples. Be creative and experiment with your own recipes, use the highest quality ingredients, and feed your activity. It really is as simple sim ple as that. that.
CONCLUSION You now have the knowledge and the tools to implement defensive tactics and individualize them to your needs. It is time to put everything you have learned together into a cohesive strategy to start launching assaults in your war against the “Pentaverate.”
STRONG MEDICINE NUTRITION “MILITARY
INTELLIGENCE” (REFERENCES): Metab (Lond) 5 (2008): 9. Accurso Accurso A, e t al. D ie tary carb carbohyd ohydrate rate restrictio n in type 2 diabetes mel li tus and andmetaboli c syndrome: ti me f or a criti criti cal appraisal. Nutr Metab (Lond) Afi fy AM , El- Bel tagi HS, El -Salam SM, & Omran Omran AA. Bi oavail abil abil ity of i ron, zi nc, nc, phytat phytatee andphytase activi ty during soaki ng and andgermi natio natio n of white so rghum varie varie tie s. PLoS One 6 (2011): e25512. Ak il en R, Tsiami A , Deve ndra D, & Ro binson N. Ci nnamon in gly caemic control: control: Systemati c revi revi ew and meta analysi analysi s. Clin Nutr 31 (2012): 609-615. Al k azemi D, Eg el and and GM, R oberts LJ, Chan Chan HM, & K ubow S. Ne w i nsights regarding ti ssue Se andHg i nteractio ns on oxi dativ dativ e stress f rom plasma IsoP and IsoF me asures asures i n the Canadian Inuit Inuit populati populati on. J Lipid Res 54 (2013): (2013): 1972- 1979. Al le n RW, Schwartzman Schwartzman E, Baker W L, Col eman CI, & Phung OJ. OJ. Cinnamon Cinnamon use use i n type type 2 diabete diabete s: an updated systematic revi ew and meta-analysi meta-analysi s. Ann Fam Med 11 (2013): 452-459. Bouchena Bouchenak k M , & LamriLamri- Senhad Senhadji ji M . Nutriti Nutriti onal quali ty of l egumes, andtheir role in cardiometaboli cardiometaboli c risk risk preve preve ntion: a revi ew. J Med Food 16 (2013): 185-198. ents 3 (2011): 529-554. Bradbu Bradbury ry J . Do cosahexae noic aci d (DHA): an ancie ancie nt nutrie nutrie nt for the mo dern human brai brai n. Nutri n. Nutrients Broadhurst CL, Cunn Cunnane ane SC, & Crawford MA . Ri ft Vall ey l ake fi sh and andshell fi sh provided brain-specif brain-specif ic nutriti nutriti on for early Homo . Br J Nutr 79 (1998): 3-21. Chamberlain Chamberlain J G. The possi ble rol e of lo ng-chain, ng-chain, omega- 3 fatty acids i n human uman brain phyloge phyloge ny. Perspect Biol Med 39 (1996): 436-445. Chamberlain Chamberlain J G. D ie tary li pids and evol ution of the humanbrain. brain. Br J Nutr 80 (1998): 301-302. Chuengsamarn engsamarn S. Curcumin Curcumin extract for preve preve ntion of type 2 diabete diabete s. Diabetes s. Diabetes Care 35 (2012): 2121-2127. Chuengsamarn engsamarn S. Re duction of atheroge atheroge nic risk in patients wi th type type 2 diabetes by curcuminoi cuminoi d extract: a ran randomize domize d controll controll ed trial. J Nutr Biochem 25 (2014), 144-150. Nutr 89 (2009): 1627S-1633S. Craig WJ. Health effects of vegan diets. Am J Clin Nutr Craig WJ . Nutritio n concern concerns and and heal th effe cts of veg etarian die ts. Nutr Clin Pract 25 (2010): 613-620. Crawford MA, & Broadhurst CL. The rol e o f docosa-hexaenoic and the marine food we b as dete rminants of evo lutio n and homi homi nid brain brain deve deve lo pment: the chall enge f or human sustainabil ity. Nutr Health 21 (2012): 17-39. Cunnane nane SC, Pl ourde ourde M , Stew art K, & Crawford MA. Docosahexaenoic acid and shore-based diets in homini n encephali zatio n: a rebuttal. Am J Hum Biol 19 (2007): 578-581. Dale y CA, Abbott A, Doyl e PS, Nader GA, & Larson S. A revi ew o f fatty acid profi profi le s and and antioxi antioxi dant dant content content in grass-fe grass-fe d and andgrain-fe d bee f. Nutr J 9 (2010): 10. Fernand Fernandez ML. Re thinki thinki ng dietary chole chole sterol. Curr Opin Clin Nutr Metab Care 15 (2012): 117-121. Atheroscler Re p 12 (2010): 377-383. Fe rnan rnandez dez ML , & Call Call e M , Re vi siti ng die tary chol chol este rol recommendatio recommendatio ns: does the the evi dence dence suppor supportt a li mit of 30 0 mg/d? Curr Atheroscler Lipids 45 (2010): 947-962. Forsythe CE, e t al. L imi ted ef fe ct of die tary satur saturated ated fat on plasma saturated fat in the context context o f a l ow carbohyd carbohydrate rate diet. Lipids Lipids 43 (2008): 65-77. Forsythe CE, e t al. Comparison of l ow f at and low carbohyd carbohydrate rate diets on circulating fatty acid composi composi tio n and marke marke rs of i nflammation. Lipids Griffi n JD, & Li chtenst chtenstei ei n AH. Di etary etary Cholesterol and Plasma Lipopr Lipoprotein otein Profil es: R andomiz domiz ed-Controlle ed-Controlle d Trials. Curr Nutr Rep 2 (2013): 274-282. Gupta Gupta SC, Patch Patchva va S, & Aggarwal BB. T herapeutic rol es of curcu curcumin: l essons l earned earned from cli nical trial s. AAPS J 15 (2013): 195-218. Neuropharmacology 63 (2012): 211-223. Ha SK, e t al. 6-Shogaol, a gi nger produ product, ct, modulates modulates neuroi neuroi n-fl ammation: a new approac approach h to neuroprotection. Neuropharmacology Janssens PL, Hursel Hursel R, & Westerterp-Plantenga MS. Capsaici Capsaici n increases increases se nsatio nsatio n of full ness in energy balance, balance, and decreases desi re to e at after dinner dinner i n negati negati ve e nergy balance. balance. Appetite 77C (2014): 46-51. Jo nes JL, et al. A M edite rranean rranean-styl -styl e l ow- gl ycemi c-l oad diet i mprove mprove s variable variable s of metaboli c syndr syndrome ome i n wome n, and and additio additio n of a phytoch phytochemi cal-ri ch medical f ood enhances ances benef benef its on li poprotei poprotei n metaboli sm. J Clin Lipidol Lipidol 5 (2011): 188-196. Kang JH , et al. Di etary capsa capsaici ici n attenuates attenuates metabol metabol ic dysregulation in geneticall y obese diabetic mice. J Med Food 14 (2011): 310-315. Kanter M M, K ris-E therton PM, F ernandez M L, Vi cke rs KC, & Katz DL. Explori ng the factors that that aff aff ect blood chol este rol and heart disease ri sk : is die tary chole chole sterol as bad for you as history l eads us to bel bel ie ve? Adv Nutr 3 (2012): 711-717. Kaur P, Aschner M , & Syversen T. Biochemical f actors actors modulati ng cel cel lul ar neurotoxici ty of me thylmercury. thylmercury. J Toxicol (2011): 721987 . Neurotoxicology 29 (2008): 978-987. Kaur P, He ggl and and I, A schner schner M, & Syve rsen T. Docosahexaenoic acid may act as a neuroprotector for me thylmercury-i thylmercury-i nduced uced neurotoxi neurotoxi city in primary neural neural cel l cultures. cultures. Neurotoxicology Ki m J H, G upta S C. Turmeric (Curcuma cuma l onga) inhibi inhibi ts i nflammatory nucle nucle ar factor (NF)-k appa appaB B and NF-k appa appaB-regulate B-regulate d gene produ products cts and and induces death receptors le ading ading to suppresse presse d prol if eration, i nduced uced Nutr Food Res 56 (2012): 454-465. chemose chemose nsitiz ation, and and suppressed osteocl astogenesi s. Mol Nutr Nutrition 29 (2013): 821-827. Kumar S, Verma AK, D as M, J ain SK, & Dwi vedi PD. Cl ini cal complicatio ns of ki dney bean (Ph (Phaseol aseol us vulg aris L.) consump consumptio n. Nutrition Lee da Y, et al. A nti-i nflammatory activ activ ity of sulf ur-containing ur-containing compounds ounds from garli garli c. J Med Food 15 (2012): 992-999. Mahluji S, Ostadrahimi A, Mobasseri M, Ebrahimzade Attari V, & Payahoo L. Anti-inflammatory effects of zingiber officinale in type 2 diabetic patients. Adv Pharm Bull 3 (2013): 273-276. Obersby D, Chappell DC, Dunnett A, & Tsiami A A. Pl asma total homocysteine status of ve getarians compared compared with omnivores: a syste matic revi ew and and meta-analysi meta-analysi s. Br J Nutr 109 (2013), 785-794. Pawlak R, Parrott SJ, Raj S, Cull Cull um-DuganD, & Lucus Lucus D. How preval preval ent is vi tamin B(12) defi cie ncy ncy among vegetarians? Nutr Nutr Rev 71 (2013): 110-117. Ralston NV. Selenium health benefit values as seafood safety criteria. Ecohealth 5 (2008): 442-455. Ral ston NV, & Raymond LJ . Die tary sel enium’s protecti ve ef fe cts against methylme rcury toxicity. Toxicology 278 (2010): 112-123. Nutr 62 (2011): 106-110. Rani M P, et al. I nhibi tory potential potential of gi nger extracts extracts against enzyme s li nke d to type 2 diabetes, diabetes, i nflammation and and induced uced oxidative stress. Int J Food Sci Nutr Ray B, Chauhan NB, & Lahiri DK. The “aged garlic extract:” (AGE) and one of its active ingredients S-allyl-L-cysteine (SAC) as potential preventive and therapeutic agents for Alzheimer’s disease (AD).
Curr Med Chem
18 (2011): 3306-3313. Ray B, Chauhan han NB. & Lahiri DK. Oxidative insults to neurons neurons and and synapse synapse are prevented by aged garli c extract and and Sall Sall yl -L- cystei ne treatment in the neuronal neuronal culture and APP-Tg mouse model . J Neurochem 117 (2011): 388-402. Shehzad Shehzad A, R ehman G, & Lee YS. YS. Curcumin Curcumin in infl ammatory ammatory dise ases. Biofactors 39 (2013): 69-77. Tome D, & Bos C. Lysi ne require ment through through the human li fe cycle. J Nutr 137 (2007): 1642S-1645S. Vafa Vafa M , et al . Ef fe cts of ci nnamon consu consumption mption on glycemi c status, l ipi d profi le and and body composi composi tion i n type type 2 diabeti diabeti c patie patie nts. Int J Prev Me d 3 (2012): 531-536. Volek JS, F ernandez M L, Fe inman RD , & Phinney Phinney SD. Di etary carboh carbohydr ydrate ate restricti on induc induces es a unique metaboli c state state positi vel y affe cting atheroge atheroge nic dysl dysl ipi demia, fatty acid partitio partitio ning, and metabol ic syndrome. Prog Lipid Lipid Res 47 (2008): 307-318. Volek JS, e t al. Carbohyd Carbohydrate rate restriction has has a more favorable favorable impact on the m etabolic syndrome than a low fat diet. Li pids pids 44 (2009): 297-309. Volek JS, e t al. W hey protein suppleme ntatio ntatio n during uring resi stance stance training augments augments l ean body body mass. J Am Coll Nutr 32 (2013): 122-135.
Z eval lo s VF, et al. al. Gastroi ntestinal Eff ects of Eating Quinoa (Chenopodium enopodium quinoa quinoa Wi ll d.) in Cel iac Patie Patie nts. Am J Gastroenterol 109 (2014): 270-278.
BATT BATTLE LE PLAN PLA N III
PUTTING PUTTING IT ALL TOGETHER
“Though “T hough no one can go back and and make make a brand brand new start, st art, anyone can start from now and make a brand new ending.” —Carl Bard
“If you always always put lim limits on everything you yo u do, physical physical or anythi anyt hing ng else, it will will spread into into your work and into your life. There are no lim limits. T here are only plateaus, plateaus, and you must must not stay st ay there, t here, you yo u must must go beyond them.” them.” — Bruce Lee
PUTTING IT ALL A LL TOGETHER TOGETHE R I
LIFESTYLE LIFESTYLE CHANGE: CHA NGE: “THE NECK OF ROY BUCHANA BUCHA NAN’ N’S S GUITAR” GUITAR”
Underg Undergro ro und guitar guitar legendleg end- Roy Buchanan Buchanan The authors are both musicians; Chris is a guitarist and Marty a jazz pianist. Many of our conversations together center on our mutual love for music and musicians. Sometimes there are some universal truths that can be applied to health and fitness lurking beneath our shared anecdotes. Marty’s tale of the guitar neck of Roy Buchanan is one of these... I was always struck by the modesty of Roy Buchanan’s guitar gear. His beat-tohell scarred-wood Telecaster was as plain as an Amish farmer. When he had a few
beers and was feeling good and relaxed, he was incredible. His playing was extremely subtle with lots of soaring, sustained anthem-like riffs. Roy was majestic, elegant, loud, and crystal clear. His patented “ghost tones” and effortless threeoctave speed runs were all done with the greatest of ease, as he exhibited ho-hum nonchalance that added added to the effect. He was was a r elaxed, laid back, rural r ural dude creating amazing music with effortless pyrotechnics. I once watched Roy from a front table, stage left, from a distance of perhaps 15 feet. He rolled into an extended arpeggio with his pick-holding right hand tracing a perfect oval on the six strings; touching each string at precisely the right instant in time over and over, creating a cascade of crystalline glass notes, all perfectly timed. I imagined if he had a piece of chalk in his hand instead of a guitar pick, and a blackboard instead of a guitar, the result would be a series of perfectly drawn ovals. Often, Roy would turn his back to the crowd as he played. Early on I noticed the back of the neck of his Telecaster was r ubbed raw in a o ne-inch wide pathway pathway up up the exact center. Over the years, this path had been worn away as a direct result of nothing more than Roy’s palm repeatedly passing lightly up and down the neck. He would move his hand with great smoothness, gentleness, and dexterity—he used the lightest of touches. I wondered how many passes up and down the neck of Roy Buchanan’s guitar it took to wear off that varnished finish? Undoubtedly, hundreds of thousands of ever-so-light palm passes were needed to wear off the factory varnish—perhaps a million hand passes were needed. There is
a great lesson to be learned: virtuosity comes with a price, and lifestyle change doesn’t happen overnight. While Buchanan was certainly gifted, the more he practiced, the more gifted he became. When talent collides with a serious time investment, and you add in patience and a single-minded dedication to a craft, the results are astounding. astounding. Physiological quantum leaps happen in direct proportion to the amount of quality time invested in lifestyle change. Roy didn’t baby himself; he immersed himself. In your own more limited and modest way, you too should seek to emulate Roy’s dedication to his art. Train smart, train intense, eat right, and rest big. Do copious amounts of healthy outdoor cardio training to keep the internal plumbing working at peak efficiency. Let’s Let’s follo fol low w Roy’s example and put in the work. wor k. When all the elements are in place and executed in that consistent, balanced fashion for weeks on end, synergy occurs and results accelerate. Our system relies on the expert use of basic tools with simplistic and effective methods—with periods of enforced r est and and the support support o f nutrient-dense nutrient-dense and and seasonally appropr iate food.
Transformation is achieved by implementing a bare bones basic strategy in a systematic fashion. We need to understand the simple core themes, plan how to weave minimalistic new activities into our lifestyle and reality. You must incorporate “the process” within the time constraints of your life. This takes planning, patience, and persistence, but is achievable for all.
We are not here to be your personal cheerleaders; you only need to supply t he mot mot ivat ivation ion and we’l we’lll take you t he rest o f the t he way way..
PUTTING IT ALL A LL TOGETHER TOGETHE R II STRONG MEDICINE LIFESTYLE
CHANGE—STRATEGIC PLANNING
PUMMEL THE “PENTAVERATE” Circadian disruption, chronic stress, obesity, gut inflammation and inactivity are the enemy. They are the prime sources of chronic oxidative stress and inflammation —the real re al under lying lyi ng causes ca uses of o f chr o nic disease. dis ease. The effects of each of these sources add up to cause the preventable diseases listed in the black box. To achieve optimal health of your mind and body, you will have to implement the Strong Medicine tactics from each chapter to attack each
enemy. Any of the 5 sources left unchecked will overflow your stress cup (allostatic overload), overl oad), and over time result in destr destr uction uction o f your health. health. Keep reading and we will show you how to strategically plan your own assault on chronic disease, achieving victory with optimal health.
The Strong Medicine Defensive Tactics Tactics will break br eak the links of the Pentaverate, Pentaverate, and prevent the chr chr onic inflammatio i nflammation n and oxidative stress that lead to to disease. di sease. Star Star t by assessing assessing which member( member(s) s) of the the Pentaverate Pentaverate is(are) most mo st problematic for you.
STEP 1: SELF ASSESSMENT
As Sun Tzu said in the Art kno w the the enemy and know the Art of War , “If you know yourself, you need not fear the result of a hundred battles.” As a result of your hard training tr aining,, you now know the enemy. enemy. It is time to take a look lo ok at the the curr ent stat statee of o f your mind-body and and your environment. Decide which members of the “Pentaverate of Pestilence” are your biggest enemies in your o wn pri privat vatee war against poor health. health. For some, circadian cir cadian disruption and the poor sleep that accompanies it is the biggest obstacle. Chro Chro nic stress stress affects most of us and most likely is a problem fo r you as well. well. Do Do you have recurr ent digestive digestive problems o r gastroint gastro intest estinal inal issues? Are you overweight, diabetic, or have the activity level of a three-toed sloth? You get the idea. It is cr ucial that you you do this self-assessment and be honest with with yourself. your self. Once you have identified which members of the “Pentaverate” are most problematic, you can formulate an initial assault plan.
STEP 2: TAR TARGE GETED TED ASSAULT SSAULT Once you have identified which enemy is your biggest obstacle to health, pick a few Str Str ong Medicine Defensive Tactics Tactics fr om that section. If If you ar e over weight or diabetic, pick a couple of tactics tactics in the Obesity section. If poor sleep is your biggest issue, start start with with tactics tactics from fro m the Cir Circadian cadian Disruption Section. Implement these tactics in your daily life to start your targeted assault on your selected “enemy. “enemy.” Only implement i mplement the amount of defensive tactics that you can handle at once. o nce. Change itself (even po sitive change) is is inherently inher ently str str essful. Many Many new trainees ar e super-motivated super- motivated at first and charge the enemy lines lines with with all of o f their guns g uns blazing, blazing, trying to change too much too soon. These trainees inevitably fail to truly incorporate the defensive tactics into their lifestyle change. Stick with with a few of the defensive tactics tactics and incor por ate them them consistent consi stently ly until until they no long er feel like stressful changes, but but become become part par t of your normal routine.
STEP 3: REASSESS THE BATTLEFIELD Once you have had an initial successful assault o n your enemy, enemy, go back to to STEP 1 and reassess the battlefield. Try to identify the next enemy that represents the biggest obstacle to achieving your health and fitness goals. Do not hurry and try to conquer the enemy in one massive assault by attacking all of your obstacles at once. This is what happens to millions of people every year around January when they try to “fix” themselves as part of o f a New Year Year ’s resolution. reso lution. By By mid-February mid-Febr uary they realize r ealize they have tried to make too many changes at once. Their battle plan collapses and they lose the gr ound they have gained, allowing the enemy to to advance again—lost weight is gained back, and their gym memberships go unused. This pattern pattern repeats itself itself the follo wing wing Januar Januar y. No No true pro gr ess is ever made. Our slow and methodical approach will ensure that you truly make lasting lifestyle changes which can be built upon. By the the time next year r olls ol ls around aro und,, you will be leaner, healt healthier, hier, and more mor e fit, instead instead of starting starting from fr om square one. If it takes you several years to achieve complete victory over your enemy, enemy, so be it. This is how wars are ar e won, battle by battle. battle. Instant Instant gratification with quick weight loss plans and “Hollywood” exercise progr pro gr ams will fail and have no place in true lifestyle lifestyle change.
IT’S IT’S ALL A LL CONNECTED... Using Using t he Strong Medicine battle batt le plan, plan, assaulting one o ne mem member ber of t he “Pentaverate” often causes collateral damage to the others.
Over time you will assimilate the Strong Medicine Defensive Tactics into your lifestyle. You will truly be on your way to becoming a Strong Medicine Warrior ready to r ecruit new trainees for the the war against chronic chro nic disease. disease. For those of you who like to track your accomplishments and enjoy goal setting we have created a Strong Medicine “rank structure.” The rank structure makes use of a point po int syste system; m; you will pr ogr og r ess to a higher “rank” as you accumulat accumulatee a defined number number of points.
STRONG MEDICINE TACTICS: “GOLD” = 15 POINTS
STRONG MEDICINE TACTICS: “SILVER” = 10 POINTS
STRONG MEDICINE TACTICS: “BRONZE” = 5 POINTS Points will be awarded for every Strong Medicine Defensive Tactic you incorporate successfully into your lifestyle. If you have used a defensive tactic consistently for 90 days, it is safe to say it is part of your lifestyle and you may claim the points. Some of the tactics will not apply to your situation (i.e. tactics for trainees with cancer). Do not concern yourself with missing possible points from these tactics as the rank progression in the Strong Medicine will account for the “special population” tactics (such as cancer) in the point ranges. You can promote yourself to the next rank once you have achieved the requisite points for each (note that you can also be “demoted” to a lesser rank if you lose enough points by “falling o ff the wago wagon” n” if you yo u stop consistently consistently using using a previously previo usly incorporated defensive tactic).
Use of the rank structure is not required, but can be motivating for many trainees. It will will keep you honest by forcing for cing you to periodically per iodically assess your pr ogr og r ess. As we move up the ranks, it will be beneficial to have other measures of our progress besides points. We want to see the beneficial changes that accompany promotions in the Strong Medicine rank structure. The following section on Analyt Analytics ics will cover co ver “stuff you can measure” for fo r tracking the physical, physical, physiolo physiologic, gic, and metabolic changes in your flesh machine as you progress through your battle plan. There are countless metrics we can measure as potential markers of health (biomarkers). We have picked the four biomarkers we find to be the most useful and meaningful meaningful for tracking physical physical impr ovement during lifestyle lifestyle change.
BATT BATTLE LE PLAN PLA N IV
ANALYTICS: “STUFF YOU CAN MEASURE”
“Not “Not everythin everythingg that can be be counted counts, and not not everythin everythingg that counts can be counted.” —Albert Einstein Einst ein
STUFF STUFF YOU CAN CA N MEASUR MEA SURE: E: INTRODUCTION
BIOMARK BIOMARKERS ERS AND AN D THE “HOLY “HOLY GRAIL” OF CORRELA CORRELATION TION AND A ND CAUSATION
The conceptual framework of the “stress cup”—using the concepts of hormesis and allostatic load to inform your daily health and wellness decision making— makes sense on an intellectual level. But, many of us would like some way to measure our self-experiments in lifestyle management as we wage our war against chronic disease. disease. In this section, we will cover some of these measurements, known as “biomarkers.” They can be measured with procedures like blood work and heart monitoring.
CORRELATION ≠ CAUSATION Keep in mind that many of these biomarkers only correlate with health and disease. This means that they do not necessarily cause health or disease, but are
associated with it . In the first section discussing cholesterol and lipoproteins, we’ll see that smalldense LDL and oxidized LDL measured from our blood in a laboratory test are associated with an increased risk of heart disease—but higher LDL hasn’t been pro ven to cause heart disease. In In other words, wor ds, when when heart disease is pr esent, this this type of LDL seems to be around more, but we haven’t fully determined exactly how it causes causes heart disease (although (although there are ar e some strong str ong theor theor ies). Correlations from things we can measure to disease can lead us astray if we are not very careful. This is especially true with observational studies as we discussed in the nutrition section very early in the book. Here is an example of jumping to the wrong conclusion based on correlations found in observational studies: 100,000 people filled out questionnaires regarding their lifestyle (food and activity) and any diseases that they may have. We analyze the questionnaires and find that the people who drank the most coffee had the highest rate of lung cancer. From the data we see that coffee drinking is correlated with having lung cancer. The media gets wind of our early study results and releases a story saying that drinking coffee will give you lung cancer. This scenario isn’t that far-fetched as we see stories every day in the news media about red meat, eggs, and saturated fat all
stemming from observational studies.
After coffee sales start drop as a result of the news media releasing their “coffee=lung cancer” story, we realize that we forgot to ask about smoking in our questionnaire. When we re-analyze the data, we find a very strong correlation with cigarette smoking and lung cancer. It also turned out that the coffee drinkers in
our study were also more likely to smoke. Coffee drinking was correlated with lung cancer, but was not the cause of lung cancer seen in our observational study. Smoking, a known cause of lung cancer (proven with actual laboratory studies), was not accounted for in our original study. In the study results, smoking is a confounder.
Coffee drinkers were more likely to smoke, and smokers are more likely to get lung cancer. Coffee was correlated with lung cancer because of the relation of coffee coff ee drinkin drinkingg t o smoking smoking in our o ur study, study, not because coffee causes lung cancer. The hard part with any observational study is controlling confounders. Researchers try to think of all the other possible things in the environment that could have an effect on a correlation with an exposure (coffee) and the disease (lung cancer). cancer). It It is impossible to contro l for fo r all confound confo unders—whic ers—which h is why observational studies should primarily be used to form hypotheses for future studies when a correlation is found. Finding a correlation with coffee drinking and lung cancer doesn’t make much sense from what we know about the mechanism of lung cancer. There isn’t a plausible mechanism for coffee to cause lung cancer. The researchers could have used the correlation of coffee and lung cancer to generate a hypothesis that they could test further, but certainly should never draw any conclusions that coffee Unfor tunately tunately,, this happens very often, and the news news media does causes lung cancer. Unfor all of o f us a r eal disservice by gener ating ating sensational sensational headlines. headlines. This leads to fur ther ther confusion among the general public. Invariably, another observational study will come out the the follo wing wing mo nth nth showing showing an opposite o pposite cor cor relation. We are spending time talking about this because many of the biomarkers we will discuss have correlations with disease. Some have stronger correlations than others, and some have been studied enough to approach showing that they contribute to a cause for the disease. We have to use biomarkers as “ engine warning lights ” (a car analogy) that we may be going the wrong direction with our lifestyle choices, but the biomarkers themselves may not be a cause of disease. The “witch scene” from the classic movie, Monty Python and the t he Holy Grail is a gr eat examp example le of how correlation cor relation can go wrong with with disastro disastro us consequence consequences. s. The scene starts with the villagers trying to decide if a woman is a witch, and Sir
Bedevere and King Arthur come in to “school” them on correlation and causation...
ar e ways of telling telli ng whether she is a witch. BEDEVERE: Quiet, quiet. Quiet! There are ar e they? they? CROWD: Are there? What are BEDEVERE: Tell me, what do you do with witches? VILLAGER #2: Burn! bur n them them up! CROWD: Burn, burn what do you burn bur n apart fr om witches? witches? BEDEVERE: And what Mor e witches! witches! VILLAGER #1: More VILLAGER #2: Wood! BEDEVERE: So, why do witches burn? [pause] VILLAGER #3: B--... ‘cause they’re made of wood...? BEDEVERE: Good! CROWD: Oh yeah, yeah... BEDEVERE: So, how do we tell whether she is made of wood? VILLAGER #1: Build a bridge out o ut of her. BEDEVERE: Ah, but can you not also build bridges out of stone? VILLAGER #2: Oh, yeah. BEDEVERE: Does wood sink in water? VILLAGER #1: No, no. VILLAGER #2: It floats! It floats! Thr ow her into the pond! pond! VILLAGER #1: Throw CROWD: The pond! BEDEVERE: What also floats in water? VILLAGER #1: Bread!
VILLAGER #2: Apples! VILLAGER #3: Very small rocks! Cider ! VILLAGER #1: Cider VILLAGER #2: Great gravy! VILLAGER #1: Cherries! VILLAGER #2: Mud! VILLAGER #3: Churches—churches! VILLAGER #2: Lead—lead! ARTHUR: A duck. CROWD: Oooh. BEDEVERE: Exactly! So, logically..., VILLAGER #1: If... she.. weighs the same as a duck, she’s made of wood. BEDEVERE: And therefor therefor e—? VILLAGER #1: A witch! CROWD: A witch! We shall use my larg er scales! BEDEVERE: We
DON’T GET NEUROTIC The best way to use the biomarkers covered below is to periodically monitor them so you can correlate the results with “how you are feeling”. If your periodic testing shows “bad” results, and you have gained fat mass and generally feel lousy, it stands to reason in this case the tests are reinforcing the conclusion that you are on the road to poor health. Those of you who have type-A personalities and/or obsessive “tendencies” could easily fall into the trap of stressing over this testing, or testing too frequently. The idea behind using these biomarkers is to hone your intuitive sense of your body’s state, day-to-day. Ideally, as you dial-in the ability to “listen” to your body, you will need to use the biomarker testing less and less. We’ll discuss in detail the backgro backgro und and rationale for measuring the the following fo llowing biomarkers. These sections are very technical, but are necessarily so for understanding what you are measuring and its significance—along with each biomarker’s limitations. Here’s what will be covered:
I. Lipid Panel Pa nel (AKA Cholest Choles t erol) ero l) II. Physical Measurements III. III. Markers of Inflam Inflamm mation at ion IV. IV. Heart Rat e Variabili Variabilitt y
We’ll start by measuring cholesterol, which shouldn’t be controversial if you understand the science. Unfortunately, a great deal of misunderstanding and outright misinformation surrounds cholesterol in general, not to mention the blood testing of “cholesterol.” Hopefully we can clear things up a bit before we come to the conclusion that cholesterol is “a witch.”
STUFF STUFF YOU CAN CA N MEASUR MEA SURE EI
CHOLESTEROL: CHOL ESTEROL: WHA WH AT ARE WE WE MEASURING?
“Saturated fat and cholesterol in the diet are not the cause of coronary heart disease. That myth is the greatest ‘scientific’ deception of t he century, and perhaps perhaps any century.” century.” —George V. V. Mann, M.D. M.D.
SCIENTISTS AS HERETICS Dr. Mann was one of the co-directors of the Framingham Heart Study, and spent his career attempting to determine risk factors for heart disease. His contention that cholesterol (and saturated fat) from the diet was not a contributor to heart disease was very controversial to say the least. As a society, we have been completely “brainwashed” by constant messages about the evils of cholesterol, that statements such as Dr. Mann’s are like going against gospel. Cholesterol has been demonized more even than saturated fat in the past 50 years. The marketing of “low cholesterol” foods and anti-cholesterol public health messaging has been so effective that to even suggest taking a second critical look at the basis for these recommendations puts us at risk of being labeled “medical heretics”. The anti-cholesterol movement has approached a level of religious
fervor. fer vor. As with with saturated fat in the nutr nutr ition section, let’s take take a step back, loo k at the science, science, and and make infor med opinions reg arding cholestero l.
WHA WH AT IS CHOLE CHOLESTEROL? STEROL? Before we discuss measuring cholesterol as a biomarker, it is crucial to understand the biochemistry and physiology of cholesterol and lipoproteins (more on this in a bit). Only with this foundation will you be able to make sense of the laborat labor ator or y testing testing and make infor med decisions about your health. health.
CHOLESTEROL This is what the fuss is all about...... Cholesterol is an absolutely ESSENTIAL compound for normal brain and body function. Here ar e a few of its i ts uses: • Proper Pro per cell cell membrane membrane funct function. ion. Cholestero Cholesteroll is a stabilizing stabilizing structure structure and an antioxidant antioxidant in the the cell membranes (remember our lipid pero xidation xidation discussion) that can stop membrane-damaging free radical chain reactions.
A piece of cell membrane in cr oss-section, oss-section, showing the double layer of fats fats called phospholipids, phospholipids, and cholestero cholesteroll in the ro les of membrane stabilizers stabilizers and antioxidants. Without cholesterol to stabilize the membrane surrounding the cell, our cells would need a cell wall like plants have, and would would be susceptible to damage by oxidation.
• Cholestero Cholest eroll is necessary for fo r effective effect ive nerve cell cell com co mmunication unicatio n —it is an integral part of the nerve “insulation” called myelin. Myelin is wrapped around the the axon “transmitters” “transmitters” o n nerve cells, similar to the insulation/coatin insulation/coating g on
electrical wiring. It ensures that nerve signals can be carried quickly and efficiently efficiently from fr om one nerve cell to another. another. In fact, cholesterol has been found to be the “rate-limiting step” in the formation of myelin in the brain and nerves outside the brain. In other words, the speed of myelin production depends on a steady supply of cholesterol. It is therefore no surprise that cholesterol is crucial for the developing brain during childhood, and for slowing the rate of the degeneration of brain connections in old age. Recent studies have shown that as people approach old age, those with the highest cholesterol have
been shown to live the longest. • Cholesterol Cholesterol is the the molecular building building block for the making many importa impor tant nt hormones, hor mones, including including cor tisol, aldostero aldostero ne, pro pro gesterone, testost testostero ero ne, estro estro gens, and vitamin D.
• Cholesterol Cholesterol is the the molecular building building block for making many importa impor tant nt hormones, hor mones, including including cor tisol, aldostero aldostero ne, pro pro gesterone, testost testostero ero ne, estro estro gens, and vitamin D.
A simplified pathway showing some of the important hormones made from cholestero cholestero l. The hormo nes testost testostero erone ne and estr estr ogen og en have obvious impor tance tance to us. Aldosterone is involved in maintaining electrolyte balance in the kidneys and cortisol cor tisol is a critical hor mone involved in the the str str ess response.
• Cholestero Cholest eroll is also the t he buildi building ng block for bile bile salt salt s, crucial for digestion and and absor ption of o f dietary fats f ats (and fat soluble sol uble vitamins, A, A, D, E, E, and K). K). • Cholestero l is present pr esent in significant sig nificant amounts in human breast milk—a vital component for infant brain development. Because of cholesterol’s very important functions, your body has a system to keep levels adequate for these vital functions. Because of this system, you can’t significantly significantly alter cholester cholester ol levels by changing dietary dietary intake. intake.
CAN YOU CHANGE CHOLESTEROL LEVELS LEVE LS IN YOUR BLOOD BY CHANGING HOW H OW MUCH MUCH CHOLESTEROL YOU EAT? Research has shown that most people can only change their blood levels of cholestero cholestero l about 5% in either either direction by changing changing how much cholesterol they eat in their diets. When you do get a small increase in cholestero cholestero l in your bloo d from fro m increased dieta dietarr y cholesterol cholesterol,, there there also is an increase in HDL associated cholesterol, and more of the large buoyanttype of LDL cholesterol carriers. (More about this later, but both are good things!) Changing ho w much cholestero l you yo u eat (despite (despite what you may have heard) does not alter alter blood blo od levels of cholesterol much for mo st people. people. The small change that may happen doesn’t affect your risk for heart disease, according to recent scientific studies. If you take in less cholesterol than your body needs in the diet, the body will produce more. If you take in more cholesterol in the diet, the body will produce less. The bottom line is that your body knows what it is doing with cholesterol
(even ifif you or o r your doctors doct ors don’t).
Based on the above information, it would follow from a “first principles” perspective that artificially lowering cholesterol levels with pharmacology may have unintended consequences. We are seeing more of these unintended consequences in some of the side effects recently observed by artificially lowering cholesterol levels using using drugs. dr ugs. • Memory emor y loss (cholesterol (cholesterol is needed needed for pro per nerve functioning functioning in the the brain) • Muscle damage (thoug (thought ht to be due to depletion of CoQ10, a crucial cr ucial antioxidant which shares part of the same pathway as cholesterol for its synthesis) • Erectile dysfunctio dysfunction n (possibly (poss ibly due to low lo w testoster testosterone one from fr om depleted cholestero cholestero l, testosterone’s testosterone’s building block)
QUICK QUICK MEDICAL MEDICA L NOTE: There ar e certainly some individuals individuals who who can benefit benefit from fro m cholesterol lowering medication, such as males who have already had a heart attack. Most of us can change change our “lipid pro files” in the rig ht dir direct ection ion with proper nutrition, lifestyle, and exercise—without any of the side effects listed above. Current science is starting to catch up with the “first principles,” even though many in the scientific and medical community can’t seem to let go of the idea that cholesterol itself is the problem. The current science points to problems arising from lipoproteins, the the car car riers ri ers o f fat and and cholesterol cholesterol..
KEY POINT: As we we will soo n show you, cholestero cholesteroll itself does not lead to heart disease, but certain types of cholesterol carriers that are thought to be problematic.
LIPOPROTEIN LIPOP ROTEINS S 101 Fat and cholesterol transport (carrier) molecules—lipoproteins—come in a variety of “flavors” and have very different functions. An important idea to keep in mind is that recent research has shown that it is the amount and type of dietary carbohydrate which is one of the biggest factors in how lipoproteins can “go bad”—not dietary cholesterol or saturated fat. This overview is very simplified, but hopefully the message is clear.
HDL. The major classes of lipoproteins are: chylomicrons, VLDL, LDL, and HDL You may have heard about a couple of these lipoprotein “carriers” of fat and cholesterol while talking with your doctor. The message we will keep repeating is that that none none of these ar ar e cholestero cholestero l, they they ar ar e carriers carr iers o f cholestero cholestero l!
TYPES OF LIPOPROTEIN LIPOPROTEINS S (CARRIERS) CHYLOMICRONS Chylomicrons are the primary form of lipoprotein that transport dietary lipids
(i.e. (i.e. t he fat that t hat you eat). • Triglycerides Trig lycerides (fat) from fr om the the diet associated associated with with chylomicrons chylomicro ns are tr tr anspor anspor ted ted through the lymph system first before they enter the bloodstream (except for short shor t chain chain and medium medium chain fats). fats). This preven pr events ts a large larg e amount of lipids fr om rapidly enteri entering ng the bloodst bloo dstrr eam. • Tissues Tissues with with a high need need for trig lycerides (skeletal (skeletal and cardiac muscle for energy, adipose adipose tissue for storage) storag e) have an enzyme enzyme called lipoprotein lipopro tein lipase lipase in nearby blood bloo d vessels. This enzyme separates separates the dietary dietary triglycerides trigl ycerides from fr om the the chylomicr chylomicr ons to allo w the the cell to to use the fat (for energy or o r structural structural requirements).
The picture above depicts the basic structure of a lipoprotein particle in cross-section. The actual particle is a 3 dimensional sphere. The phospholipids lining the outside have 2 tails (in black) each composed of an unsaturated fatty fatty acid. These unsaturated fats with with double bonds ar e suscept susceptible ible to oxidation (fr om our discussion discussion o f fats in Nutrition Nutrition 101). The apolipopr otein par par t of the particle particle (in red) r ed) is the the prote pro tein in responsible r esponsible for r ecognition by vario vario us receptor receptor s. The type type of apolipopro apolipo prote tein in present on the particle par ticle is the “calling “calli ng car d” that distinguishes LDL, HDL HDL,, and chylomicrons. chylomicro ns. Free cholesterol (yellow) is present pr esent in the phospholipid phospholipid membrane, helping to give it structural support and to act as an antioxidant. The inner core consists of the fats called triglycerides (in gr een) and and cholesterol cholesterol esters esters (yellow (yello w outlined outlined in orange). The cor e contains contains the the “cargo” “carg o” of o f cholesterol and tr tr iglycerides, iglycer ides, which which is delivered to to the various cells o f the body body for use. Cholestero Cholesteroll ester ester s are made of cholesterol with a “tail” consisting of various types of fatty acids.
VERY LOW DENSITY LIPOPROTEIN (VLDL) • VLDL VLDLss are ar e pro duced and r eleased by the liver. • VLDL VLDLss carr car r y int int ernally ernally produced fat and cholesterol. cholestero l. Very low density lipoproteins lipopr oteins carry carr y the the triglycerides trigl ycerides produce pro duced d fro m excess glucose when when the the liver “glycogen “glycog en tank tank”” is full. They are also the initial initial carr ier fo r cholestero cholestero l pro duced duced in the liver that is needed by tissues for the crucial functions cholesterol provides (mentioned above). • VLDL VLDLss also interact with lipopr lipo protein otein lipase, an enzyme enzyme that t hat releases fat from
utilization by other other tissues tissues for t he VLDL VLDL carrier carrier for fo r storag st oragee in fat cells cells or utilization energy or structural structural uses. • After After much of the trig lyceride lycer ide has been r emoved, the VLDL is transformed
into a relatively cholesterol-rich LDL.
LOW DENSITY LIPOPROTEIN (LDL) LDL is the carrier unfortunately known as “bad cholesterol”. It is neither cholesterol nor always bad. Its function is to carry cholesterol from the liver to supply the body’s various cells with needed cholesterol. This cholesterol is then used by the cells to perform the essential functions listed above. Under normal circumstances, the LDL travels through the blood vessels and “docks” with an LDL r eceptor at its delivery deliver y site. You can think of o f LDL as a commuter co mmuter bus that arr ives at a station station (the (the LDL LDL r eceptor) eceptor) and dro dro ps off its carg o o f cholesterol.
KEY POINT: LDL is not cholesterol, despite being called “bad cholesterol.” Cholesterol is cholesterol regardless reg ardless of o f what what car car ries ri es it. LDL LDL is a cholesterol carr ier. As always, the “devil is in the details”. It turns out that the LDL carrier exists in subclasses according to size: small-dense LDL (sdLDL), and large-buoyant LDL (lbLDL). The latest science shows that these subclasses may act VERY differently in contributing to heart and vascular disease, and the amounts of each can be largely influenced by diet. Much mor e on this soon. so on.
HIGH HIGH DENSITY LIPOPRO LI POPROTEI TEIN N (HDL) Known as “good cholesterol”, even though it also is NOT cholesterol, but another cholesterol carrier. In basic terms, this carrier takes the excess cholesterol not used by tissues, tissues, and carr ies it back to the liver.
KEY POINT: HDL is not cholesterol despite being called “good cholesterol.” Cholesterol Cholesterol is cholesterol cholestero l r egardless egar dless of what what carries carr ies it. HDL HDL is another cholest cholesterol erol carrier.
SMALL-DENSE LDL AND LARGE-BUOYANT LDL We just introduced the idea that the LDL carrier has size “sub-classes”. The differences between the two main subclasses of large buoyant LDL and small dense LDL are much more than just size—they act very differently in the body for the development of heart disease. Both types of LDL carry cholesterol. The cholesterol they carry is identical,
but the carriers themselves are different. Just as you are the same person whet whether her you travel t ravel by by bus or by t axi. axi. The different types of LDL, small-dense and large-buoyant are formed from VLDL. Genetic factors determine the ratio of lbLDL to sdLDL someone has, but what we eat is a huge player in how much of each will be formed. The key point to understand is that the cells in your body need cholesterol and the the liver makes the the lipoprotein lipopr otein carr iers which which deliver the amount of cholesterol the the body needs at any one time. Large-buoyant LDL carries more cholesterol than a small-dense LDL carrier, so it takes fewer large-buoyant LDL particles to carry t he same same amount amount of cholesterol. cholestero l. If you are making small-dense LDL particles, you need more of them to carry enough cholesterol to meet the body’s demands. This has extremely impo r tant health consequences as we we will see shor sho r tly. tly. Put simply, think of large buoyant LDL as a commuter bus that can carry many “passengers” (cholesterol) and small dense LDL as a taxi that can carry far fewer “passengers” “passengers” (cholesterol). (cholesterol ). The following section will use the “commuter bus” and “taxi” analogy to show you how the different types of lipoproteins are formed. Once you understand this, you will better understand the lab tests your doctor draws to look at your cholestero cholestero l levels.
CHOLESTEROL “TRANSPOR “TRA NSPORTA TAT TION” To briefly review, lipoproteins are the carriers of fat (triglycerides) and cholesterol:
• Chylomicrons are the carriers that transport the fat and cholesterol that you get directly fro m food fo od when you you eat. ar e the carr carr iers that that tr tr anspor anspor t the the fat (tr (tr iglycerides) iglycer ides) and • VLDL and LDL are cholestero cholestero l made or processed pro cessed in the the liver. tr anspor anspor ter ter of cholesterol cholestero l from fr om the liver to the the rest of the • LDL is the primar y tr body.
• HDL is the carrier that takes any excess cholesterol from the body and transports it back to to the the liver for “recycling.” “recycling.” The process starts when VLDLs are made in the liver and “packed” with triglycerides (fats) and cholesterol. The amount of triglycerides in each VLDL depends on your diet and your “metabolic health.” A quick review of STEP 6 in the Diabesity Intervention section will remind you that excess glucose and fructose in the diet will be made into triglycerides (fat) by the liver. Also remember from the Diabesity section that if you have insulin resistance or diabetes, the fat cells are not doing their storage job well and are releasing triglycerides to be processed back in the liver. Both excess sugar in the diet and insulin resistance will cause more triglycerides to be either created or processed by the liver (usually both are happening). These triglycerides are packaged into the VLDL carriers by the liver, in the hope that they can be delivered to muscle or fat cells for use or storage. The liver is trying to get the triglycerides out of the liver so they don’t build up and become toxic (as in forming a “fatty liver”).
VLDL packed with triglycerides with a small amount of cholesterol.
If ther ther e are high amounts of triglycerides trig lycerides fro m excess excess dietary dietary sugar and/or insulin i nsulin r esistance, the the “packaging” pro cess will lo ad the VLD VLDL L with with trig lycerides, lycer ides, without without much roo m left for shipping shipping out the the cholesterol to the body body..
VLDL with more cholesterol as “cargo” and fewer triglycerides.
A healthy person who doesn’t eat excess sugar or have insulin resistance will not have an excess of trig lycerides lycer ides cr eated in the the liver. When the the VLDL VLDL is made to transport triglycerides trig lycerides and cholesterol cholesterol out to to the body, body, there there is mor e ro om to “package” cholesterol in the VLDL because there are not as many triglycerides around. The VLDL will leave the liver and travel to deliver the triglyceride cargo first to muscle or fat cells for energy use or storage. Once the triglyceride cargo is offloaded, the VLDL undergoes processing and is transformed into a LDL. The LDL is left with a cargo of cholesterol to deliver to the body.
The type of LDL formed depends on how much triglyceride content was present in the original VLDL. • A VLDL VLDL that was “stuffed” with trig lycerides lycer ides will will be transfor transfo r med into a small dense LDL after the triglyceride cargo is dropped off. The resulting small dense LDL has relatively little cholesterol cargo, because there wasn’t much room for cholestero cholestero l in the the or iginal triglyceride-pac trigl yceride-packed ked VLD VLDL. L.
• A VLDL VLDL with a “nor mal” amount of tr tr iglycer ig lycerides ides and mo morr e cholesterol cholester ol,, will be transformed transfor med into into a larg l arge-buoyan e-buoyantt LDL LDL once the the triglyceride trig lyceride carg o is dropped dro pped off. The large-buoyant lar ge-buoyant LDL LDL has more mor e cholesterol cargo carg o because because there there was mor e room for cholesterol in the original VLDL.
LARGE-BUOY LARGE -BUOYAN ANT T LDL (LBLD (LBLDL) L) Large-buoyant LDL LDL for med fro m nor mal VLDL VLDL carr y a relat r elatively ively larg e amount of cholesterol cargo carg o on each “particle” of lbLDL. lbLDL. These particles travel to the cells in your body that need cholesterol and drop off their “cargo”.
When the lbLDL arrives at a cell to drop off cholesterol, it pulls up to a designated “statio “station” n” (like a bus pulling pulli ng up to a bus station). The “statio “station” n” is an LDL receptor. The lbLDL particle “docks” with the LDL receptor to drop dro p off the the cargo carg o of cholester cholester ol. This is what LDL LDL particles are supposed to do as a transpor transpor ter ter o f cholester cholester ol.
The larger lbLDL particles are also less prone to damage from free radicals radicals and can stay in the bloodstream bloo dstream long longer er without becomin becomingg oxidized. The lbLDL is like li ke a commuter bus with with cholesterol cholester ol as passenger s. A bus is larg e, sturdy sturdy,, less pro ne to damage, and also also less likely to be in an accident while while traveling—much tr aveling—much like l ike an lbLDL particle.
The lar ge-buoyant ge-buo yant LDL LDL “Commuter Bus” packed with with cholesterol cholester ol..
INNOCENT INN OCENT BYSTAN BYSTANDE DER? R? The cholesterol theory of heart disease started early in the 20th century after cholesterol was found in the walls of the arteries from people who had recently died from heart attacks. This finding started the demonization of cholesterol as a cause of heart disease, especially in the last 50 years. Recent science has shown that cholesterol itself that is not leading to the buildup of plaques and narrowing of the arteries, but the lipoprotein carriers, especially the small-dense LDL LDL we we just descr ibed.
SMALL-DENSE LDL (SDLDL) The small-dense LDL particles formed from triglyceride-packed VLDL don’t act like the large-buoyant LDL. First, they are only transporting a small amount of cholester cholester ol, so it takes takes more o f them them to carr y the the same amount of cholesterol “passengers” than the large-buoyant LDL.
Small-dense LDL particles (sdLDL) are also more susceptible to damage by free radicals, which turns them into a highly reactive and dangerous particle called cal led “oxidized “o xidized LDL” LDL” (oxLDL). (oxLDL). Small-dense LDL particles are also more likely not to arrive at the designated designated “stations” “stations” (LDL (LDL r eceptors) eceptors) to deliver their their cholestero cholestero l cargo car go..
T hey are more more likely likely to get in “accid “accidents”—st ents”—st uck in in the t he walls walls of your yo ur arteries. To summarize, the sdLDL is a particle that can’t carry much cholesterol, is susceptible to damage by free radicals, and gets into “accidents” by crashing into the walls walls of your yo ur ar ter ter ies. They are also not r eliable for arr iving at the the designated designated drop-off dro p-off stations stations for cholestero cholestero l.
The small-dense smal l-dense LDL “taxi” with with little cholester ol. ol . Early studies showed that cholesterol is present in “artery clogging” plaques, and that continues to be true. We now know that cholesterol was more of an innocent bystander, carried into the walls of the arteries by the lipoprotein carriers, especially small smal l dense LDL. LDL. Blaming cholesterol for causing artery plaques is like blaming the fare-paying taxi passenger for an accident on the interstate. The passenger (cholesterol) was just r iding in the taxi, taxi, and had nothing to do with the the accident. The faulty logi lo gicc would be: we found the passenger at the scene of the accident, so they must be responsible for the damage. It obviously makes no sense to leap to the conclusion of blaming the passenger, so why are we doing it with cholesterol?
The large-buoyant LDL (lbLDL) are operating as they should, transporting large amounts amounts of cholester cholester ol from fr om the the liver, thro thro ugh the bloodstream to their their designated designated “stations” (LDL receptors) on the various cells in the body that need cholesterol for the vital vital functions we discussed at the the beginning of this section. Large-buoyant LDL—for the most part—don’t cause problems by crashing and lodging themselves into the sides of the artery walls. Many medical providers and public health entities continue to refer to the cholesterol carried by LDL particles in general as “bad cholesterol.” The lbLDL is unfortunately lumped in as “bad cholesterol,” even though your doctor does not measure what types of LDL particles you have; they only measure the cholesterol passengers. We will discuss this much more very soon.
This is a “cross-section” “cr oss-section” of an artery. Imagine Imagine looking lo oking at your artery as you would the end end of a gar den hose. You You can see the lumen where the blood bloo d travels has no narrowing narr owing or o r “blockages”. The healthy healthy cholestero cholesteroll transport transpor t syste system m of mostly lbLDL lbLDL is operating cor co r rectly and not causing causing problems. pro blems.
The small-dense LDL particles (sdLDL) are very prone to cause serious problems in the the walls walls of your arteries while carr carr ying their their “cargo “car go”” of cholesterol alo ng with with them. The sdLDL can bind with the artery walls in places that they are not supposed to bind. These are unap-proved stops in their journey to deliver cholesterol. Instead of stopping stopping at designated designated dropoff dro poff stations stations (LDL r eceptors) eceptors) for their their cholestero cholestero l passengers, sdLDL particles are prone to “crash” into the walls of the arteries, damaging the cells lining the the arte ar terr ies (endothelial (endothelial cells). Once the sdLDL sdLDL particle penetr penetr ates the the endothelial cells cel ls lining l ining the artery arter y wall, and move into the muscular muscular layer of the the arte ar tery, ry, they they are r eadily oxidized by free r adicals. Now Now the sdLDL sdLDL is a highly hi ghly r eactive oxidized LDL (much like a car car o n fire after after crashing into the guard rail). rail ). The immune system system go es on high hig h alert. Cells Cells of the “innate “innate guardi g uardian” an” immune system, known as macrophages, respond to the scene of the accident, accident, much like police do in an automobile automobi le accident on the interstate. interstate. These macrophages “know” that the sdLDL particle (with cholesterol passengers) is not supposed to be inside the artery wall. To protect the body from this reactive oxidized oxidi zed sdLDL, sdLDL, the the macrophag macr ophages es engulf the sdLDL sdLDL particle. The macrophag macr ophages es that engulf the sdLDL sdLDL particles turn into foam cells. The body recruits r ecruits mor e of the the immune system system to wall the the area ar ea off, turning the area into an atheroma. This atheroma atheroma bulges up thro thro ugh the artery wall fro m the inside and leads leads to the narrowing narr owing of o f the arteries in heart disease.
Looking at the cross-section of the artery again, the atheroma described below has narrowed the area in the artery where blood flows (lumen). Also note that the area of the athero athero ma is hig hly inflamed. This is ho w sdLDL sdLDL in particular, par ticular, contributes contri butes to to heart disease. Imagine this process in the very small blood vessels supplying your heart. Over time the the narr owing will become worse, leadi leading ng to t o a heart heart attack att ack..
TESTING CHOLESTEROL When my doctor tests my cholesterol, what are we testing? The typical lipid panel (cholesterol test) reports HDL cholesterol, VLDL, triglycerides (TG), total cholesterol, and LDL cholesterol. The VLDL, LDL, and HDL numbers represent the amount of cholesterol associated with these
lipoproteins. In other wor ds, we we are ar e measuring the the amount of cholestero l “passenger “passenger s” that that are riding ri ding on each of the different different car car rier ri er lipopro lipo prote teins. ins.
KEY POINT: Convent Conventional ional cholestero cholestero l labor atory tests tests only o nly measure the amount of cholestero cholestero l (passengers) associat asso ciated ed with with each type type of lipopro lipo prote tein in carr ier. These values tell us very little about the number and size of the lipoproteins themselves. Additionally, the value measured for LDL-associated cholesterol is not even a direct measurement, it is calculated by a mathematical formula known as the Friedewald Friedewald equation equatio n. The Friedewald equation gives us only an estimate of the passengers (cholestero (cholestero l) being carr ied by LDL LDL particles.
THE FRIEDEWALD EQUATION To estimate the amount of cholesterol associated with your LDL particles, the following equation is used:
LDL LDL cholesterol cholestero l = tot to t al cholest cholesterol erol - HDL HDL cholestero cholesteroll - trigly t riglycerid cerides/5 es/5 Again, the LDL cholesterol tests are measuring cholesterol “riding” on LDL carriers, and do not tell us how many LDL carriers are present or what type of LDL is present. Both of these missing pieces of information are extremely important
t o predict predict your risk of developing developing heart and vascular vascular disease.
Conventional cholesterol cholestero l test ing ing is measuri measuring… ng… cholesterol passengers… and is not measuring lipoprotein carriers.
Knowing your particle number and particle size is important because recent research shows that both are more predictive of developing heart disease than just measuring the amount of cholesterol passengers associated with the LDL particles. To illustrate il lustrate why this this makes sense, let’s let’s create cr eate a scenario .
“PA “PATIENT TI ENT A” Patient A goes to his doctor and has a cholesterol test. His results show a (calculated) LDL cholesterol of 150 mg/dl. His doctor is concerned and says it is too high. He is told to reduce the amount of cholesterol he is eating in his diet—this advice continues to be given despite the science! After arguing with his doctor, he is given gi ven a second test that that evaluates evaluates his LDL particle size and number. The results r esults show a relatively low actual LDL particle (carrier) number, and mostly large-buoyant LDL LDL par particles ticles (mo stly “buses”).
Patient A has mostly “commuter buses” carrying his cargo of 150 mg/dl of cholesterol, and the actual number of the buses was normal when checked, but he was given advice to lower his cholesterol based only on the initial blood test showing 150 mg/dl of cholesterol “passengers.” Patient A has a relatively low heart attack risk with our information on particle number and size, despite his “high” initial cholesterol test.
“PATIENT B” Patient B comes in the following day for his annual check up. He gets his cholesterol test and it shows an LDL (calculated) cholesterol level of 125 mg/dl. His doctor tells him his “bad cholesterol” level is pretty good, but a little on the high side, and tells him he should watch how much cholesterol he eats. One month later, Patient B has a minor heart attack and was found to have blockages in the small arteries o f his heart. He He gets a stent placed and and the cardio cardiolog log ist caring for him in the hospital also orders an LDL particle size and particle number test.
The test results show a higher than normal particle number and mostly smalldense LDL LDL particles par ticles (mostly (mo stly “taxis”). “taxis”). Patient Patient B is mystified and tells the cardiolo cardio logi gist st that that his “bad “bad cholester cholester ol” was was nor mal on o n a check-up check-up 1 month ago. The cardio log ist explains that although the amount of cholesterol “passengers” counted was normal, they are being carried on a high number of small-dense particles, known to correlate cor relate strong ly with with heart disease. You can see how Patient A could have a larger amount of cholesterol “passengers” carried in his large-buoyant LDL commuter buses, than Patient B. but have a fewer number of particles (he has a fewer number of “buses” than Patient B has “taxis”). Unfortunately, Patient B had a larger number of LDL particles overall, and most were of the small-dense type associated with heart and vascular disease. Because the small-dense particles carry less cholesterol per particle, the standard cholesterol test came back as normal because it was just count c ounting ing the t he passengers. passeng ers. Patient A had more passengers overall, but less LDL particles, because his largebuoyant LDL particles can carry more passengers. The large-buoyant LDL particles are also less likely to cause problems in the walls of his arteries. His “high bad cholesterol” in this case was not a risk to his heart health. The different scenarios of Patient A and Patient B show some of the problems with relying solely on conventional cholesterol testing when figuring your risk for heart disease. However, the conventional lipid panel is far from useless. We will show you how to gather some very valuable information from this test outside of the LDL LDL cholesterol cholester ol amount. First, Fir st, let’s let’s discuss particle size si ze in a bit mor e depth. depth.
WHAT AFFECTS MY LDL PARTICLE SIZE? While genetic genetic factors certainly predispose some people to have mor e small-dense LDL, nutrition plays a larger role for most people in determining how much large-buo lar ge-buoyant yant vs. small-dense small- dense LDL they have.
KEY POINT: Genetics contribute, but nutrition plays the largest role in determining LDL particle size. We already discussed the role of nutrition in particle size previously, but it bears repeating: Forming small-dense LDL particles happens from the following diet and lifestyle factors: • Consistently eating mor e sugar and starch than your body can handle leads to mor e triglycerides triglycer ides made made fro m the the excess excess sugar. • Insulin Insulin r esistance from fr om inflammation inflammatio n and oxidative stress (diabetes, obesity, to decreased fat storage storag e poor poo r sleep, gut g ut inflam inflamm mation, at ion, chroni chro nicc stress) st ress) can lead to in fat cells (they are al r eady stuffed stuffed full with fat). The excess comes co mes to the liver for processin pr ocessing. g. • The liver deals deals with with the the triglycerides triglycer ides (fat) (fat) from both of these these sources sour ces and packages the trig lycerides lycer ides into VLDL VLDL.. These VLD VLDL L are ar e stuffed with tr tr iglycer ig lycerides, ides, and have little little room ro om for fo r cholestero l. • A small-dense small- dense LDL LDL is formed for med after the the trig lyceride-stuffed lycer ide-stuffed VLDL VLDL dro ps off the the triglycerides. You can see that excess starch and sugar coupled with insulin resistance is
primaril primarilyy responsible res ponsible for fo r for f orm mation at ion of o f sm s mall-dense all-dense LDL. LDL. If you are ar e already alr eady insulin r esistant, esistant, and eat a diet heavy in starch and sugar, the fat in the diet will contribute to formation of small-dense LDL by increasing triglycerides further. However, fat in the diet is not the specific underlying problem as many would have you think. The problem is fat eaten with sugar and starch in an insulin r esistant state. state.
TECHNICAL NOTE: The type of fat that you eat is also very impor i mpor tant. tant. High amount amo untss of of omega-6 PUFA PUFA in vegetable vegetable oils from fr om fast foo d and processed foo d will increase inflammation, oxidative stress, and worsen insulin resistance. As insulin resistance becomes worse, it will decrease carbohydrate tolerance, resulting resulting in mo r e triglycerides trigl ycerides produce pro duced d and pr pr ocessed by the the liver—leading to mo r e sdLDL. sdLDL. The sdLDL sdLDL that that is for med is mor e pro ne to oxidation as some o f the omeg a-6 PUFA PUFA will be inco r por ated into into the sdLDL sdLDL particle.
Notice that cholesterol in the diet does do es not lead to small-dense LDL. Reducing cholesterol in the diet only causes the body bo dy to produce prod uce more cholesterol “from scratch” as needed.
Forming large-buoyant LDL particles happens when you are insulin sensitive and don’t eat more starchy carbohydrate and sugar than your body can handle. The liver does not have to produce triglycerides from excess sugar and starch, and the fat cells cells are ar e able to to stor e triglycerides trigl ycerides so the liver does not have to to pr ocess them. them. • With fewer tr tr iglycer ig lycerides ides for fo r the the liver to package package in VLDL VLDL,, a “nor mal” VLD VLDL L is formed with more room for cholesterol “passengers.” • After After the the small amount of tr tr iglycer ig lycerides ides is dropped dr opped off, off , the VLDL VLDL is transformed into a large-buoyant LDL. • Not eating high amounts amounts of pro-inflam pro -inflammator matory y omeg a 6 PUFA PUFA will also help reduce inflammation, reduce oxidative stress, and help maintain insulin sensitivity leading to fewer triglycerides and more lbLDL.
TECHNICAL NOTE: Eating Eating more mo re dietary cholesterol causes causes your body to produc pro ducee less cholestero cholestero l. Any Any short-t shor t-term erm small increase in cholester cholester ol in i n the the body fro m eating eating more mo re cholesterol cholestero l will cause a small short-t shor t-term erm incr ease in largebuoyant LDL, not small-dense LDL. Most dietary dietary satur saturated ated fat has the same effect of a shor t-ter t-term m small increase incr ease in lar ge-buoyant ge-buo yant LDL LDL.. Satur Satur ated fat and cholesterol cholester ol in the diet also increase the amount of HDL, the cholesterol scavenger (known as “goo d cholester cholester ol”). The only satur satur ated ated fat to to avoid avo id is the proinflammatory palmitic acid that we have discussed extensively in previous sections.
IS ST STAN ANDA DARD RD CHOLESTEROL CH OLESTEROL TESTING USELESS? There is some very useful information in a standard cholesterol test (commonly called a lipid panel), without resorting to testing for particle size and particle number. I. It is generally gener ally accepted accepted that higher HDL-associated cholesterol cholester ol levels are correlated (remembe (r ememberr cor relation vs. causation) causation) with with a lower r isk of heart disease. A high HDL-associated cholesterol cholester ol value says that HDL HDL is doing do ing a go od job jo b of carr car r ying excess cho lester ol back to the liver. li ver. As As cholester cho lester ol itself is not no t causing vascular disease, it is unclear what the actual mechanism resulting in is not much decreased risk may be, but it is an active area of research. T here is
more we can say about HDL, except that higher levels generally show lower risk of heart disease. disease.
KEY POINT: High HDL-associat HDL-associated ed cholestero cholesteroll is well well cor co r related with with a lower r isk of heart and vascular disease. II. High tri triglyceri glycerides des are well well cor related with with a higher r isk of heart disease. disease. The medical community community generall generally y used used to to ig nore nor e the the triglyceride triglycer ide level level on labor ator ator y
tests tests unless it i t was was very ver y high. hig h. We have established a pretty strong stro ng mechanism m echanism showing how high triglycerides triglycer ides lead to the for mation mation of small-dense small-dense LDL— LDL—aa strong risk factor for heart disease. As we have repeatedly discussed, high trig lycerides lycer ides are ar e associated asso ciated with with obesity, obesity, diabetes, and fatty fatty liver disease, which are all inflammatory diseases. We also know that heart disease is primarily an inflammatory disease and is accelerated by obesity and diabetes. More medical providers pro viders are paying closer atte attent ntion ion to trig lyceride levels for this this reason. r eason. III. III. A patter pattern n usually usually seen on standard lipid panels panels is high trig lycerides lycer ides with with low lo w HDL. HDL. It is also common comm on to have lo w tr tr iglycer ig lycerides ides associated asso ciated with with high HDL levels. Recent science has shown that the HDL/tri HDL/triglycer glyceride ide ratio is a better standard d LDL cholesterol cholester ol predict predictor or of o f risk of heart disease disease and diabetes diabetes than standar levels: • High HDL HDL and low lo w trig lycerides lycer ides = LOW RISK • Low HDL HDL and high trig lycerides lycer ides = HIGH RISK IV. There Ther e is also a patter pattern n seen with with the HDL HDL/tri /trigl glyceri yceride de ratio and LDL LDL particle par ticle size:
WH AT NUMB WHA NUMBERS ERS ARE “GOOD” ON THE STANDARD LIPID PANEL? First remembe r ememberr that that any any lab values on cholesterol testin testing g are only cor r elated elated with with health and disease. Remember to use them as “engine warning lights” and make sure they are viewed in the context of any other risk factors for heart disease you may have. Family history of heart disease, high blood pressure, obesity, diabetes, and smoking all are well-known risk factors for heart and vascular disease. The lipid panel panel (cholesterol (cholestero l and trig lycerides) is just another another piece of o f the puzzle. puzzle. We have just spent a great deal of time showing the differences between largebuoyant and small-dense LDL, especially sdLDL’s proposed contribution to heart and vascular disease. Keep in mind that all the risk factors listed above contribute to the development and progression of heart and vascular disease, and the underlying main mechanisms mechanisms of o f disease are chronic chro nic inflammation inflammation and oxidat o xidative ive stress.
“Bad” lipid profiles such as the pattern of low HDL, high triglycerides, and small-dense LDL are usually seen in the setting of inflammatory conditions such as diabetes, obesity, and high blood pressure. Most people with heart disease have most of the risk factors present at the same time, not just unfavorable lipid panel values in isolation. “Fixing” obesity and diabetes lowers inflammation and oxidative stress, and often “fixes” high blood pressure and abnormal lipid panels, changing smalldense LDL LDL to lar ge-buoyant ge-buo yant LDL LDL without without directly dir ectly “tr “tr eating” cholestero chol esterol. l. The purpose of this long-winded discussion is to emphasize that we shouldn’t be looking at any of these laboratory tests in isolation, without taking other factors into account. We should also avoid the habit of “treating” laboratory values, instead we need to treat the person, and often the lab values “fix” themselves. Use the lipid panel as one of the measures to gauge your progress in your pursuit of health. All this this being said, below are so me suggest sugg ested ed targets for the the traditional lipid panel:
PATTERN A (FAVORABLE)
• Triglycerides Trig lycerides 100 mg/dl or less • HDL HDL 60 mg/dl mg/ dl or g r eater • LDL-associated LDL-associated cholestero l may vary, but this patt patter ern n is generally general ly associated associ ated with with large-buo lar ge-buoyant yant LDL LDL particles Note that that the the triglycer trig lyceride ide target targ et is set at 100 mg/dl or less. Most Most tests set “nor mal” at less than 150 mg/dl. My My bias is to set s et the the target targ et a bit lower fo r triglycerides. I don’t consider 150 mg/dl to be “metabolically healthy.”
PATTERN B (UNFA (UNFAVORA VORABLE BLE)) • Triglycerides Trig lycerides 150 mg/dl or great gr eater er • HDL HDL 40 mg/dl mg/ dl or less • LDL-associated LDL-associated cholestero l may vary (can be “nor mal”), but this patt patter ern n is generally associated with small-dense LDL particles
TECHNICAL NOTE & RESEARCH UPDATE : Tests to measure LDL particle size are currently available but sometimes don’t give consistent results. The tests will likely become more reliable as technolog technology y impro ves, so ask your doctor which which test test is curr ently ently the most reliable if you want to test particle size directly (especially if you are considering starting starting medication). medication). The NMR test for particle number is currently the most reliable and can be very useful if you are ar e trying to sort so rt out o ut a confusing confusing lipid panel, and and are trying to make a decision about starting medication.
Current Current science science shows t hat t he tot t ot al LDL LDL particle num number (not LDL LDL cholesterol cholestero l number) number) has the t he best correlation with heart disease. disease. A high high LDL particle number is often associated with small-dense particle size (but not always).
IT GETS MORE COMPLICATED ....... Believe it or not, the topic of cholesterol and lipoproteins is even more complicated. No wonder people are confused! Here are some highlights for those who want to dig deeper: • Lipoproteins Lipopr oteins such as LDL LDL are ar e involved invol ved in the immune r esponse to bacterial invasion, and are elevated when we have to fight off an infection. If your blood work is done do ne during this time, time, your numbers may be abnormal.
• The amount of LDL LDL r eceptors eceptor s (“statio (“stations”) ns”) can change in r esponse to various vari ous situations. For instance, thyroid hormone controls how much LDL receptor is made. If you have low thyroid function (hypothyroidism), you will have low LDL receptors. Low LDL LDL r eceptors eceptors can cause cause some major problems: pro blems: — The lipopr lipo proteins oteins need to “dock” with with the LDL LDL r eceptors (“statio (“stations”) ns”) to offload offlo ad their their cholesterol car go for the the cells to to use. — If there there are not enough LDL LDL r eceptors eceptors (“stat (“stations” ions” to drop dro p off passenger passengers), s), the normal sized large-buoyant LDLs stay in the bloodstream longer. — The longer lo nger the the LDLs LDLs stay in the bloodstr blo odstream, eam, the mo morr e susceptible they are ar e to oxidation o xidation (even lar ge-buoyant ge-buo yant LDL LDL). ). You You can think of o f this as a ship shi p in the water water too long l ong.. Even the the hulls of o f the best-made best-made ships will r ust if they are in the water for long enough. — “Fixing” “Fixing” a poor ly functioning functioning thyro thyroid id can “fix” your cholestero cholestero l and lipoprotein lipopr otein problem pro blem by making making mor e “stations”(L “stations”(LDL DL receptors) for LDL LDL particle “docking.” • Statin-ty Statin-type pe cholesterol cholester ol dr dr ugs don’t change the propo pr oporr tion of small-dense small- dense LDL; LDL; they theoretically may even make the proportion worse. This may be because one effect of statins is to cause cells to make more LDL receptor. This is good for the large-buo lar ge-buoyant yant LDL LDL,, but remember that small-dense small- dense LDLs LDLs don’t bind well to normal nor mal LDL receptor “stat “stations. ions.”” This will preferentially pr eferentially leave mor e small-dense LDL in circulation—and small-dense particles are more easily oxidized! There are plenty of people having heart attacks with “normal” cholesterol while taking statins. This may be why.* why.* *A r ecent ecent article by a gr oup of researchers resear chers addressed the the observat obser vations ions that statin-t statin-type ype drugs make the the propor pr opor tion of small-dense small-dense LDL gr eater eater during cholesterol lowering therapy. While it is true that the clinical significance of the higher small-dense LDL proportion with statin therapy is somewhat uncer uncer tain, tain, there there is strong stro ng biolog bio log ical plausibility plausibility to support suppor t the the alter alter ed proportion of small-dense LDL may indeed be problematic. The point of this technical note is that the researchers authoring the article in question dismissed the increase in proportion of small-dense LDL with statin statin therapy as a potent po tentiall ially y pro blematic finding. finding . Of particular interest
is that t hat ALL ALL of t he autho authors rs of t his his paper paper had strong stro ng tie t iess to t o t he pharmaceutical companies that make statin drugs. Several of the authors are even employees of the pharmaceutical companies, making t heir heir opinions/findi opinions/findings ngs subject to t o massive massive pot potential ential conflict conflict of int int erest. erest . This type type of conflict of int i nterest erest in cholesterol r esearch is unfor tunat tunately ely far
from rare. • The amount of oxidative oxidative stress and inflammation inflammation pro pro duced duced from fr om pro pro cessed food, environmental pollution, and metabolic derangement (diabetes) contributes to how fast LDL LDL is oxidized o xidized in the bloo dstream. • Small-dense LDLs LDLs carr car r y a r elatively low lo w amount of chol cholestero esteroll with each sdLDL sdLDL particle. Remember that cholestero l itself i tself is an antioxidant, antio xidant, and and the low amount of cholesterol may be a reason for the the increased oxidation rate of sdLDL sdLDL.. The subject of lipoprotein and cholesterol is complex enough even at this level to make your head swim when wondering how to really interpret your lab values. The bottom line is that laboratory values for cholesterol and lipoproteins only correlate with health and disease. Although we are getting a pretty good idea that oxidized lipoprotein particles and their interaction with our immune system play a MAJOR ro le is the the development development of heart disease, they they still still just j ust represent a stro stro ng corr co rr elation elation with the disease process. We still can’t definitively call what we measure in blood work causative causat ive.. There are so many other factors in play and context is extremely important.
SUMMARY, TAKE SUMMARY, TAKE H OME ME MESS SSAGE AGES, S, CONSIDERATIONS 1. High trig lycerides lycer ides and low lo w HDL HDL usually indicate an unfavor able metabolic state state and can be gr eatly modified modifi ed by diet. 2. High trig lycerides lycer ides and low lo w HDL HDL are ar e often of ten associated associ ated with small-dense LDL, LDL, which which is more mo re suscept susceptible ible to oxidation and for mation mation o f ather ather osclerotic oscler otic plaques. plaques. High triglyceride trigly ceridess and low HDL HDL are strong strong predictors of i nsulin resistance resis tance and diabetes. 3. Very high overall over all cholestero cholestero l numbers numbers on a lipid profile pro file (high total total cholesterol and high LDL—even high HDL) can be due to several underlying issues which need to to be addressed: addr essed: • Poor thyr thyr oid funct function: ion: treat the the thyro thyroid id and cholestero cholestero l numbe numberr s will likely improve. • Recent infection: lipopr lipo proteins oteins are ar e involved invol ved in the immune r esponse to invading bacteria.
• An underlying underlying genetic genetic abnormality resulting in poor LDL receptor funct function. ion. This is called familial hypercholesterolemia. Be sur sur e to discuss this possibility with your doctor, especially if there is a family history of the condition. • Very er y high cholestero l levels are ar e often associated associ ated with an LDL LDL r eceptor eceptor dysfunctio dysfunction n and should be appro ached cautio cautiously. usly. Remember that even largelar gebuoyant LDLs left in circulation too long are susceptible to oxidation. 4. Look Loo k for number patter patterns ns moving movi ng in the r ight ig ht direction, dir ection, and don’t get too hung up on the specific numbers themselves. For instance, triglycerides decreasing below 100 with increasing HDL is generally a good sign. Don’t wring your yo ur hands hands over o ver whether whether a triglyceride trigl yceride value of 70 is better better than than 80. 5. Curr ent science shows that total LDL particle cholester ol part icle number number (not LDL cholesterol number) has the best corr cor r elation with heart disease. High LDL particle number is usually associated asso ciated with with small-dense par ticle size (but not always). Hig High h total LDL particle numbers may require statin use while the underlying cause (genetic, thyroid, etc.) is being determined. 6. Dietar Dietary y cholesterol cholester ol (and most saturated fat) has very little to do with with heart disease risk. Altering how much you eat either way does little to change blood cholesterol cholester ol levels. Maybe Maybe Dr. Mann isn’t such a heretic her etic after all. al l. 7. Labor Labor ator ator y values values of lipoproteins lipopr oteins and cholester cholester ol are correlates of disease or health. Remember to use them as “engine warning lights”. The body is INCREDIBLY complex and we haven’t completely figured out all of the moving parts. Hopefully this section at least gives you the knowledge to clear up misconceptions and misinformation, and can help you make a more informed decision regarding your health. If you are still somewhat confused, you are not alone. As science advances, we will get a clearer picture of the role lipoproteins and cholestero cholestero l play in our health. health. If all we we have done done is to stop you fr om saying “goo “g ood d cholesterol” and “bad cholesterol,” then it has all been worth it!
STUFF YOU CAN MEASURE II
PHYSICAL MEASUREMENTS MEA SUREMENTS
AN UNHEAL UNH EALTHY THY OBSESSION OBSESSION WITH WEIGHT In popular culture, measuring lifestyle change success has focused on “weight loss” as measured on the scale. People often brag about how much weight they have lost in short amounts of time on the latest fad diets. Rapid weight loss often comes with with radical r adical caloric calor ic r estr estr iction, and as discussed discussed previously, previously, a significant sig nificant amount of the weight is lost from valuable muscle mass. But, it is not just popular culture that is centered on weight as a measurement of health. The scientific and medical communities co mmunities have long lo ng used the Body Mass Index Index (BMI) as a health marker. The BMI formula incorporates height along with weight and is the method currently used to determine if someone is “normal,” “overweight,” or “obese.” Recent science has shown that BMI may not be the best marker to gauge body fat and health. The problem with using BMI is that it does not adequately account for muscle mass.
• People with large lar ge amounts amounts of muscle mass can be classified classifi ed as “over weight” even though their body fat per centage is low lo w. Many Many athletes’ athletes’ BMIs BMIs catego catego r ize them as “overweight” when it is obvious by looking at their lean bodies that they are far fro m overwe over weight ight or unhealt unhealthy hy.. • People with very ver y low lo w muscle mass (not a go od thing) are ar e categor ized by BMI BMI as “normal” even though they have a significant amount of body fat and may even have a metabolic disease such as insulin resistance or diabetes.
“NORMAL WEIGHT OBESITY” Using the weight-focused BMI has given us a new classification of unhealthy people— normal normal weight obese . These people have a “normal” BMI, but also have a high amount of body fat as compared to their muscle mass. They often carry this excess body fat around their midsection (central obesity). Recall from the Obesity chapter that this type of body fat is highly inflammatory and certainly far from healthy even though their weight is considered “normal.”
GET RID OF YOUR SCALE Weighing yourself to gauge g auge pro gr ess with with lifestyle changes changes is not a scientific scientific way to measure health benefits. It also creates a source of stress and can become neurotic. Body weight can fluctuate on a day to day basis, primarily due to shifts in fluid gain and loss, not body fat loss. We have seen many frustrated and stressed dieters weighing themselves daily and not understanding how they gained two pounds overnight. They respond by restricting calories further or crushing themselves in the the gym based so lely on o n what what they they saw on the scale that that morning. mor ning.
This practice is not good for mental health and contributes to creating an unhealthy relationship with food and exercise. This is a huge factor in the long-term failure of dieting and can create the vicious cycle of weight gain, weight loss, rebound weight gain, and the demoralization that goes with it. The diet industry is invested in continuing this futile cycle and reinforces the message of “weight loss”
in their advertising. Stop falling victim to obsessive weighing and put your scale out with the other garbage. We need another simple but scientifically sound measurement to monitor our progress that does not focus on the unreliable measurement of body weight. We want a measurement measur ement that that corr cor r elates well with with health. The waist to height r atio is such a measurement.
THE WAIST TO HEIGHT RATIO (WHR) The waist to height ratio (WHR) is a simple formula that is easily calculated.
1) Measure easur e the circumfer cir cumference ence of your waist at the level of the the umbilicus (belly button). button). You You can use inches or o r centimeter centimeterss as long lo ng as you yo u are consistent when when you measure your height. 2) Measure your height (most of us know this this already). 3) Divide your waist waist measurement measur ement by your height measurement. measur ement. The r esult is your waist to height ratio (WHR).
WAIST AI ST TO HEIG H EIGH H T RATIO (WHR) (WH R) EXAMPLE CALCULATION RecUsing one of the author’s (Chris) measurements, the WHR is calculated as follows: • Chris’s waist waist measur measur ement (cir cumference) cumfer ence) at the level of the umbilicus (belly button) button) is i s 32 inches. • Chris’s height is 69 inches (5 feet 9 inches). • To find the WHR, WHR, we we divide 32 by 69. • 32/69= 0.46 0.46
Chris’s waist to height ratio (WHR) is 0.46
We want to keep our WHR below 0.5 for optimum health and to avoid chronic diseases. WHRs WHRs above 0.5 have have been corr cor r elated with with the the follo fol lowing wing diseases: • • • •
Diabetes High High blood pressure Heart disease High triglycerides trigl ycerides from fr om metabolic metabolic syndro syndro me
These are the same diseases associated with the chronic inflammation and oxidative stress from obesity.
KEY POINT: Keep your your waist to to height hei ght ratio r atio (WHR) below 0.5 0.5 to prevent pr event development development of chronic diseases such as diabetes, heart disease, and high blood pressure. It is impor impo r tant to note that many people at risk r isk for fo r these diseases may be classified classifi ed as healthy if we used used the weig weight-based ht-based BM BMI for screening. scr eening. The “nor mal weight obese” o bese” perso n would be classified classifi ed as healthy by by the BM BMI, but would would be cor r ectly identified as unhealthy by the the WHR. WHR. Using Using only the BMI would miss people at risk for the above diseases. Most of us strive for a healthy, lean physical appearance—even if we are not particularly concerned about our health. Most people would not approach a prospective mate and say, “Sure you look really fit, but I will have to pick you up to make sure you don’t weigh too much.” This scenario sounds ridiculous but isn’t that the message we are sending by being preoccupied by weight? A lean, well-muscled person is healthy and attractive regardless of what the scale shows. The WHR is the best measure of how healthy you are and how your clothes will
fit. Developing lean muscle mass is also the best prevention from chronic disease and accelerating aging. Lean mass will increase body weight. Here are a couple of scenarios to illustrate the advantages of using WHR over scale weight:
SCENARIO 1: JILL Jill started at 5’6 inches tall, 180 lbs., and had a 38” waist. Jill went on a calorie restricted crash diet and monitored her weight loss with a scale. At the end of 4 months her results were: • • • •
Weight eig ht dropped dr opped from fr om 180 lbs. to 150 lbs. (30 lbs. lost) lo st) Waist circumfer cir cumference ence dro pped from fr om 38” to 34”. 34”. BMI BMI dropped dr opped from fro m 29 (overweig (o verweight) ht) to 24. 24.2 (nor mal). WHR dropped dr opped from fr om 0.58 0.58 to to 0.52. 0.52.
SCENARIO 2: 2 : KATHERINE KATHERINE Katherine started with identical proportions to Jill at 5’6 inches tall, 180 lbs., lbs., and a 38” waist. Katheri Katherine ne started lifestyle change chang e using Strong Stro ng Medicine tactics. At the end of 4 mo nths nths her r esults were: • • • •
Weight eig ht dropped dr opped from fr om 180 lbs. to 155 lbs. (25 lbs. lost) lo st) Waist circumfer cir cumference ence dro pped from fr om 38” to 31” 31” BMI BMI dropped dr opped from fro m 29 (overweig (o verweight) ht) to 25.0 25.0 (overweight). (overweig ht). WHR dropped dr opped from fr om 0.58 0.58 to to 0.47. 0.47.
SCENARIO SCENA RIO ANAL AN ALYSIS YSIS If you look just at weight loss, it would seem that Jill’s crash diet was more effective that Katherine’s Strong Medicine approach. After all, Jill lost 5 more pounds than Katherine, right? If we followed BMI as a measure of progress, Jill went from overweight to normal while Katherine was still technically classified as over weight at the the end of 4 mo nths. nths. If we look beyond weight loss, we see that Jill only lost 4 inches off of her waist circumference while Katherine dropped 7 inches. Jill finished her 4 months of dieting with a WHR still above 0.5 and still at risk for chronic disease. Katherine’s WHR dropped into the healthy range at 0.47. Katherine is also leaner and able to wear smaller sized clothes than Jill despite less total weight loss. What gives here? Jill lost more weight so why isn’t she leaner than Katherine?
Jill went on a calorie restricted crash diet with inadequate food to fuel her activity. As far as her brain was concerned, her reduced food intake was a threat and the threat response system was initiated to prevent starvation. High levels of cortisol from the stress-threat system cannibalized muscle mass to produce glucose to feed the brain during starvation mode. The high cortisol levels made body fat loss around her belly very slow. Upon further investigation, it was found that of the 30 pound weight weight loss, 10 pounds wer wer e lost fr om muscle and only 20 pounds pounds were lo st as fat. Katherine followed Strong Medicine tactics and fed her activity levels. The emphasis on food quality helped restore her hunger communication system in her brain. She spontaneously ate enough calories to fuel her activity without sending a threat message to the brain, preventing high cortisol levels. She also followed the Strong Medicine exercise plan and added 5 pounds of muscle in 4 months (while Jill lost 10 lbs. of muscle starving herself). Further investigation showed that Katherine lost 30 pounds of fat. Despite losing less overall weight than Jill, Jill , Katherine lost 10 pounds more fat and added muscle muscl e mass. Katherine also looks leaner and more physically fit even though she weighs 5 pounds more than Jill. She also now wears clothes 2 sizes smaller than Jill. From these scenarios you can see how following weight (and BMI) can be a poor measure of progress with lifestyle change and can even lead you astray. The WHR is a much better measure of improvement both inside your body from a health perspective, and outside from an aesthetic sense. As you make your journey through lifestyle change using Strong Medicine tactics, heed the two take-home messages fro m this section. section.
TAKE HOME MESSAGE: 1) Keep your waist waist circum circumference less than t han half half of o f your yo ur height height.. 2) Throw your scale away and replace it with a tape measure!
STUFF YOU CAN MEASURE III
MARKERS OF INFLAMMATION
Long-term low l ow level inflammation and oxidative stress stress are the the underlying causes causes of preventable chronic diseases as we have discussed throughout this book.
C-REA C-R EACTIVE CTIVE PRO PROTEIN TEIN (CRP (CRP)) Laboratory tests to reliably measure chronic oxidative stress are not readily available in the clinic setting at this time, but there is a good marker for chronic inflammation. inflammation. This “marker of inflammation” inflammation” is called C-reactive Protein (CRP). CRP is a protein produced by the liver in response to inflammation. Doctors classify CRP within a group of proteins called acute phase reactants. The acute proteins are produced during periods of high levels of inflammation hase reactant proteins as part of a defense response to stresses such as injury—especially invading bacteria.
Recall from Basic Training that immune cells produce chemicals called cytokines to carry the inflammatory message throughout the body to stimulate wound healing after an injury, or to repel the attack of foreign bacteria. When the liver detects cytokines produced by immune cells, it starts making acute phase reactants such as C-reactive protein to aid in defense of the body.
TECHNICAL NOTE: There ar e many potent potential ial markers mar kers of o f inflammation that that are curr ently ently being studied studied for use as as predictor predictor s of r isk of chronic chro nic inflammatory inflammatory diseases such as heart disease and diabetes. CRP has been shown to be the most predictive and and the the only one o ne we recommend following follo wing to track your progr pro gr ess if you are engaged in lifestyle change change to to treat or prevent diabetes, obesity, or heart disease. Modern medicine has used the fact that CRP levels are elevated during inflammation, and physicians can routinely measure it with blood tests. In the clinic, CRP CRP can be used to help differ dif ferentiat entiatee bacterial bacteri al and vir al infections. i nfections. We We will use CRP to help identify the low level chronic inflammation that is a risk factor for numerous preventable diseases. Indeed, CRP has been shown to be highly predictive as a marker for the development of diabetes and heart disease, and CRP is consistently elevated in o besity. besity.
KEY POINT: Elevated Elevated CRP CRP is highly hig hly predictive pr edictive for developing type type II diabetes and heart disease. CRP is also elevated in obesity.
CRP AND AN D RISK OF HEART HE ART DISEASE DISEA SE
Elevated C-reactive protein has been found to be a better predictor of developing heart disease in the future than LDL cholesterol levels or high blood pressure. The National Academy of Clinical Biochemistry Laboratory Medicine recently found that CRP was the only biomarker that met criteria for use in the prevention of heart disease.
HIGH SENSIT SENSITIVITY IVITY C-REACTIVE C-REACTIVE PROTEIN PRO TEIN (H SCRP) When CRP was first used as a laboratory test for inflammation, the technology to measure low levels of CRP was not available. Since chronic inflammation is usually present at very low levels, we needed to develop testing that could accurately measure low levels of CRP. This was accomplished with the development of the high sensitivity C-reactive protein (hsCRP) test. Now we are able to measure the very low levels of CRP that accompany chronic inflammation.
Each member of the Pentaverate produces low level chronic inflammation, so it is no sur prise pr ise that elevated elevated levels o f hsCRP have been found with each one.
CRP IS NON-SPECIFIC The often cited “drawback” of using hsCRP is that it is a nonspecific marker for inflammation. That means that it can be elevated by anything that increases the inflammatory response by the immune system. The test may not be useful for doctors trying to diagno se a specific disease. disease. For the the Strong Medicine trainee using hsCRP to monitor progress in reducing the sources of chronic inflammation leading to prevent pr eventable able disease, the non-specificity non-specifici ty of hsCRP is a strength. str ength. Circadian disruption, chronic stress, obesity, gut inflammation, and inactivity all roduce low levels of inflammation and will elevate hsCRP.
The nonspecific nature of hsCRP elevation from any source of low level inflammation means we can follow hsCRP levels as a marker of progress as we attack attack each member of the Pentaverate. Pentaverate.
KEY POINT: The nonspecific nature of hsCRP elevation with any source of low level inflammation inflammation means we can follow hsCRP hsCRP levels levels as a marker mar ker o f prog pr ogress ress as we attack attack each member of the Pentaverate. Pentaverate.
WHAT IS A GOOD LEVEL OF HSCRP? Most of the research with hsCRP has studied the correlation of hsCRP levels with the risk of heart disease. These levels are shown in the table below:
hsCRP level Less t han 1.0 mg /L 1.0 t o 3.0 mg/L g/ L Great er t han 3.0 mg/L g/ L
Risk Risk for fo r Heart Disease Disease LOW INT INT ERMEDI ERMEDIA AT E HIGH HIGH
The Strong Medicine trainee’ trai nee’ss goal g oal is to keep hsCRP hsCRP belo below w 1.0 1.0 mg/L. mg /L.
KEY POINT: The goal is to keep hsCRP levels below 1.0 mg/L as you are tracking your pro gr ess in the battle battle against the Pentaverate. Pentaverate.
TECHNICAL NOTE: Increased hsCRP above 1.0 mg/L will also increase risk for developing other pr eventab eventable le chro nic diseases such such as diabetes, diabetes, high blood blo od pr essure, and cancer but the actual correlated levels of hsCRP and risk for these diseases diseases are ar e not as well characterized characterized as it is for f or heart disease. disease.
QUICK QUICK MEDICAL MEDICA L NOTE: Since CRP is a non-specific marker for inflammation, people with inflammator inflammator y diseases such as rheumatoid rheumatoid arthritis or o r active active cancer cancer will have elevated elevated CRP CRP far above the nor mal levels. Active infections or injury will also cause very high levels of CRP. If any of these situations applies to you, measurement of hsCRP to monitor risk for chronic chro nic diseases diseases will not be useful. useful. High sensitivity C-reactive protein can be a useful part of the “Stuff You Can Measure” to monitor your progress in your personal battle to prevent chronic disease. • Corr ecting ecting circadian disruption and getting getting r egenerative sleep will lower
hsCRP levels. • Contro Contro lling chr chr onic stress with with brain training will will diminish diminish your hsCRP hsCRP.. • Reducing Reducing body body fat and insulin r esistance through thro ugh the 8-step prog pr ogrr am will minimize minimi ze hsCRP levels. • Stopping gut inflammatio n will bring bri ng down high hsCRP hsCRP. • Exercise crushes cr ushes inactivity-induced inflammatio n and brings bri ngs down hsCRP hsCRP levels as well. As part of your Strong Medicine battle plan, work with your doctor to get a hsCRP blood test (along with a lipid panel) at your regular preventive checkup.
STUFF YOU CAN MEASURE IV
HEART EA RT RATE RATE VA VA RIABIL RIABILITY ITY
If you had to pick just one single biomarker of health to measure, heart rate variability vari ability (HRV) (HRV) would be the one. HR HRV is your “desert island” isl and” biomar ker. In our opinion, HRV deserves this exalted status because it is the best window to view the day to day st atus of your stress st ress cup.
REV IEW OF HEA REVIEW H EAR RT RA RATE VARIA VARIABILITY BILITY (HRV)
We discussed HRV briefly in the Chronic Stress chapter along with the subject of biofeedback. HRV in simplistic terms is the natural variation of the length of time between each heartbeat. Heart rate is controlled by the two branches of the autonomic nervous system (ANS), specifically the sympathetic “flight or fight” nervous system (SNS), and the parasympathetic “rest and digest” nervous system (PNS). Go back and review your Basic Training on the Stress-Threat system if you need a refresher on this topic. topic. The “flight or fight” sympathetic nervous system (SNS) causes the heart rate to speed up in r esponse to any threat. It also also causes the heart to beat with a machine-like between each heartbeat. regularity , with minimal var iation o f the time between
The SNS (flight or fight) causes heart rate to increase, and for the heart to beat with precise regularity—very little variation in time between each heartbeat. This regularity is shown by the nearly identical lengths of the red arrows above. These arr ar r ows show sho w that that the the time between between each heartbeat is the same. This is called call ed LOW LOW
heart rate variability (Low HRV). When the “flight or fight” SNS is dominant, heart rate variability (HRV) is LOW. There are no health consequences to having periodic SNS dominance, such as while actively exercising or responding to an emergency. The health consequences show themselves when the SNS remains dominant most of the time due to chronic stress and diseases. The “rest and digest” parasympathetic nervous system (PNS) slows down the heart after a threat has passed. For most of the time, the PNS should be the active system controlli contro lling ng how ho w the the heart beats. A healthy hear heartt controlled contro lled by a r elaxed (PNS dominant) nervous system shows differing times between each heartbeat.
The PNS (rest and digest) causes the heart rate r ate to to decr ease after the threat has passed (or exercise is completed) and for the heart to beat with a variation of time between each heartbeat. This variation is shown by the different lengths of the green arrows above. These arr ows show the time between between each each heart beat is differ ent, with with arr ows having darker shades of green correlating with increased time between heart beats and lighter lighter gr een arrows arr ows for shorte shor terr times betw between een beats. beats. This variat vari ation ion in i n time
between between beats is called HIGH HIGH heart rate rat e variability variability (High HRV). HRV).
HRV AS A WINDOW WIND OW INTO YOUR “STRESS “STRESS CUP” Chronic stress, poor fitness, poor sleep, and a broken metabolism are all sensed as “threats” by the brain. In response to these daily threats, the “flight or fight” sympathetic nervous system is always on. The low level of “flight or flight” in which many of us live our daily lives causes chronic inflammation and oxidative stress. The always-on “flight or fight” system overfills our stress cup on a daily basis leaving the brain and body fighting a losing battle to adapt. Measuring heart rate variability (HRV) lets us see the current state of our autonomic nervous system—is it dominated by the “flight or fight” SNS, or by the “rest and digest” PNS? For optimum health, we want PNS dominance most of the time.
Most of the Strong Medicine Medicine defensive tactics tactics in this book boo k have the ultimate effect of maximizing PNS dominance, and turning down the level of the “flight or fight” SNS. We can track our autonomic nervous system status over time as we incorporate Str Str ong Medicine defensive defensive tact tactics ics to measure o ur progr pro gr ess. o ur nervous ner vous system system by the the “flight or • Low Lo w HRV HRV cor responds to dominance of our fight” SNS. SNS. This is not a good go od sig n. We are ar e moving in the wr wr ong direction for fo r our health, and and low HRV HRV indicates indicates that our “stress cup” has been over flowing. flo wing.
• High HRV HRV corresponds to dominance by the “rest and digest” PNS. This is the natur natur al state of the flesh machine and l eads to o ptimum health. High HRV HRV is a good go od sig n that that we we are curr ently ently within within the the limits of our “str “str ess cup”. cup”. We used a variation of this idea in the high intensity “burst cardio” protocol when we measured heart rate recovery after exercise, even though we were not measuring HRV.
HRV AND HE HEAL ALTH TH Our view that HRV is a window into the “stress cup” is supported by recent scientific research. Recall from Basic Training that we presented allostasis and allostatic overload (the state of your “stress cup”) as a way of looking at chronic
disease as a whole. Cur Cur rent research r esearch shows that that allostatic allostatic overlo o verload ad (overflowing (over flowing the the “stress cup”) has been associated with obesity, diabetes, heart disease, high blood pressure, anxiety, and depression. The same diseases are also associated with low HRV. HRV is emerging as a predictive marker for the development of chronic disease (and of health). • Low HRV HRV has been shown to predict predi ct the development of high bloo d pressur pr essure. e. • Low HRV HRV predicts predi cts poor poo r glucose gluco se tolerance toler ance and insulin r esistance seen in diabetes. • Low HRV HRV predicts predi cts development of heart disease better better than than most mos t other risk ri sk factor factor s such as high bloo d pressure and lipid test testing. ing. • High HR HRV predicts pr edicts long lo ngevity. evity. The longest long est lived li ved people peo ple have the highest hig hest HRV HRV into into old o ld age.
• Exercise is is the t he mos mostt powerful po werful stim st imulus ulus t o raise HRV HRV (as long as you do not overfill overfi ll your “stress cup” by by overtraining). The overarching concept that links low HRV to poor health is chronic activation of the str str ess-threat system.
The stressed-out brain constantly activates the threat system which keeps the “flight or fight” sympathetic nervous system (SNS) turned on. This creates dominance of the SNS and reduces HRV. This is why low HRV is associated with so many diseases, and is present even before the diseases become clinically apparent (before they can be detected by your doctor). In this way, HRV is the “canary in the coal mine” for heading down the road to poor health. As you learned in Basic Training, Traini ng, both bo th exter external nal and internal “threats” “thr eats” activate activate the the stress-threat stress-thr eat system. system. • An internal threat of swol swollen len fat cells in obesity causes inflammatio n. Inflammation activates the stress-threat system and lowers HRV. • An external threat—a stressful wor wor k environment—will envir onment—will activate activate the stressthreat threa t system, decreasi decr easing ng HRV HRV. • An internal threat threat of bacter bacterial ial infectio infection n or injur inj ury y will lower HR HRV in the shor tterm for these types of threats. • An external threat of pr pr ocessed foo d will cause inflammation inflammatio n and oxidative
stress. The stress-threat system is activated as the free radicals from processed foo d overwhelm o verwhelm the ADS ADS “bouncers.” This causes low lo w HRV HRV and predicts the development development of a broken bro ken metabolism. metabolism. • An internal internal threat threat of rumination rumination and and worr y causing causing chro chronic nic psycholo psychological gical stress will lower HRV because of the “ramped-up” flight or fight system. • An external threat of consi consistent stent over training traini ng from fr om “boo “boott camp beat down” exercise exerci se prog pr og r ams is a threat thr eat to to the body causing r educed HR HRV. • Chronic Chro nic stress is a threat that leads to anxiety and depression. depressi on. People with with anxiety and depr de pressi ession on have low l ow HRV HRV. • An internal threat threat of inadequate inadequate sleep and disrupt disr uptio ion n of the the circadian cir cadian r hythm hythm is a huge threat to the brain. It also results in low HRV.
HRV AND CIRCADIAN CIRCADIAN RHYTHM HRV HRV follo fol lows ws a natural circadian cir cadian rhyt r hythm hm with increased incr eased HRV HRV during r egener ation mode. mo de. This makes sense, as increased i ncreased HRV HRV is associated associ ated with with the dominance of the “rest “r est and digest” parasympathetic parasympathetic system. An overflowing “stress cup” results in loss of the high HRV during the night and leads to poor recovery and regeneration. Loss of high HRV at night also predicts development of diabetes. You can see why HRV is potentially a very good measurement for assessing the state of your “stress cup” and overall health. There are some scientists who even think that measuring HRV should be done in the clinic as part of a preventive checkup to help predict development of disease. You doctor could potentially use HRV to measure both physical and psychological psychologi cal wellness, something that blood tests cannot capture. capture. As a Strong Medicine trainee, you know that the physical and psychological are one, linked by the mind-body.
MEASURING ME ASURING HEA H EAR RT RA RATE TE VARIA VARIABILITY BILITY Not so long ago, measuring HRV required specialized equipment costing tens of thousands of dollars and was beyond the reach of the average person. Now we can get fairly accurate measurements of HRV with a smart phone and a chest strap heart rate monitor.
Calculation of HRV is fairly complex and requires some relatively sophisticated mathematics. Modern smart phone applications read the heart beat input from the chest strap and do the calculations for us. The result is a HRV score that is scaled co r r elate with with high hig h HRV HRV. from 0-100. Higher scor es cor High HRV scores usually correlate with a healthy state of the nervous system and low levels indicate activation of the stress-threat system. The higher your HRV score, the more you are in a parasympathetic nervous system (PNS) dominant state —a g oo d thing. thing . The lower lo wer your HRV HRV scor sco r e, the mo morr e you are ar e dominated dom inated by the “flight or fight” sympathetic nervous system (SNS) which indicates an overflowing “stress cup”.
FOLLOWING FOLLOWIN G YOUR HRV SCORE SCORE The HRV score is a very individual measure and should not be compared with scores from other people. But, higher HRV scores are often found in physically fit, healthy people. The idea is to get a baseline score to evaluate the current state of your health and fitness, then follow it as you incorporate defensive tactics from the Strong Medicine program. Your overall HRV scores will slowly improve as you reduce your stress, get better sleep, clean up your nutrition, lose body fat, and get regular exercise. exercise. It is important to note that your HRV will fluctuate day to day depending on your current situation. A night of bad sleep, increased stress, overdoing your exercise, or a particularly bad couple of days of “dietary “dietary indiscret i ndiscretion” ion” will cause your scores scor es to drop temporarily.
WHEN WHE N AND A ND HOW H OW TO TO MEASURE? MEASURE? Ideally, HRV measurement should be done at the same time every day and while attempting to reproduce the same method of measurement as closely as possible. We prefer to measure HRV immediately after waking in the morning while still in bed. This way the time of day is the same (and accounts for circadian changes in HRV) and the body position during measurement is the same. HRV is very sensitive to changes in your environment. We also like waking measurements because the various stresses of the upcoming day have not yet affected your body and brain, giving a measurement that has fewer variables to affect it. You can use these measurements to make lifestyle decisions—especially regarding reg arding exercise—and avoid avoid overfilling overfi lling your “str “str ess cup”. cup”.
USING HRV TO TO PLAN ACTIVITY A CTIVITY
To illustrate il lustrate the use of a daily HRV HRV score, scor e, let us construct constr uct a hypothetical hypothetical case.
HRV CASE REVIEW: Chri Chriss is a 44 year year old male with no chro nic diseases diseases and a relat r elatively ively high level of o f fitness. His HRV HRV scores scor es usually fall in the range rang e of 80 to 85. He nor nor mally exercises three to four times per per week week and generally gets good sleep. Chris wakes up after a restless night of sleep due to an upper r espirator espir atory y infection. His His HRV HRV score scor e (usually in the 80s) is 68 that mor ning. His exercise schedule had a planned squat wor wor kout that evening. Chri Chriss comes home ho me after after work (an unusually unusually stressful work wor k day) and perfor ms his squat wor wor kout with with a 10 minute minute burst burst cardio protocol pro tocol afterwards. The next morning his HRV is down to 58. He feels exhausted and the upper respiratory infection is worse. Chris had a drop in his usual HRV score of at least 12 points after a night of bad sleep due to an illness. Instead of modifying his workout plan, he continued with his planned workout of squats and a burst protocol that put a high amount of stress on his body. This caused an already mostly full “stress cup” (from poor sleep and illness) to overflow. We saw the results of Chris not heeding his falling HRV score the next day with a further 10 point drop in HRV. He should have altered his workout plan that day to be either a rest day, or at most a short walk instead of the taxing squat squat wor wor kout. He is now at risk for fo r the the relat r elatively ively minor upper upper respir ator ator y infection infection to become much worse due to his immune system becoming suppressed from an overfilled overfi lled “stress cup”. cup”. If he would have taken a rest day on the morning of the HRV score of 68, he would have recovered. Most likely, he would have had a higher score the next day and been able to do his squat workout without overfilling his “stress cup”.
GUIDELINES There ar e no hard har d and fast fast rules for r esponding esponding to a falling HRV HRV score, but we do have some suggestions. • If your scor e dro dro ps 10 10 points points or mor e, consider taking taking a rest day day from exercise and add a brain training session. • If you you scor e drops dro ps for two two consecu co nsecutive tive days, days, you really need to to pay attention attention to what could be causing the drop. dro p. Sleep is the usual culprit culpri t for this this so prio ritize ri tize getting getting regenerative r egenerative sleep that that night night (using tactics tactics from fr om the Circadian Disruption chapter) and certainly forget about any heavy physical physical training. tr aining. Following your yo ur HRV HRV can can be very powerful for making sure you yo u do not over train. You can also al so use it to see the impact of various vari ous Strong Str ong Medicine defensive tactics. If Chris would have replaced the planned squat workout that day with a 30 minute session of mindfulness breathing practice, his HRV score the next day would likely have been back up in the the 80-85 range r ange instead i nstead of 58 and feeling feeli ng sick si ck and exhausted. exhausted. You can use a falling score scor e as motiv mo tivat ation ion to incorpor incor porat atee an appropr iate defensive defensive tactic tactic that day to to br ing you yo u back fro m an over flowing flo wing “stress cup”. A dropping dr opping HRV HRV score might motivate you to pay more attention to your sleep that night, clean up your diet, or engage in some brain training.
HRV EQUIPMEN EQUIPMENT T As technology advances, there will be more options available to perform daily HRV HRV monitoring at home. There are current curr ently ly some good go od pr oducts oducts available. To get g et you started, here are two systems we have personally used (we have no financial or personal relationships with with either either developer developer): ): SweetWater Health. This is a smartphone smar tphone application that is • SweetBeat™ by SweetW low lo w priced and is r eliable for f or measuring measur ing HRV HRV. It r equires equir es a Bluetooth heart r ate
monitor strap such as the Polar® H7. It has other features related to food sensitivity and weig weight ht loss that we have have not used or o r evaluated, evaluated, so we cannot comment on these features.
• BioForce HRV. This is a HRV measurement package developed by top MMA (mixed martial arts) tr tr ainer Joel Jo el Jamieson. This pro duct is a bit mor e pricey but comes with an excellent excellent guide on using usi ng HRV HRV with with physical training. trai ning. The BioFor ce HRV HRV uses a smartphone application applicatio n and a Bluetoo Bluetooth th heart rate monitor mo nitor chest str str ap. It also has a go od website to to track tr ack your measurements. measur ements. Chris used this this product for 3 months and found it reliable for tracking HRV and to plan his training. Special Note: The accompanying manual has extensive technical information on HRV and allostasis (much to our surprise and pleasure). From reading the manual, it is obvious that Mr. Jamieson is extremely well versed on allostasis, allostatic load, and has applied the concepts very well to training high-end athletes. Highly recommended.
CONCLUSION HRV HRV measurement truly is i s a window to the state state of your nervous nervo us system and your “stress cup”. This is one of the most powerful and relevant biomarkers in this Analytics section. We strongly suggest you consider routinely checking your HRV to keep your “stress cup” fro m overflo o verflowin wing. g. Managing Managing your “str “str ess cup” effect effectively ively will have downstream benefits and HRV is currently the best way to keep an eye on it. By successfully managing your “stress cup” with HRV, you will likely see the other three biomarkers in this section improve as well. This is truly your “desert island” biomarker. This also marks the end of the Stuff You Can Measure (Analytics) section. Use these biomarkers appropriately, remembering the difference between correlation and causation. Also, do not get neurotic when measuring these biomarkers and turn them them into sources sour ces of stress.
ANALYTICS “MILITARY INTELLIGENCE” (REFERENCES): Re v 13 (2012): 275-286. Ashwel l M , Gunn Gunn P, & Gi bson S. Waist-to- height ratio i s a bette bette r scree ning tool than waist ci rcumfe rence rence and BMI for adult cardio cardio metaboli c risk factors: systematic revi ew and meta-analysi s. Obes Rev Nutrients 4 (2012): 1015Barona J, & Fe rnan rnandez dez M L. Di etary chol esterol affe cts plasma plasma li pid lev el s, the intravascu intravascular lar processi processi ng of li poprotei poprotei ns and and reve rse chol chol esterol transport wi thout increasing the the risk for heart disease. Nutrients 1025. Lipids Health Dis 9 (2010): 136. Bays H, et al. Are post-treatment low-density lipoprotein subclass pattern analyses potentially misleading? Lipids Obes (2013): 269038. Bener A, e t al. Obesity index that bette r predicts predicts metaboli c syndrome: body mass mass i ndex, w aist ci rcumfe rence, waist hip ratio, or wai st height ratio. J Obes (2013): Bittner V, et al. The triglyceride/high-density lipoprotein cholesterol ratio predicts all-cause mortality in women with suspected myocardial ischemia: a report from the Women’s Ischemia Syndrome Syndrome Eval uation uation (WI SE). Am SE). Am Heart J 157 (2009): 548-555. Comp Physiol 285 (2003): R1250-R1252. Blak e GJ , & Ri dker PM. C-re active protein: a surrogate surrogate risk mark er or mediator mediator of atherothromb atherothrombosi s? Am s? Am J Physiol Regul Integr Comp Blankste in R, et al. Predictors of coronary coronary heart disease e vents among among asymptomatic asymptomatic persons persons with low l ow- density li poprotei poprotei n chol chol este rol M ESA (Multi -Ethnic Stud Study of Atheroscle rosis). J Am Coll Cardiol 58 (2011): 364374. Brosschot J F, Van Van Dij k E, & Thayer J F. Dail y worry i s rel ated to low heart rate variabil ity during wak ing and the subsequent sequent nocturnal rnal sl ee p peri od. Int J Psychophysiol 63 (2007): 39-47. Browning LM, Hsi eh SD, & Ashwel Ashwel l M A. systemati c revie w of w aist-to -hei ght ratio ratio as a screening screening tool for the predictio predictio n of card cardio io vascular vascular disease and diabete diabete s: 0.5 could be a suitable suitable gl obal boundary value. Nutr Res Rev 23 (2010): 247-269. Brunon Brunonii A R, e t al. He art rate rate variabil ity i s a trait mark er of maj or depressiv depressiv e disorder: evi dence dence f rom the the se rtrali rtrali ne vs. el ectric current current therapy to treat treat depressi depressi on clinical study. Int J Neuropsychopharmacol 16 (2013): 19371949. Chapma Chapman n MJ , et al. T rigl yceride- rich li poprotei poprotei ns and and high-density l ipoprotein chol chol esterol in patie patie nts at at high risk risk of cardio cardio vascular vascular disease: e vi dence dence and guidance for manageme manageme nt. Eur nt. Eur Heart J 32 (2011): 1345-1361. Choi CU , et al. Statins do do not decrease small , dense dense l ow- density density l ipoprotein. Tex Heart Inst J 37 (2010): 421-428. Davidson MH, e t al. Cli nical util ity of infl ammatory ammatory markers andadvanc advanced ed li poprotei poprotei n testi ng: advice advice from an expert panel panel of l ipi d speci ali sts. J Clin Lipidol 5 (2011): 338-367. El Harchaoui K, e t al. Value o f l ow- density l ipoprotein particl particl e number and siz e as predictors of coronary coronary artery disease in apparently arently healthy men and and women: the EPIC-N orfol k Prospecti Prospecti ve Populati on Study. J Am Coll Cardiol 49 (2007): 547-553. Fernand Fernandez ML. Re thinki thinki ng dietary chole chole sterol. Curr Opin Clin Nutr Metab Care 15 (2012): 117-121. Gale ano ano NF, Al- Haideri M , Key serman F, Rumsey SC, & Decke lbaum RJ . Small dense lo w density li poprotei poprotei n has increased increased aff aff ini ty for LDL receptor-i ndependent ependent cell surface surface binding binding si tes: a potential mechanism f or increased atheroge atheroge nicity. J Lipid Res 39 (1998): 1263-1273. Gazi I F, Tsimi Tsimi hodimo hodimo s V, V, Tsel Tsel epis AD, El isaf M , & Mi k hail hail idi s DP. Cli nical importance and therapeutic therapeutic modulation of small dense l ow-density l ipoprotein particle particle s. Expert Opin Opin Biol Ther 7 (2007): 53-72. Gerber PA, PA, e t al. Small , dense LDL particle particle s predict predict changes in i ntima media thick ness andinsuli n resistance resistance i n men with type 2 diabetes andprediabetes—a prediabetes—a prospecti prospecti ve cohort cohort study. PLoS One 8 (2013): e72763. Goh LG, Dhali wal SS, Wel born born TA, Le e AH , & De ll a PR. Anthropometric Anthropometric measureme measureme nts of general and central central obesi ty and the predictio predictio n of cardiovascular cardiovascular dise ase risk in wome n: a cross-sectio nal nal study. BMJ Open 4 (2014): (2014): e004 138. Grad E, & Danenberg Danenberg HD. C-reactive protei protei n and atherothrombosi s: Cause or ef fe ct? Blood Rev 27 (2013): 23-29. Gratas-De Gratas-De lamarche A, De rbre rbre F, Vincent S, & Cil lard J. Physi Physi cal inactivi ty, insuli n resi stance, stance, andthe oxidative -i nflammatory loop. Free Radic Res 48 (2014): 93-108. Haensel Haensel A, M il ls PJ, Ne le sen RA, Z ie gle r MG, & Di msdale msdale J E. The relationship relationship between heart heart rate rate variabili variabili ty and and inflammatory inflammatory markers markers i n car cardiovasc diovascular ular diseases. Psychoneuroendocrinology 33 (2008): 1305-1312. Hayashino Hayashino Y, et al. Ef fe cts of exe rcise on C-reactive protei n, inflammatory cytoki ne and adipoki ne in patie patie nts wi th type 2 diabete diabete s: A meta-analy meta-analy sis of randomize d contr control ol le d trial trial s. Metabolism 63 (2014): 431-440. Hovingh GK, Davidson MH, Kastelei n JJ , & O’Connor AM. Di agnosis agnosis and treatm treatment ent of f amili al hyperch hyperchole sterolaemia. Eur Heart J 34 (2013): 962-971. Nutr 65 (1997): 1747-1764. Howe ll WH, M cNamara cNamara DJ, Tosca M A, Smith BT, BT, & Gaines JA . Plasma li pid and and li poprotei poprotei n responses to die die tary fat and and choleste choleste rol: a meta-analy meta-analy sis. Am J Clin Nutr Cardiol 167 (2013): 855-861. Jarczok MN , Li J , Mauss D, Fischer JE, & Thayer Thayer JF. He art rate variabil ity i s associated wi th gl ycemi c status status after controll controll ing for components components of the metaboli c syndrome. drome. Int J Cardiol Ther 17 (2013): 147-164. Jo hnson TV, TV, Abbasi Abbasi A, & M aster VA. VA. Systemati c revie w of the e vi dence dence of a relati onship onship betwee n chr chronic onic psychosocial stress and and C-reactiv C-reactiv e protein. Mol Diagn Ther Kemp AH , & Quintana Quintana DS. The rel ationship betwe betwe en mental and physical heal th: insights from the study of heart rate variabili ty. Int J Psychophysiol 89 (2013): 288-296. Kemp AH, Quintana DS, Fel mingham KL, Matthews S, & J el inek HF. De pressi pressi on, comorbid anxiety disorders, and and heart rate variabil ity in physi call y healthy, unmedicated patients: i mplicatio ns for card cardio io vascular vascular risk . PLoS One 7 (2012): e30777. Li bby P, P, Ri dke r PM, & Hansson GK. I nflammation in atheroscle atheroscle rosis: from pathoph pathophysi ysi ol ogy to practice practice . J Am Coll Cardiol 54 (2009): 2129-2138. Mae da S, et al. Associ ations betwe betwe en small dense LDL, H DL subfractions subfractions (HDL2 (HDL2 , HDL3) andrisk of atherosclerosi s in Japanese -Ame ricans. ricans. J Atheroscler Thromb 19 (2012): 444-452. Mak i K C, Dick li n MR, D avidson MH, M iz e PD, & Kulk arni K R. I ndicators of the atheroge nic li poprotei poprotei n phenotype measured measured with density density gradient ultracentrifugation ultracentrifugation predict predict changes anges i n carotid carotid intima- media thickness i n men and women. Vasc Health Risk Manag 8 (2012): 31-38. Mak i KC, Slavin J L, R ains TM, & Kris-Etherton PM. PM. Limi tations tations of observationa observationall evi dence: dence: impli cations cations for evi dence-ba dence-based sed dietary dietary recommendations. ations. Adv Nutr 5 (2014): 7-15. Atheroscler Re p 13 (2011): 373-380. Mangalmurti SS, & Davidson MH. The i ncremental ncremental val ue of l ipi ds and and infl ammatory ammatory biomarke rs in dete dete rmining residual cardiovascular cardiovascular risk risk . Curr Atheroscler Me ie r-Ewert HK, e t al. Ef fect of slee p loss on C-reactive C-reactive protein, an inflammatory inflammatory mark mark er of card cardiovascular iovascular risk. J Am Coll Cardiol 43 (2004): 678-683. Me isi nger C, Baumert Baumert J, Khuseyi Khuseyi nova N, Loewe l H, & Ko enig W. Plasma oxi dize d low-density l ipoprotein, a strong strong predictor predictor for acute acute coronary heart dise dise ase eve nts in app apparently healthy, healthy, middle- aged men from the ge neral neral popul ati on. Circulation 112 (2005): 651-657. Mi k hail hail idi s DP, DP, et al. “European panel panel on l ow density l ipoprotein (LDL) subclasses” : a stateme stateme nt on the path pathoph ophysi ysi ol ogy, atheroge nicity and cli nical si gnifi cance of L DL subclasses. subclasses. Curr Vasc Pharmacol 9 (2011): 533571. Mi ll er YI, et al. Oxi dation-speci dation-speci fi c epitopes are danger-associated danger-associated mole cular cular patterns patterns recogniz recogniz ed by pattern recogniti on receptors receptors of i nnate immunity. Circ Res 108 (2011): 235-248. Mo stafa SA, et al. The associ ation of the trigl yceride- to-H DL chole sterol ratio wi th insuli n resi resi stance stance i n white white European and and SouthAsi an men and and women. PLoS One 7 (2012): e50931. Lipids 45 (2010): 907-914. Musunur Musunuru u K. Atherogeni c dysli pidemia: cardio cardio vascular vascular risk and and die die tary intervention. Lipids My ers GL, et al. Nati onal Academy of Cl ini cal Biochemistry Laboratory Laboratory Me dicine Practice Practice guidel ines: eme rging bio bio marke rs for primary primary preve preve ntion of cardio rdio vascular vascular dise dise ase. Clin Chem 55 (2009): 378-384. Cardiovasc Dis 56 (2014): 426-433. Oliveros E, Somers VK, Sochor O, Goe K, & Lopez-Jimenez F. The concept of normal weight obesity. Prog Cardiovasc Onat A, Can G, Kaya H, & He rgenc G. “Atherogenic i ndex of plasma” (log1 0 trigl yceride/high-density l ipoprotein-chole sterol ) predicts predicts high blo blo od pressure, diabetes, diabetes, and vascular vascular eve nts. J Clin Lipidol 4 (2010): 89-98. Park Park BS, & Yoon JS. R el ative sk el etal muscle muscle mass is associated with devel devel opment opment of me taboli c syndrome. Diabetes Metab J 37 (2013): 458-464.
Peterson MM , et al . Apoli poprotei poprotei n B is an innate innate barrie barrie r against invasive staphylococcu staphylococcuss aureus aureus infecti on. Cell Host Microbe 4 (2008): 555-566. Petursson Petursson H, Sigurdsson JA, Bengtsson C, Nil sen TI, & Ge tz L. I s the the use of chole sterol in mortali ty risk algori thms in cli nical guidel ines val id? Ten Ten years prosp prospecti ecti ve data from the Norwegi an HU NT 2 study. study. J Eval Clin Pract 18 (2012): 159-168. RodriguezRodriguez- Hernand Hernandez H, Sime ntal-M ntal-M endia endia LE, Rodriguez-Ramirez G, & Re yes-R omero M A. Obesi Obesi ty and and inflammation: inflammation: epidemiolog y, risk risk factors, factors, and and mark ers of inflammation. inflammation. Int J Endocrinol ( 2013): 2013): 678159. Savva SC, Lamniso s D, & Kafatos Kafatos AG. Predicting ca card rdio io metaboli c risk risk : waist-to- height ratio ratio or BMI . A meta-analy meta-analy sis. Diabetes Metab Syndr Obes 6 (2013): 403-419. Vasc Surg 28 (2014): 375-380. Shen H, et al. Correlation between serum levels of small-dense low density lipoprotein cholesterol and carotid stenosis in cerebral infarction patients >65 years of age. Ann Vasc Tani Tani M , et al. Smal l dense LD L enhanc enhances es TH P-1 macrophage hage f oam cell formation. J Atheroscler Thromb 18 (2011): 698-704. Thayer JF. Vagal Vagal tone and the infl ammatory ammatory refl ex. Cleve Clin J Med 76 Suppl 2 (200 9): S23-S26. Thayer JF, Ahs F, F, Fredrik son M, Soll ers JJ , & Wager Wager TD. A me ta-analysi ta-analysi s of heart rate variabil variabil ity and neuroi maging studie s: impli cations for heart heart rate rate variabil ity as a mark mark er of stress and health. Neurosci Biobehav Rev 36 (2012): 747-756. Thayer JF, & Sternb Sternberg erg E. Beyo ndheart rate variabil variabil ity : vagal regulatio n of allo static systems. Ann N Y Acad Sci 1088 (2006): 361-372. Lipids Health Dis 10 (2011): 21. Toft-Pete rsen, AP, AP, e t al. Small dense LDL particle particle s—a predictor predictor of coronary coronary artery artery dise ase e valuated by by i nvasive and and CT-based CT-based techniqu techniques: es: a case-control study study.. Lipids Pharmacol (2013). Toth PP. Insulin resi stance, stance, small LDL particle s, and and risk risk for atheroscleroti c dise dise ase. Curr Vasc Pharmacol (2013). Lipids 42 (2007): 403-409. Tsimihodimos V, Gazi I, Ko stara C, Tsel Tsel epis AD, & El isaf M . Plasma li poprotei poprotei ns and and triacylg ly cerol are predictors predictors of small, dense LDL particl particl es. Lipids Tsimik as S, S, & Mi ll er YI. Oxi Oxi dativ dativ e modifi cation of li poprotei poprotei ns: mechanisms, rol e i n infl ammation and andpotential cli nical appli appli cations in cardiovascular cardiovascular disease. Curr Pharm Des 17 (2011): 27-37. Endocrinol (Lausanne) Vi nik AI. The conduc conductor tor of the autonomic autonomic orchestra. orchestra. Front Endocrinol (Lausanne) 3 (2012): 71. Wang X, e t al. Infl ammatory ammatory marke rs and risk risk of type 2 diabetes: a systemati c revie w andmeta-analysi s. Diabetes Care 36 (2013): 166-175. Wei smann smann D, & Binder CJ. The i nnate i mmune re sponse sponse to produc products ts of phosphol osphol ipid peroxi dation. dation. Biochim Biophys Acta 1818 (2012): 2465-2475. Obes (2012): 149516. Wi ndham ham BG, e t al. The re lati onship onship betwee n heart rate rate vari abil abil ity and and adiposi ty diff ers for central andove rall adiposi adiposi ty. J Obes (2012): Prog Cardiovasc Cardiovasc Dis 55 (2012): 321-331. Xhyheri B, Manfrini Manfrini O, Mazzol ini M, Pizz i C, & Bugiardin Bugiardinii R. Heart rate rate variabili variabili ty today. today. Prog Younis ounis N , Charlto n-Me nys V, Sha Sharma rma R, Soran H, & D urrington urrington PN. Gly cation of LD L i n non-diab non-diabeti eti c people: Small dense LDL i s pref pref erential ly gl ycated both in viv o and in vi tro. Atherosclerosis 202 (2009): 162-168. Zulf iqar U, J urivi ch DA, Gao W, & Singer DH. Re lation of high heart heart rate rate variabili variabili ty to healthy healthy l ongevity. Am ongevity. Am J Cardiol 105 (2010): 1181-1185.
DOC’S REFLECTIO REFL ECTION N Strong Medicine is a reflection of everything I wanted to say when my patients asked me “What can I do to get healthier?” There were only so many preventative r ecommendations ecommendatio ns I could impar t to to them in a 30 minute appointment.
The idea for this book started as a series of in-depth informational handouts that I could give gi ve my patient patientss for “homewor “homewor k” readin r eading g betwe between en office visits on topics such as nutrition, stress relief, exercise, sleep habits, etc. I researched the handouts by combing the scientific literature for the latest up-todate information that would support my recommendations. After compiling dozens of handouts, I realized that I had the skeletal framework for a book. The project took on a life of o f its own, own, growing gr owing far beyond the the original or iginal scope. Originally projected to take a month or so, this small project became a two year obsession that eventually became Strong Medicine. It spanned life events such as leaving the military, finding a new job, and relocating to a new state. This book was truly a labor of love fueled by a passion for science, medicine, and the need to contribute something meaningful to public health. I have always been frustrated when hearing flawed recommendations for health promotion and prevention that lacked any scientific foundation. I found myself ranting about this fact with with increasing increasi ng fr equency. equency. cathartic for f or me. I finally put my own cards on o n the table table and Strong Medicine was cathartic did something instead of continuing to complain about the inadequacies of conventional conventional recommenda r ecommendations tions for disease prevention. prevention. Thro ugh Strong Medicine, I offer solutions instead instead of complaint co mplaintss and criticisms. So many of our friends and family members are afflicted by chronic preventable disease and desperately want effective solutions that they can implement. We live in the the infor mation mation age, ag e, and in the the face of so much conflicting conflicting information info rmation it is difficult to find the needle in the proverbial haystack. My hope is for this book to give people the foundational knowledge to sift through the haystack of misinformation and find their “needle.” “needle.” After reading countless scientific research articles on seemingly disparate subjects, I felt the best course of action was to start with the basic processes that are the the sour ces of chronic chr onic disease and build build a prescriptive pr escriptive framework ar ound them. them.
Looking at the proposed mechanisms, it became obvious that sleep, nutrition, physical activity (or a lack thereof), stress, and obesity all contributed to a variety of chronic diseases. There was an underreported, underlying commonality that linked these maladies. Chronic inflammation and oxidative stress were the underlying mechanisms that tied together the many causes of chronic disease. Allostatic overload, the “Stress Cup,” was the overarching concept that showed how chronic stress, gut inflammation, circadian disruption, obesity, and inactivity all join hands to promote long-term inflammation inflammation and oxidative str str ess, the the precursor precurso r s to chro nic disease. disease.
The irony of writing a book on wellness, while working at a full time medical ractice, was that I consistently overflowed my own stress cup. I was more stressed and sick than I had ever been in my life! I certainly was a case study and proof o concept of allostatic overload! Hypocrisy abounded for two years while writing this book as I gave advice to my patients on stress relief while being the perfect illustration of the overflowing stress cup. I am sure I lost several layers off my telomeres. After the book was complete, my road back to health put into play the concepts outlined in this book: “Physician Heal Heal Thyself!”
The goal of Strong Medicine was to explain difficult concepts of human biochemistry, physiology, and pathology in a way the lay-person could comprehend. These interlinking, interrelated concepts would create a foundation of knowledge that could empower normal people to make beneficial lifestyle decisions. I wanted to demystify chronic disease by opening the “black box” of the flesh machine for all to see. One goal was to help people understand the effects of their lifestyle lifestyle choices and the scientific scientific foundations foundations fo r our prevention prevention recommend reco mmendations. ations.
I continue to hold strongly to the notion that when people understand and can visualize what is going on inside the body and brain as a result their lifestyle decisions, it becomes easier to become motivated and implement sustainable change. Ignorance is truly bliss, and once the veil of the unknown and unseeable is lifted by knowledge, your bad habits become harder to ignore. When bad habits are transformed into good habits, the resulting positive impact on the body creates enthusiastic enthusiastic momentum. m omentum. The military theme of this book was comfortable to me since I spent thirteen years of my life serving our country in the military—in both the Army and Navy. More importantly, I used the military theme to portray the true peril of our current public health crises. If you do not believe we are in a war against preventable disease, you are choosing to live with your head in the sand. Is it not shocking that reliable prognosticators indicate that the current generation will be the first in modern history projected to live shorter lives than their parents or grandparents? Why is this? What has bought about this horrific situation and is it preventable? Optimum health is difficult and near impossible to attain while existing in our modern environment. To acquire optimal health requires knowledge, diligence, planning and methodical application. We no longer live in the pristine environments of our distant ancestors, but can certainly learn a lot from them. They “exercised” intensely, got lots of cardio and ate pure, natural food. That template works in our present time quite nicely. However modern problems require modern solutions. We need to jettison dogmatic and unyielding paradigms—is it impolite to note that they don’t work? Strong Medicine seeks to approach the battle against chronic disease and the search for optimal health with a combination of the wisdom and practices practices of o f our o ur ancestors and advances advances of modern science. science. Strong Medicine will empower those that truly are motivated. If you have the motivation, we have shown you the game plan. If If you have had enoug h and are “sick and tired of being sick and tired” then put into play the very real and very concrete steps we outlined. We told you why something is the way it is, then related how to improve impro ve it. Every Every one of o f us can achieve achieve our health health goals, go als, but there there ar e no shor sho r tcut tcuts. s.
COACH’S CONCLUSI CONCL USIONS ONS
What is the the “take away” away” message o f this book? boo k? Self-empowerment. Self-empower ment. There is really should be no more confusion on your part regarding what you need to do to renovate your body and your life. You have a transformational roadmap. You supply the requisite mental motivation and disciplined application of our battle-tested methodology. It works every single time it is enacted fully and completely. Our systematic and appropriate strategies for exercise and nutrition are not the ever popular, one-size-fits-all mainstream health and fitness strategies. Our strategies are elite athlete practices, diluted and made user-friendly, pared down without without losing lo sing the core cor e essence that makes them effective. You can now create customized training templates that fit your lifestyle and time constraints. We have made provisions for the out-of-shape to gradually adapt to our fitness practices and procedures. Unlike the Sergeant Fury boot camp types, we don’t throw you into the proverbial deep end of the fitness pool in the first minute of your first session. We teach you how to swim first. We have established parallel strategies in related disciplines. By enacting these strategies simultaneously, we have engineered a physical transformation and psychological recalibration. Someone undergoing a profound physical transformation also undergoes a profound psychological transformation. Oscar Wilde once noted, “Perception is everything.” He was right about everything and this observation about how we see ourselves and our surroundings is no exception. While a negative self-perception is a psychic boat anchor hung around one’s neck, convert that negative perception into a positive perception— complete with some very real detoxification and high intensity, endorphin-releasing exercise—and exercise—and a man or woman is rebor r eborn n physically physically and psycholog psycholog ically. ically. I have facilitated hundreds of dramatic physical transformations, and one of the defining characteristics of true transformation is self redefinition. We enable people to reinvent themselves. Camille Paglia once described bodybuilding (the combination of nutrition and exercise to reengineer and reconfigure the human body) as “a struggle against nature.” Indeed, rather than be swept away by life and force of habit, the individual can seize control of their life. They can fight against “inevitability” and the idea of settling for whatever life hands them. We are either compliant with with our seemingly preor preo r dained dained fate or we fight. We who choose to embrace the fight understand that life itself is a struggle and
embrace it. Compliant living is mere existing. We want more—we want to improve our quality of life by methodically engaging in our parallel disciplines. Over time our practices will transform us, and we will attain and maintain vibrant muscular health and virility. vir ility. We subscribe to old school methods, rooted in intensity, sweat, and common sense. We believe in the idea of doing fewer things better; we will detoxify ourselves by practicing power nutrition and gourmet organic eating. Using powerhouse nutrients, we can expertly prepare meals we look forward to eating. We combine power nutrition with power power training. Everything you need to engineer your very own radical physical transformation is contained within the two covers of this transformation manual. This book is meant to be a workbook—so put our ideas into play and breathe life into the strategies we have shared with you. Try to avoid the cafeteria syndrome of cherrypicking our methodology. Avoid the temptation to only embrace the aspects of our system that appeal to your preconceptions and prejudices. Don’t reject parts of this holistic system that you deem unpleasant, stupid or ill-informed. Our strategies are purposefully interrelated. Break them apart and the results will be substandard. There is a tangible physical synergy when all the aspects are practiced systematically and simultaneously. If you come to love this vibrant way of living, then transformation is no longer a question of “if” but “when.”
ABOUT THE AUTHORS
CHRISTOPHER G. HARDY, D.O., MPH, CSCS Dr. Chr Chr is Hardy is emer ging as a leader in public health, health, merging merg ing his expertise expertise in nutrition, strength and conditioning, and in clinical and preventive medicine into a comprehensive appro appro ach to to treat chr chr onic disease. Dr. Hardy has a diverse background, including 13 years active military service in both the U.S. Army and U.S. Navy. He is a previous graduate of the Naval Diving and Salvage Training Center and Underwater Construction Basic Course, going on to serve as a military deep sea diver. He left the military the first time after four years of service to start his higher education. education. Dr. Hardy is a graduate of Old Dominion University, earning a bachelor of science in biochemistry. He went on to medical school at WVSOM in Lewisburg WV, WV, gr aduating aduating as a Doctor of Osteopathic Medicine. Medicine. After medical school and internship, Dr. Hardy reentered the military as a Navy physician, serving aboard the USS WASP (LHD-1) as medical officer and joining the ship on deployment in support of Operation Enduring Freedom. He then served another operational tour as a medical officer before attending Johns Hopkins University University for medical medical specialty specialty training. Dr. Hardy completed his specialty training in Occupational and Environmental Medicine at the Johns Hopkins School of Public Health where he served as Chief Resident, also earning a Master of Public Health degree with a concentration in toxicology.
Dr. Hardy is Board Certified in Occupational and Environmental Medicine under the American College of Preventive Medicine. He has also completed formal training in medical acupuncture and is a Certified Strength and Conditioning Specialist by the NSCA. He is currently enrolled in the Fellowship in Integrative Medicine at the the University of Arizo na. Chris lives in Everett Washington and is passionate about guitars, mountain biking, and health and wellness. He is still active as a trainer and gives nutrition lectures around the local community. He is married to his talented wife Carrie, a former biochemist and current student in Naturopathic Medicine at Bastyr University. His daughter Anna is a graduate student in Geophysics at Virginia Tech University.
ABOUT THE AUTHORS MARTY GALLAGHER Marty Gallagher has been involved in high-level athletics for over 50 years. He captured his first national title and set his first national records as a 17-year old teenage teenage Olympic O lympic weightlifter in 1967. In May May of 2013 he set his most mo st recent national records as a 64-year old powerlifter. He won the 1992 IPF world masters powerlifting title and has taken silver and bronze medals in world championships. He is a six-time national champion masters powerlifter.
As a coach he guided Team USA to the IPF world team title in 1991 and coached Black’s gym to five national powerlifting team titles. He was mentored by the 1st world powerlifting champion Hugh “Huge” Cassidy and Gallagher in turn mentored hall-of-fame powerlifting world dominator “Captain” Kirk Karwoski. Gallagher competition coached Ed “King” Coan, the world’s greatest powerlifter, along with iron immortals Doug Furnas, Lamar Gant and Mark Chaillet. Marty works with the military elite spec ops fighters (in this country and abroad) along with governmental special units within various agencies. As a writer Gallagher is widely read and considered one of the finest writers operating within the health, nutrition, bodybuilding, strength and athletic training genre. He has had over 1,000 articles published since 1978, including 232 weekly ‘ask the expert’ fitness columns for the Washington Post.com and 89 articles published during a ten year relationship with Muscle & Fitness and Flex magazine. Gallagher ’s biogr aphic on Ed Coan Coan was called, called, “the “the gr eatest eatest powerli powerliftin fting g book ever written,” by the late Joe Weider. Rock star Henry Rollins called the Coan book,
“Awesome!” Dr. Jeff Everson described Gallagher’s Magnus opus, The Purposeful Primitive “A literary masterpiece.” Gallagher lives in rural Pennsylvania.
ACKNOWLEDGEMENTS FROM CHRIS HARDY Attempting to give the appropriate appreciation to those who directly and indirectly supported this project is daunting. I have been fortunate to have incredible family members, fr iends, colleagues, and teach teachers ers over the the years and will will certainly have missed some who deserved to be mentioned. Thanks to John Du Cane, Derek Brigham and the Dragon Door team for making this book a reality. From the strength and conditioning world, my thanks go to: Dan Cenidoza, Chuck Miller, Mike Krivka, Lauren Bunney, Donna Pierce, Susan Simpson, Sandor Sommer, and Rob Miller. Thanks to my colleagues: Steve English, M.D., Don Berry, D.C., Maegan Knutson, N.D., Kim Broom, M.D., Dianna Chamblin, M.D., Gail English, M.D., Fran Read, M.D., Jiho Bryson, M.D. MPH, Bob Handel, M.D., Marti Bradley, R.N., Kathy Schram, R.N., Gavin Gordon, M.D., Joe Divita, M.D., Brad Olson, M.D., Chris Hoernig, R.N., Jenny Tinch, M.D. MPH, Erin Duffy, M.D. MPH, Bob Klem, M.D., Colleen Clark, John Trueblood, PA-C, Mike Puckett, CIH, Carolyn Ramos, R.N., Osama Boulo s, Phd., Phd., Carole Caro le Stonnell, and Stephanie Stephanie Cramer. Thanks to my teachers over the years whom provided friendship, mentorship and an excellent educatio education. n. The three that deserve special s pecial mention are ar e Mark Ellio tt, tt, Phd., Phd., Craig Cra ig Tho r ne, M.D. M.D. MPH, MPH, and Virg Vir g inia Weaver, M.D. M.D. MPH. MPH. Thanks to my military mil itary ship-mates: ship-m ates: Rory Ror y Miller Miller,, Sean Pear Pear son, Ken Richards, Walt Walt East, East, John Jo hn Broom, Bro om, Rob White, and Ryan Ryan De La Cruz. A very special thanks to my family and surrogate family: Marty and Stacy Gallagher, Brian and Gina Knoll and the rest of the Knoll family, the entire Randall and Thomas clan, Dennis and Karen Polli, Joe and Charlotte Coddington, Riddhi and Eric Blow, and especially to Cathy Hardy (greatest Mom on Earth), Jason and Reagan Hardy for all the love and support. Finally, there is not enough gratitude that can be expressed to Anna Hardy for
being a constant inspiration and a wonderful daughter. To my best friend, colleague, and incredibly talented wife Carrie, you were with me every step of the way. Strong Medicine would not exist without your love and support.
ACKNOWLEDGEMENTS FROM MAR MA RTY GALLAGHER GALLAGHE R I wish wish to acknowledge ackno wledge two people: Chris Chri s Hardy and my wife Stacy. Stacy. When Chris first proposed that we do a “public health” book, I was dubious – but curious. I was a huge fan of Chris and his amazing life story; I knew of him and about him before I met him and came to consider him a friend and confidant long before our book collaboration began. We had so many mutual interests past the strength, power, physical transformation-genre that initially drew us together. He was the Navy’s top medical man at Johns Hopkins and our Baltimore friend Sandy Sommer intro intro duced duced us. Our mutual interests were many; Chris was a musician working in the jazz/fusion realm and a scientist and a medical doctor. In his short life had been in both the army and the navy and recently completed a thirteen-year military career. He had life experience galore and was drawn to hardcore resistance training. We both had a fondness for Weston A. Price, Krishnamurti, the Mahavishnu Orchestra and Trailer Park Boys. So you can see why he and I hit it off immediately. He loved gourmet organic food and we consumed much together while continuing our ongoing conversation about bringing elite training and nutrition methods to the general public. I work with the elite and he works with the afflicted. I shared my idea that “detuned” and “diluted” elite methods are what is needed by the general public. Obviously, the methods of the elite work. The misconception has been that these elite methods methods are ar e too harsh, too demanding and beyond beyond the reach of ‘regular ‘r egular folk.’ folk.’ Instead, Instead, the the fitness mainstream mai nstream teaches John Jo hn Q. and Mar Mary y J. all about abo ut “moderate” “moder ate” and “sensible” fitness strategies. These mild methods don’t do a damned thing. They ever have and they never will; softball methods never work on account of insufficient intensity. Without herculean effort, there is no compelling reason for the body to to favor ably reconfigur e itself. itself. True, the elite methods need be defanged and declawed before being handed over to innocent civilians. Chris understood this. We had initial talks on how to construct user-friendly (for normal people) yet effective transformative training and nutr nutr itional pro tocols. This book is an out o utgr gr owth owth of our weir weird d synergy. We had both
arrived at the same eventual and identical conclusion to two entirely different questio questions: ns: he sought soug ht to to r ehab the damaged, I sought ways to make the best bett better. er. This book reveals the totality and breadth of Chris’ cinematic vision. While I might claim to be an inch wide and a mile deep, Chris is truly a mile wide and a mile deep. I am proud to be associated with bringing his Chekov-like vision of a bette betterr healthier healthier wor ld to fr uition. uition. I also want to acknowledge the herculean contribution of my wife, Mrs. Stacy O’Neal Gallagher, my Amazon, Spartan, tomboy, farm girl, horse whisperer, man whisperer, girlfriend. Stacy put up with my ever-increasing hermetic eccentricities and mood swings. By the end of the book writing process, I was, according to her, “One bus stop away from morphing into the Unibomber, living alone in the woods, mailings bombs to enemies.” Thank you Stacy Girl for your humor, patience and wild exuberance….
Gallop your horse Down the edge edg e of the sword, Hide in the middle of the flame. flam e. 17th century Zen poem obviously written for Stacy
INDEX Entries es in this index, index, carried carr ied over verbatim from fro m the print edition edition of this this title, title, Note: Entri are unlikely to correspond to the pagination of any given e-book reader. However, entries in this index, and other terms, are easily located by using the search feature of your e-book reader.
A See Arachidonic AA. See Arachidon ic acid Abdominal muscles, 413 See Visceral obesity Abdomi Abdomi nal nal o besity. See Visceral Abdomi Abdomi nal nal trai ning, 419 and and antianti- rotation, 41 6 basic basic plank, 41 4 high plank plank , 415 one hand hand pl ank, 4 16 plank plank row, 417–4 18 sit- ups as low back back “poison,” 413 problem s caused caused by, by, 412 –41 3 variatio ns, 412 also Premature agi ng andchroni Accelerated aging. See also Premature chroni c stress and AGEs, 244 chron chronic ic stress, 28 5 and exercise, 362 obesity and and chron chronic ic insuli n resistance, 197–198 and processed food, 246 slee p prob proble le ms, 334 See Adrenocorti ACTH. See Adr enocorti cotropic hormone Actin and myosi myosi n, 62 See Alzheimer’s disease AD. See Alzheimer’s Adaptive immune system, 8–9, 128 Adaptiv e response response and oxidative stress, 23–24 triggering, 24 Adenosine, i n brain, 325 Adenosine triphospha triphosphate, te, 3 25, 3 26 as energy currency, 98 production production of, 10 4 See Fat cell s Adiponectin Adipocytes. See Fat functio ns of, 176 production production and i nfl ammatory cytokines, 182 release, 209 Adrenal Adrenal g lands, lands, 35 Adrenali Adrenali n, 33 Adrenocorticotropic Adrenocorticotropic hormone, 14 3 See Antioxidant defense system ADS. See Antioxidant Advanced gl ycati on end-products, 201 “dock “dock ” with RAGE, 244 and elevated sugar levels, 244 in food, 245 formation formation of, 244 infl ammation and oxidative stress by, 101, 244, 246–247 Aerobic exercise recommendation, 249–250 See Advanced glycati on end-products AGE. See Advanced Age and protein intak intak e, l ink between, 65–66 See Al pha li nolenic acid ALA. See Al acid Al cohol consumption and fatty li ver disease , 58 Algae, 83–84 Allergies, 91 Allium Allium sativum, sativum, 462 Allostasis, 12, 206 definition of, 39 endorph endorphin rel ease, 40
vs. hormesis, 40 responses responses i n environmental environmental stress, 40 All ostatic ostatic l oad, oad, 206 harmfu harmfull e ffe cts of, 41–42, 45 measuring measuring marke rs of, 43 andobesi ty, 179 See Allostatic load All ostatic ostatic ove rload. rload. See Allostatic Alpha Alpha li nolenic acid, acid, 80, 89–90, 459 Alzheimer’s disease, 202, 353 Amber-tinted glasses, 350 Ami no acids acids essential, 63 side g roups roups of chemi chemi cal propertie propertie s of, 61 non-polar, non-polar, 61 polar, 62 structure of, 60 Amygdala, 275, 277, 278 Anaerob Anaerobic ic gl ycolysis, 10 3–104 Animal-based foods, 63 and and AGE fo rmation, 245 nutrient density of , 64 Animal Factory, 456 Animal foods, fat in, 455 See Autonomic nervous system ANS. See Autonomic Antibiotics and and dysbiosi s, 155–1 57 from envi ronmental ronmental sources, sources, 15 7 IBD risk wi th, th, 156 Antibodies, 9 Antige ns, adaptiv aptiv e i mmune response to, 8– 9 Anti-inflammatory response, 9 Anti-nutrie Anti-nutrie nts, 160 Antioxidant defense system, 338 andfre e radical s, balance betwee n, 11–13 functions functions of, 10 plant-based plant-based foods, 2 36 Antioxi dant dant supp supple ments, 23 Anti-rotati on and and abdominal abdominal training, 416 Apolipoprotein, 515 Arachidonic acid, 86 Aromatase, 195 Assi sted squat squat doorway/pol e squat, 381 shortened shortened rep-stroke squat, 380 towel or rope squat, 381–382 Asthma, 91 Astrocytes, 141 Atheroma, 523, 524 See Adenosine triphosph ATP. See Adenosine triphosphate Auto-antibodies, 163 Autoimmune disease, 129 chron chronic ic stress, 28 5 genetically predisposed to, 132 slee p prob proble le ms, 334 Autoimmunity Autoimmunity definition of, 9, 128 factor require d for, 129 in tissue types, 128 Autonomi Autonomi c nervous system functio ns of, 33 parts of enteric nervous system, 34 parasymp parasympath atheti eti c nervous system, 33 sympatheti c nervous system, 33 Autoxidation, 79 Axons, nei nei ghboring nerve nerve cell s, 269 Axon transmitte r, synapse synapse of, 2 70
B Bagels, metabolic response to gl ucose ucose produ production, ction, 10 7 insulin release, 107–109 reactive reactive hypoglycemi a, 109 Basic cardio “ramp-up,” “ramp-up,” 420– 422 Basic plank abdomi abdomi nal nal training, 414 Basic training, fo undatio datio ns of, 2 B-cell B-cell s, 8, 128 See Brain deri ve d neurotrophic factor BDNF. See Brain
Bedroom environment, 350 Beef pot roast, 487 Bell y breathin breathing, g, 297 Bench press te chni que, que, 3 96 dumbbel l, 397 advancing, advancing, 401 ove rhead, rhead, 402–4 04 “ pause-rel pause-rel ax-and-gri nd” style, 398–400 physiol ogical benefi benefi ts of, 401 Beta-cell failure, 189 Biof ee dback technique, technique, for stress reduction, 301– 303 HeartMath, 303 heart heart rate variabil variabil ity, 302 monitoring muscle muscle tension and ski n conductan uctance, ce, 3 02 muscle tension, 302 real-time information, information, 302 BioForce HRV, 554 Biol ogical vs. chronological chronological age, 198 Biomarkers cholesterol, 509–534 correl correl ations wi th heal th and and disease, 5 04–50 8 as engine warning lights, 506 heart heart rate variabili ty and, 546– 553 of i nflammation, nflammation, 541–545 physical measurements of, 535–545 Bloo d sugar sugar control, control, stepwise appr approach oach to, to, 26 0–261 adequate sleep, 258–259 avoiding HFCS, 242–247 gl uten-containing uten-containing produc products, ts, avoi ding, 229 insulin sensitivity with exercise, 249–258 plant-based plant-based foods, 234–24 1 antio antio xi dant dant defense wi th, 236 fe rmentable rmentable fi ber content, content, 235–2 36 fe rmentation rmentation by gut bacteria, bacteria, 234 le gumes, gumes, 237 polyphenol content, content, 239–2 40 sulforaphane ane content, content, 23 7–239 and and whol whol e w heat, 235 processed seed oil s, avoiding, 229–232 omega-6 PUFA, 230 for salad dressi dressi ng, 231–2 32 protei protei n consump consumptio n, 232–23 3 starch/glucose starch/glucose tole rance determination, 222–2 27 stress reduction techniques, techniques, 2 59 also Blo od sugar Blood sugar sugar level . See also Blo sugar control, ste pwise appr approach oach to person with normal normal i nsuli n sensitiv ity, 224, 225 pharmaceuticals armaceuticals to control, 227 unprocesse processe d whole grains and, 22 6–227 See Bright light therapy Blue light signals, brain, 330 BLT. See Bright See Body mass index BMI. See Body Body affe cts brain, brain, 288 anti-i anti-i nflammatory/ nflammatory/ca calmi lmi ng ef fects, 2 96 compositio n and and gut heal heal th, 166 unio n of mi nd, 268 Body mass index, 173, 535–536 problem with, 536 wei ght-focused ght-focused,, 536 Body-s can technique, 299 Bodywei ght squa squat, t, 372–3 73 Box deadli ft, 384 Brain, 288 axon-dendrite, transmitter-receiver, 271 changi ng, 268 fi rst principle principle s perspecti ve, 281 survi survi val advant advantage, age, 2 83 chased by bears, 27 4 as energy andgl ucose ucose hog, 9 9–100 epigenetic changes, 285 “fi ght-or-fl ght-or-fl ight” respons response, e, 31 functio ns of, 30 and gut, 125 hypotha hypothalamus, lamus, 31 3, 3 14 k etones as energy source, source, 116 and and mental heal th, 285 negativi negativi ty bias, 282 response to stress, 143 threats, threats, 2 75 Brain-based Brain-based threat response response system See “Fight or flight” system primitive and modern threats, 32 “fight or flight” system. See “Fight Brain deri deri ved neurotroph neurotrophic ic f actor, actor, 30 3, 3 04 Brain training, training, 30 7 Brain Training Training Triumvi rate, 308 Brain-train Brain-train mi nd method, method, 293 “Brain wasting,” 201 “Branched-chai “Branched-chai n” amino acids, 62 Breast cancers, 195 Breastfeeding, 147 Breathing Breathing bell y, 297 exhalation exhalation time, 296
inhalation inhalation time, 29 6 sympathetic sympathetic nervous system, 295 Bright l ig ht therap therapy, y, 341 Broccol Broccol i sprouts, sprouts, 237–23 9 Buddha’s Brain, Brain , 300 Buddhist meditati on practices, practices, 294 Bug Bug l ights, 350 “Burst Cardio” protocol, 428– 429, 432–435 Butyric acid (butyrate), 70 , 234
C Caffeine, 334, 345 Caloric restriction restriction diet, 474–476 Calories calculation calculation,, 207 andhunger hunger communicati on syste m, 220 Cancer Cancer cell s, phenomenon phenomenon of, 193 Cancers characteristics of, 192–193 chron chronic ic stress, 28 5 dependent dependent on gl ucose, ucose, 1 93–19 5 li nk wi th obesi ty and and chronic chronic insuli insuli n resi stance, stance, 192– 196 sensitive to estrogen, estrogen, 195 slee p prob proble le ms, 334 trigger for, 193, 196 uncontrolled cell growth, 193 Capsaicinoi Capsaicinoi ds, 463 Capsicum annum, num, 463 –46 4 Carbohydrates, 55 fiber, 59 health health effe cts of, 119 misconception about, about, 1 19 starches, 57 sugar, 56 –57 fructose, fructose, 57 glucose, 56–57 sucrose, sucrose, 58 Carbohydrate to le rance, 4 65–46 8 low carb carb eating, eating, 466–468 LSS eating pattern, 466– 468 overvie w, 465 Cardio training foundation, foundation, 420 –422 Cardio vascular training, 250, 363 , 436, 44 4 Carrot noodles, 4 85 Cayenne, 463–464 See Correl ated color te mperatur CCT. See Correl mperaturee See Clostridium difficile CD. See Clostridium See Centers for Disease Control CDC. See Centers Celiac disease, 129 Centers for Disease Control exercise recommendation “moderate intensity” aerobic, 249–2 51 “steady-state” “steady-state” exercise, 252 “vi gorous gorous intensity,” intensity,” 251–252 Chain Chain reactions of fre e radicals, radicals, 11 Chin-ups, 405– 406 Chipotl e butternut squash soup, soup, 48 0 Cholesterol, 509–534 in artery cloggi ng plaques, plaques, 521 buil ding ding block f or bil bil e salts, 512 for cell communication, 511 cell membrane function of, 510 chemi chemi cal structur structuree o f, 5 10 for deve lo ping brain brain during during chil dhood, 511 dietary, 455 in human human breast breast mi lk , 512 li poproteins, 514–517 as molecular buil buil ding blo ck f or hormones, hormones, 511–512 standa standard rd li pid panel, panel, 529–5 31 testing of, 524–527 transportation, sportation, 517–5 24 Chole Chole sterol esters, 515 Cholesterol levels, in blood, 513 Chronic Chronic disease, 45 Chronic inflammation, 129, 164, 221 causes of, 125 and and chronic preve preve ntable ntable disease, 14–15 definition of, 9 of gut, 123 sources of, 14 outside “e nvironment,” 15 Chronic intestinal permeability, 130–131, 164 Chronic Chronic preve preve ntable ntable dise ases, 14 Chronic stress and threat response, 3 2
Chronob Chronobio io lo gy, 342 Chron Chronologi ologi cal cal vs. biologi cal cal age, 198 Chylomi crons, crons, 514 transport sport of fat and chol chol este rol, 516 Cinnamomum spp, Cinnamomum spp, 463 Ci nnamon, nnamon, 463 See Sl ee p proble ms, circadian disruptio Ci rcadi an disruption. See Sl isruptio n Ci rcadi an rhythm, 312 , 500 See Conjugated CLA. See Conju gated linolei c acid acid Clostridium dif fi cile , 155 Coconut oil, 71, 72, 232 Coffee drinking correl correl ation wi th lung lung cancer, cancer, 505–5 06 relation to smoking, 506 Colonocytes, Colonocytes, 59 Color additives, additives, 219 Combinatio Combinatio n antibi antibi oti c therapy, therapy, 156 Compli mentary mentary protei protei ns, 64 Compound multi-joint exercises, 367 Confounders, 51 Conjugated linoleic acid, 95 Conventional vs. organic organic produce, 46 1 Cooking methods and AGEs, 245 strategy strategy,, 49– 491, 4 90–491 Correlated color temperature, temperature, 34 7, 348 Corticotropin rel rel easi ng hormone, hormone, 143 Cortisol, 274 Cortisol receptor resistance, 286, 287 C-reactive C-reactive protein, protein, 541– 542 high sensiti sensiti vity, 544–545 nonspecific, 544 and and risk risk of heart dise dise ase, 542 See Corticotropin rel easi ng hormone CRH. See Corticotropin hormone See C-reactive protei CR P. See C-reactive protei n Culi nary nary consensus, consensus, 447–464 deadly deadly meat, 455–45 6 food quali ty demand fo r, 456 for omnivore, omnivore, 449–455 for vegetarian, vegetarian, 457–460 herbs and spice s, 46 1–464 cayenne, 463–4 64 cinnamon, 463 fi ve health-pr health-promoting, 464 garli garli c, 462 ginger, 462 turmeric, turmeric, 463 lo cal foo d and and, 449 Curcuma longa, longa, 463 Curcumin, Curcumin, 46 3 Cytoki nes, 8, 9, 177–178, 182, 184
D Dawn simulator, 346 Deadlift, 383 “bodybuilder stiff-leg,” 384 See Box deadli ft box. See Box commonfl aws in, 393–394 conventional, 384 See Stiff-le g dead stiff-leg. See Stiff-le deadli ft See Sumo sumo. See Su mo deadli deadli ft tactics, 388 variations, 384 Deep squat, 369, 371 Defe nsive nsive tactics, tactics, 2–3 Dementia, 202 Dendrites, Dendrites, nei ghboring nerve nerve cell s, 269 Depression andchroni chroni c stress, 2 85 and and slee p problems, problems, 33 4 Descartes, Descartes, R ene, 267 See Di homogamma DGLA. See Di homogamma li nolenic acid acid See Docosahexaenoic acid Diabesity, 180 DHA. See Docosahexaenoic also Bl ood sugar control, ste pwise appr Diabetes. See also Bl approach oach to; Type 1 diabetes; Type 2 diabetes causes of, 53 andchroni chroni c stress, 2 85 anddepressi on, 288 muscle muscle mass maintenance as defense against, 365 nutriti on and exercise , 340 and and “prediabetes,” laboratory laboratory tests for charts, charts, 205
fasti ng blood sugar, sugar, 203–2 04 HbA1c test, 203 OGTT, 204 risk for developing, 206 and and sle ep problems, problems, 334 Diabetics, whole grains for, 226–227 Die tary tary chole chole sterol, 455 Di etary sources sources arachi donic acid, 86 gamma linolenic acid, 86 linoleic acid, 86 Diets, 21 and and epige netic changes, 18 fail ure ure i n long-term, long-term, 50, 54 Digestion, 222 Dige stive tract tract messengers, messengers, 215 and satiety, 214–215 Dihomogamma Dihomogamma li nole nic acid, acid, 90 DNA damage damage by free radical s, 10 discovery discovery of, 16 mutatio mutatio n, 20 Docosahexaenoic acid, 82, 89–90 Dopamine Dopamine rel ease, 217 Double Double bonds, bonds, 79 Dumbbel Dumbbel l bench press te chni que, 3 97 advancing, 401 overhead, 402–404 “pause-relax-and-grind” style, 398–400 Dysbiosis causes of antibiotic use, 155–156 LPS level s, 154 processed processed foods, 152–1 53 saniti saniti ze d food supply, 155 definition of, 149–150 dietary source of, 155 diseases and and diso diso rders rders associated wi th, 151
E Eastern meditation tact tactics, ics, 2 93 E. coli O157:H7, coli O157:H7, 455 Edison, Thomas, 329 See Enteric glial cells Egg scramble, 478 EGCs. See Enteric Ei cosanoi cosanoi ds, 87 Ei cosapentaenoic cosapentaenoic acid, acid, 82, 89–9 0 Elaidic acid, 93 Elite athletes, 442 Endometri Endometri al cancer, 195 Endorph Endorphin rel ease and and all ostasis, 4 0 Endorphins, Endorphins, 14 0 Endotoxemia, 154 Endotoxi Endotoxi n, 154 Energy drinks, 247– 248 Energy generation from fat catabolism, 105 from glucose catabolism, 103–104 See Enteric nervou ENS. See Enteric nervouss system Enteric gli al cel ls, 141 Enteric nervous system, 3 4 and and brain, simi larity betwee n, 141 components of, 141 enteric enteric glial cells, 141 gut-brain gut-brain axi s stress reduction, reduction, 143 two- way communication communication network , 142 vagus nerve, 142 neurotransmitte otransmitte rs, 1 41 response to stress, 143 as “se condbrain,” brain,” 3 4 Environment, 18 Environmental challenge. See Environmental Environmental stresse s Environmental signals chan changes ges i n epigenome, 2 0 epigenetic system response response to, 17–18 for health, 21 Environmental Environmental stresse s adaptations/responses in, 40 adap adaptations tations through through all ostasis in, 4 0 dosage dosage of, 23 dose of food and exercise, 26–27 andhormeti c wi ndow, 27 importance of, 22–23 Environmental Environmental stressors, 21 Environmental Environmental stress sensor, 241
See Eicosapentaenoic acid Epigenetics, 21, 202, 284 EPA. See Eicosapentaenoic case study, 19 definition of, 16 of fetus, 20 response to environmental signals, 17–18 Epigenome, 20 and and environmental stressors, 21 See Adrenalin Epinephrine. Epinephrine. See Adrenalin Epithelial cell barrier, 126 Essential amino acids, 63 Essential amino acids deficiency, 457 Essential fatty acids, 80–81 Excess fat, 190–191 Exercise, 21, 24, 351–352. See also Progressive also Progressive resi stance stance training benefi benefi ts of regular, regular, 351 CDC recommendation recommendation for, 249–25 0 defensive tactics, tactics, 363 and and epige netic changes, 18 health health benefi benefi ts of, 361–36 2 and and hormesi hormesi s, 26–2 7 and insulin sensitivity, 249–258 See High intensity interval training HIIT. See High “moderate intensity” aerobic, 249–2 51 “steady-state,” “steady-state,” 252 “vi gorous gorous intensity,” intensity,” 251–252 reasons for avoi avoi ding, 250 recommendations, recommendations, fundamenta fundamentall fl aws i n, 48 for reducing obesity and and chronic stress, 50 0 scheduling, scheduling, 35 2 sle ep enhanc enhancing, ing, 35 2 and and “stress cup,” cup,” 42 –43 timing, 351 Exercise i ntensity definition of, 250 and HRmax, 250–252 Exhalation Exhalation time , 296 Exorphins, Exorphins, 1 40
F “Fad die die ts,” 49 “F ast pathway,” 33 Fast pathway and HPA axi s, 35 Fat cell cell s adiponectin release, 209 definition of, 174 as energy storage facilities, 102, 177 functio ns of, 174 metamorph metamorphosis of, 175, 177–1 79 bloated adipocyte, adipocyte, 177 cytoki ne release, 177–178 obesity-related inflammation, inflammation, 178–179 Fat loss, stepwise approach to, 260–261 adequate sleep, 258–259 avoiding HFCS, 242–247 gl uten-containing uten-containing produc products, ts, avoi ding, 229 insulin sensitivity with exercise, 249–258 plant-based plant-based foods, 234–24 1 antioxidant defense with, 236 fermentable fiber content, 235–236 fe rmentatio rmentatio n by by gut bacteria, bacteria, 234 legumes, 237 polyphenol polyphenol content, content, 239–24 0 sulforaphane ane content, content, 23 7–239 and and whol whol e w heat, 235 processed seed oil s, avoiding, 229–232 omega-6 PUFA, 230 for salad dressi dressi ng, 231–2 32 protei protei n consump consumptio n, 232–23 3 starch/glucose starch/glucose tole rance determination, 222–2 27 stress reduction techniques, techniques, 2 59 Fats, 55 in animal foods, 455 break break down, 187 burning burning for energ y, 119 functio ns of, 67 gl ucagon ucagon stimulating burning burning of, 113 and and glucose, balance balance betwee n use of , 102–1 03 glucose conversion into, 102 metaboli sm, 102 as primary primary e nergy source, source, 101 See Saturated fat (trigl saturated. See Satu (trigl yceride) catabol ism, 105 Fatty acids carbon chai n double oubl e bond configurations, 92–93 carbon chain of, 69 Fatty liver, 58 Fatty liver disease, 58 Fe eding, for training and activi activi ty, 470–476
caloric caloric restriction restriction diet, 474–476 in high intensity interval training, 472–473 low carb carb die t, 474–476 LSS eati ng pattern, pattern, 475 in non-traini non-traini ng days, days, 470 –471 carboh carbohydra ydrates tes as fe rmentable rmentable fi ber, 470 fat intake from protei protei n sources, sources, 471 25- 30 grams of high quali ty protei protei n, 471 sugary sugary fruit and and starchy starchy foo d intake , 471 in training days, days, 471–47 4 “Fe el -good” satisfaction satisfaction respons response, e, 216–2 17 Fermentable Fermentable f iber and gut health, 153 health health benefi benefi ts of, 235 and and non-fe non-fe rmentable rmentable fi ber, 60 in plant-based plant-based foods, 235–2 36 sourc sources es of, 235–236 Fermentation, 59 definition of, 157 product of, 158 Fe rmented foods and probioti cs, 157–15 8 Fetus, epigenetics of, 20 Fiber, 59 health health benefi benefi ts of, 60 in whole wheat, wheat, 235 “Fi ght-or-fl ght-or-fl ight” response, response, 31, 40 “Fight or flight” system, 297, 338 See Autonomic nervous system hypothalamic-pituitary-adren See Hypothalami components of autonomic autonomic nervous syste m. See Autonomic hypothalamic-pituitary-adrenal al axis. See Hypotha lami c-pituitary-adrenal c-pituitary-adrenal axi s conditi conditi ons trig trig geri ng, 38 decreases activation of, 303 health health eff ects of, 37 sympatheti c nervous, 162 yi n/yang concept, 36 Fi sh oil capsu capsule le s, 90 Fl avor add additi ves, 219 Flaxseed, 80 Flesh machine, 314 Foam cells, 523 Foie gras, 58 also Diets Food, 53. See also Diets and exercise, 26–27 andnutrit nutrit i on, 25 Food and Drug Admi nistration, 93 Food label, 86 trans fats, 93 Food processing and gluten-related diseases, 135–136 Food quali quali ty demand for, 456 for omnivore, omnivore, 449–4 55 for ve getarian, getarian, 457–460 Formula Formula f eeding, 147 Free radicals and and ADS, balance balance betw ee n, 11 chain chain reactions, 1 1 DNA damage by, 10 “i mportin mporting,” g,” 13 and and prematur prematuree aging, 1 97–19 8 unpaire paire d el ectron of, 10 andunsaturated unsaturated fatty acid, 7 9 Free-weight exercises, 367 Free-w ei ght lifti ng techniques, iques, 367 “Frozen statue” row, 408–411 Fructose, 57 and AGE, 244 chemi chemi cal structur structuree o f, 5 6 in energy drinks, drinks, 248 in fruit drink s, 248 in fruit fruit j uices, 248 in fruits, 242 intak intak e and fatty li ver disease, 58 in soft drinks, drinks, 247 “Fruit-fl avored” avored” drinks, drinks, 247–248 Fruit Fruit j uices, 248 See “Frozen statue” row FSR. See “Frozen
G Gamma linolenic acid, 86 Garli Garli c, 462 Gastrointestinal problems, 140 Genes collections of DNA, 16 definition of, 17 expressi on and and environment, 15 functio ns of, 16 mutatio mutatio ns, 17 “turnin “turning g of f,” 17–18
“turning on,” 17 –18 Genetic variations, 16 Genome, 146 definition of, 17 See Growth hormone Ginger, 462 GH. See Growth See Gamma linolenic acid Gliadins and glutenins, 134 GLA. See Gamma Gl ucagon ucagon functions of, 111–112 release, 111 stimulati ng fat burning, rning, 11 2–113 Gluconeogenesis, 100, 188 Gl ucoraphani n, 238 Glucose as brain fuel, 99–100 chemi chemi cal structur structuree o f, 5 6 connected in chai chai ns, 57 conversion into fat, 102 in energy drinks, drinks, 248 andfat, bal ance ance betw ee n use of, 102–103 in fruit drink s, 248 in fruit fruit j uices, 248 and and insuli n, contr control ol li ng interaction interaction betwee n, 101 metaboli sm, 101 anaerob anaerobic glycolysi s, 103 production production of, 18 8 in soft drinks, drinks, 247 tolerance, 222 Glucose meter, 222 Gl uten-contai ning products roducts health consequenc consequences es for, 1 40 Gluten free diet, 124 for type 1 diabetes, 165–166 Gl uten-free processed processed produc products, ts, 229 Gluten-rel Gluten-rel ateddiseases celiac disease, 135 autoi autoi mmune and and infl ammatory ammatory disorders IN, 137–1 38 causes of, 136–1 37 diagnosis of, 138 microvill i destru destruction, 139 prevalence prevalence of, 136 food processing i mpact mpact on, 135 gluten sensiti sensiti vity, 135 and and cel iac disease, diff erence betwee n, 139 symptoms of, 139 and and metaboli c disorders, 136 spectrum of, 135 Good nutriti nutriti on, 49 Google, 294 Grain-based Grain-based fi bers, 60 Grains genetic modif modif ication of, 136 Gram-negative bacteria, 154 Groupthink, 52 –53 Growth hormone functio ns of, 116 release during slee p, 116 signals for release of, 115 Gut bacteria species, 145 and brain, 1 25 chronic inflammation of, 123, 125 as fi rst barr barrie ie r, 125 intestinal intestinal lumen, 125 nutrie nutrie nt absorption, 125 response to stress, 143 villi , 125 125 Gut bacteri bacteri a and and auto-antibodies, auto-antibodies, 163 beneficial Afri canchil chil dren, dren, 155 European chil dren, 155 fi ber transformation by, 157 health health benefi benefi ts of, 148 opportuni sti c pathoge ns and, balance balance betwee n, 148, 150 signaling Treg cell s formation, formation, 149 in traditional fermented foods, 157–158 diversity of, 145 and and enteric nervous system, 16 2 imbalance, correcting, correcting, 14 7 in infants, factors influencing, 146–147 infl uence uence on hormones, hormones, 16 3 infl uence uence o n mood and behavior, behavior, 16 1–163 microbiome, 146 restoring “balance” in, 161 and and Treg Treg cel ls, 1 49 Gut-Brain axis, 307 Gut health andbody composi composi ti on, 166 and and fermentable fi ber, 153 Gut immune system, 125 adap adaptiv tiv e i mmune syste m. See
Adaptiv e i mmune syste m as first line of defense, 126–127 innate innate i mmune syste m. See Innate i mmune syste m members members of, 127 stimulation stimulation of, 123 See Treg cell T-regulator T-regulatory y cell s. See Treg cell s Gut inflammation, 164 and and chronic chronic disease , 1 44 Gut inflammation, inflammation, triggers f or, 133 dysbiosis, dysbiosis, 145 gluten See Gluten-related diseases prolamin protein, 134 and and gl uten-related diseases. See Gluten-related toxi c components of, 134 variance variance among among responses responses to, 135 stress and intestinal permeability, 141–144
H See Hi gh density HDL. See Hi density li poprotein HDL/triglyceride ratio, 101 Health and and lacto-fe rmenting bacteria, bacteria, 160–1 61 and and muscle muscle mass maintenance, maintenance, 3 65–36 6 Heart and and vascular vascular dise ase risk , 196 Heart disease, chronic chronic stress, 285 HeartMath, 303 Heart rate rate variabili ty, ty, 302, 546–554 and ci ci rcadi an rhythm, rhythm, 5 50 equipment, 553–554 exercise and, 549 and and heal heal th, 548–55 1 high, 547, 548 high/low, 302 low, 547, 548 measurement of, 551–553 for plan activity, 552–553 review of, 546–547 scores, scores, 551–553 stress-threat system and, and, 550 Heart/vascular disease, sleep problems, 334 Heat (Calor), 7 Heme iron, 459 Herbs and and spice spice s, 461 –464 cayenne, 463–464 cinnamon, 463 fi ve health-p health-promot romoting, ing, 464 garli garli c, 462 ginger, 462 turmeric, 463 Hi gh blo blo od pressur pressure, e, sl ee p problems, 334 Hi gh carbohydra bohydrate te me als (bagels), me tabol tabol ic response to gl ucose ucose produ production, ction, 10 7 insulin release, 107–109 reactive reactive hypoglycemi a, 109 Hi gh-density carbohyd carbohydrate rate foo ds and and dysbiosi dysbiosi s, 15 2 High density lipoprotein, 516 Hi gh-fructose gh-fructose corn syrup syrup, 24 2 and AGEs, 24 4 bad bad press press on, 242– 243 comparison comparison wi th table sugar, 24 3 consumpti on by ave ave rage American, 243 and NAFLD, 58 High i ntensity ntensity i nterval nterval training, training, 252–258, 420 benefits of, 253, 425 gl ucose ucose transporters, 255–2 56 increased increased insuli insuli n sensitivi ty, ty, 257–258 muscle glucose storage, 254–255 buil t-in safety system, 430–431 “Burst “Burst Cardio,” 428–429, 432–435 for diabetes and prepre- diabetes, 257 –258 effectiveness of, 425 ef fo rt and high target heart rates of, 420 example of, 426 with exercise types, 427 feeding for training and activity in, 472–473 and and glucose glucose l evel s, 472–473 and hormetic dose, 427–428 HRmax calculation, calculation, 425, 42 8–429 prepara preparatio tio n, 420– 421 for short short periods periods of time, 252–253, 424 and stress cup, 427–429 Hi gh plank plank abdominal abdominal training, 415 High sensitivi ty C-reactive C-reactive protein, 543, 544–545 in chronic chronic disease, 545 level of, 544–545 nonspecifi nonspecifi c CRP, CRP, 544 Hi gh temperatur temperaturee cook ing andAGE, 2 45 See High intensity interval training HIIT. See High Hi ppocampus, ocampus, 276, 278
stress, 275 Hormesis, 12, 21, 362 adverse and beneficial effects, 28–29 vs. allostasis, 40 concept of, 25–27 definition of, 23 fo od and nutriti on, 25 graph of, 26, 27 Hormetic zone, 26–28 Hormones cortisol, 35 epi nephri ne andnorepine phrine phrine , 35 Hormone sensitive lipase, 113 See Hypothalamic-Pituitary-Adrenal axis; HPA HPA axi s. See Hypothalamic-Pituitary-Adrenal Hypothalami Hypothalami c-pituitary-adrenal axi s See Maxi mum heart HRmax. SeeMaxi heart rate See Heart rate variability HRV. See Heart HRV score, 552–553 See High sensitivity C-reactive protein hsCRP. See High See Hormone sensitive lipase Human genome, 17 HSL. See Hormone Hunger, 208 Hunger Hunger communicati communicati on system, 20 9 gut-brain gut-brain axis and and satiety sig nal nal digestive tract tract signaling messengers, messengers, 214–215 protei protei n, 215–2 16 le ptin, ptin, 209 communicating wi th brain, brain, 210 functio functio ns of, 210–2 12 and hypothal hypothal amus, 210 in obese people people , 211–212 resistance, 211, 213 palatable f oods andreward center, 216–217 and and restricti restricti ng calo calo rie s, 220 signal to stop eating, 210–213 Hunger drive, 208–209 Hunter-gatherer Hunter-gatherer cultures, 3 64 Hydrogenation, 94 Hyperextended spine, 393–394 Hyper-l Hyper-l ordosis, ordosis, 393 Hyperplasia, 179 Hypertrophy, 179 Hypothalami Hypothalami c-pituitary-adrenal axi s adrenal adrenal g l ands, 35 diabeti diabeti cs experie nce nce chronic activation, 288 fast pathway, 274 fast pathway and, 35 health health effe cts of, 37 hormones cortisol, 35, 37 epi nephri ne andnorepine phrine phrine , 35 hypothal hypothal amus, 34 pituitary gl and, and, 34 slo w pathway, pathway, 274 sl ow pathway and, 35 stop, stress response, 284 stressed-out brain, brain, 2 80 stress response, 273, 275, 276, 278 sympathetic sympathetic nervous system’s threat-stress response system, 2 88 Hypothalamus, Hypothalamus, 34, 1 00
I See Irritable bowe l sy ndrome Ice cream and IBS. See Irritable andcake , metaboli c response response to fat storage, 118–119 insuli insuli n rel rel ease, 118 See Intraepithelial lymphocytes IEL. See See Individual glucose tolerance test IGT test. See Individual Immune system, 8, 13 See Adaptive adap adaptiv tiv e. See Ada ptive i mmune syste m early development of, 147 infl ammatory ammatory response, 9 See Innate innate. innate. See Inna te i mmune syste m Individual glucose tolerance test, 226–227, 465 Inflammation, 6, 285 acute andchroni chroni c, 9, 8 7 acute, basic basic process process o f, 8 beneficial effects of, 12–13 benefits of, 12 cardinal signs of, 7–8 insuli insuli n sensitivi sensitivi ty l oss by, 181–183 long-term, 14 and and omeg a-3 PUFA, 87– 88 and and oxidative stress by AGE, 101 all ostatic overl oad by, 42
stimulati ng threat threat response, response, 38 trans fatty acids li nked wi th, 92–93 primary primary ge nerator nerator of, 8 short-te short-te rm increases i n, 13–14 Inflammation Inflammation markers, 541–545 C-reactive C-reactive protein, protein, 541 –542 high sensiti sensiti vity C- reactive reactive protein, 543, 5 44–545 Inflammatory Inflammatory cytoki nes and and insuli insuli n receptor, receptor, 181 –182 oxidative stress triggering, 184 Infl ammatory ammatory response response by cells, 8 palmi palmi tic acid triggering, 76 Inhalati Inhalati on, sympathetic sympathetic nervous system, 2 95 Inhalation time, 296 Innate Innate i mmune syste m, 8, 127 Insulin functions of, 107–108 gl ucose ucose and and fat for e nergy, nergy, 103 health health effe cts of, 119 misconception about, about, 1 19 Insuli Insuli n/glucagon n/glucagon ratio ratio , 114 Insuli Insuli n receptor resistant, 183 sensitive, 182 short-ci short-ci rcuite d, 181–1 82 Insulin resistance, 110, 188 causes of, 187, 222 chronic, chronic, co nsequences of accel accel erated aging, 197–1 98 “brain wasting,” 201 cancer risk , 192–1 96 excess fat, 190–191 fat break break down, down, 187 gluconeogenesis, 188 heart and and vascular disease risk , 196 high insuli insuli n le vel s, 188 high palmi palmi tate le vel s, 190–191 muscle muscle wasting, 189 definition of, 187 infl ammation reduction reduction and, and, 50 0 from inside, 186 muscle muscle mass maintenanc maintenancee as def ense against, 365 Insuli Insuli n-resistant obese obese restri cting starchy carbohydrates carbohydrates and sugars in, 22 8 Insuli n sensitivi sensitivi ty
and and blo od sugar sugar leve ls, 2 22 of cell, 110 definition of, 109–110 and and exercise, 249–258 See High intensity interval training “moderate intensity” aerobic, 249–251 HIIT. See High “steady-state,” “steady-state,” 252 “vi gorous gorous intensity,” intensity,” 251–252 loss by inflammation and oxidative stress, 181–183
Interna Internall ti mek eeper, 313–319 adrena adrenall g land’s clock , 316 fat clock, 317 gut clock clock , 317 heart heart clock , 316 immune clock , 317 ki dney clock, 317 li ver clock, clock, 316 muscle muscle clock , 317 panc pancreas reas clock , 316 Intesti nal nal barrie barrie r as first line of defense, 125–127 Intestinal permeability, 127 andautoim muni muni ty, 129 consequences of, 129–131 short short term i ncreases ncreases i n, 133 See Gut Intraepithelial lymphocytes, 139 Intesti nal nal tract. tract. See Gut See I ntestinal IP. See I ntestinal permeabil ity Iron defi defi ciency, 459–460 Irritable bowel syndrome, 139
K Ketogenic diets, 201 Ketones, 116 Ki dney dysfunction and protei protei n intake, 66 Knees collapsing inward, 379–380 shooting forward, 378–379 Krebs cycle, 104
L LA, 89–90 Lactic acid, 103 Lacto-fermentation, 158–159 Lacto-fe rmented fruits and veg etables anti-i anti-i nflammatory nflammatory effe cts of, 161 health health benefi benefi ts of, 160 Lacto-fe rmenting bacteria bacteria and health, 160–1 61 See Light at night Large-buoyant LDL, 517, 519, 520, 522 LAN. See Light particles, formation of, 529 Lauric acid (laurate), 71 See Large- buoyant LDL LBLDL. See LargeSee Low density li poprotein LDL. See Low LDL particle number, 534 LDL receptors, 532–533 LED-ge nerated nerated light, 349 Legume preparation, for toxi city, 458 Legumes, 237 Lifestyle change, 54, 494–502 defensive tactics in, 497–502 neck of Ro y Buchan Buchanan an’s ’s guitar, case study, study, 494–49 5 strategi strategi c planning, planning, 496–502 Light at night, 331 asleep, 332–333 chronotherapy, chronotherapy, 33 3 circadian disruptio disruptio n, 333– 334 exposure, 332 poor sle sle ep, 333 caffeine, 334 space space at night, 33 1 Light pollution, 331 Li ght squa squat, t, 370– 371 Linoleic acid, 80, 86, 230 Lipid peroxidation, 79 Lipid peroxide, peroxide, 79 Li popol popol ysaccharide, 154 Lipoproteins, 514 chyl chyl omi crons, 514 high density, 516 low density, 516 structu structure re o f, 515 types types of, 514–517 very l ow density, density, 516 Li ver cancers, cancers, 192 Liver metabolism, 100 Local Local food, 449 Long-chain Long-chain f atty acids long chain omega-3 fats, 459 and and metabol metabol ism, 72 Long- chain saturated saturated fat palmitic acid, 73 stearic acid, 75 Long-term eating eating si gnal, gnal, 214 Low carbdiet, 466–468, 474–476 Low density l ipoprotein, ipoprotein, 516 Friedewald equation for, 525 in i mmune response, 532 large- bouyant bouyant,, 519 oxidized, 523 particle particle number, 534 particle size, 527–529 small small -dense, -dense, 519 transport sport of f at and chol este rol, 5 17–51 9 Low starch/high starch/high protei protei n meal, me tabol tabol ic response to carbohydrate component, 11 1 fat burning, 112– 113 glucagon glucagon release, 111–112 insuli insuli n rel rel ease, 112 Low starch/su starch/sugar (LSS) eating pattern, pattern, 4 66–46 8, 4 75 LPS. See Li popol popol ysaccha ysaccharide ride
M Macronutrie nt ratio ratio , 25 M acronutri ents biochemistry perspective, 55 See Carbohydrates carbohydrates. See Carbohydrates See Fat fat. See Fat See Protei protei protei n. See Prot ei n
Macrophages, 177 , 523 Mal nutriti on and hormesi s, 26–27 Margarine, 94 Mast cells, 143 Master clock cortisol cortisol l evels, 318 hormone levels, 318 in hypothalamus, hypothalamus, 319–3 20 leptin levels, 318 malfunctioning, 335–337 blood sugar, sugar, 336 diabetes, 336, 339–340 diabetes, loss of insuli insuli n, 337 disrupt sle ep, 336 fatty li ver disease, 336 heart, 336 heart disease, 337 infl ammation, chronic, chronic, 337 insuli n resi stance, stance, 336 poor athle athle tic performance, 337 slee p, 339–340 stroke, 337 melatonin levels, 318 Maximum heart rate, 250–251 definition of, 250 determinat determination ion of, 250–251, 42 0–421 Maxwel l’ s Equations, ations, 51 See M indfulness-based stress MBSR. See M stress re duction MCTs. See Me dium-ch dium-chain ain triglycerides Me dicine, future of, 45 Meditation tactics biofe edback edback te chniqu chnique, f or stress reduction, 301– 303 HeartMath, 303 heart rate variabili ty, 302 monitori ng muscle muscle tension and and sk in conductan uctance, ce, 302 real-time information, information, 302 eastern/western hig hig h technology, 293–2 94 exercise, 303–305 interventions, 294 mindfulness practice, practice, 29 4 body-scan, body-scan, 299–3 01 mindful breathing, breathing, 295–2 98 Me dium-chain dium-chain fatty acids l auric auric acid, 71 and and metabol metabol ism, 72 Me dium-ch dium-chain ain triglycerides, 232, 471 Melatonin benefi benefi ts, 338 connectio n, 338–339 gateway hormone hormone f or regeneration mode, 321 natu natura rall li ght’s ght’s e ffe cts, 330 suppleme ntatio ntatio n, 353 temporary use of, 353 Me ntal ntal chall chall enges, 271 Me ntal ntal defect, physical brain chan changes, ges, 285 M ental he alt h and and brai brai n chan change s, 28 5 Me taboli c respons responsee to food intak intak e, 106 high carbohydrate ohydrate me als (bagel (bagel s) gl ucose ucose produ production, ction, 107 insuli insuli n release, 107–109 reactive reactive hypoglycemi a, 109 ice cream and and cake fat storage, storage, 118–119 insuli insuli n release, 118 lo w starch/high starch/high protei protei n meal carbohydrate carbohydrate component, 111 fat burning, rning, 112–1 13 glucagon glucagon release, 111–112 insuli insuli n release, 112 during sleep GH release, 115–116 k etone produ production, ction, 116 li ver gluconeogenesis, 116–117 Metabolism, 95 fat, 101–103 gluconeogenesis, 100 glucose, 99–101 le an and and athle athle tic yo ungster, 99 li ver, 100 100 mitochondria, 103 muscle, 101 obese person, 99 Metformin, 188, 227 Me thylmercu thylmercury ry (MeHg) i n fish, 453–454 Me xican ch chick en with sautéed k ale, 4 81 Mi nd, 31 Mi ndfulness-based stress reduction, reduction, 300 Mindfulness training, 294–301 Mi nd, union of body, body, 268 Mi sinformation, sinformation, 53 Mi tochondria dria as energy factories, 103 fat cataboli cataboli sm, 105 gl ucose ucose cataboli cataboli sm, 104
oxidative stress in, 183, 185–186 Mitohormesis, 200 “M oderate oderate intensity” intensity” e xercise definition of, 250 HRmax of, 251 Mo dern and and primi primi tiv e threats, 31–32 “M oist” cook ing methods methods,, 245 Mol ecular ecular mimi cry, cry, 163 Mo nosacch nosaccharide, aride, 56 M onounsaturated fatty acid chara characteristi cteristi cs of, 78 chemi cal bonds, 77 health health effe cts of, 78, 80 li quid at room te mperatur mperature, e, 7 8 oleic acid, 78 Monty Python and the Holy Grail, Grail, 506 Mo ther’s womb and and epigeneti c changes, anges, 2 0 See Mo nounsaturated fatty aci d MUFA. See Mo Muscle buil buil ding, ding, dietary signal for, 65 Muscle cannibalism, 100 Muscle mass and strength strength retaining, retaining, 36 5–366 “use it or lose it” scenario, 364 Muscle mass maintenance and health, 365–36 6 Muscles gl ucose ucose storage by, 101 primary primary e nergy source source of , 101 Muscle tension, 301, 302 Muscle wasting, 189 Mutations definition of, 16 of genes, 17 Myelin, 269 Myostatin, 189–190
N See Non-alcoholi NAFLD. See Non-alcoh oli c fatty live r disease disease National Sleep Foundation, 259, 344 “Nature vs. nurture” rture” envi ronment ronment argument, 20 Negativity bias brai brai n reacts, 28 2 first principles perspective, 283 Nerve cell cell s connectio ns, 271 dendrite receivers, 279 drawing drawing of , 269 glial cells, 268 pref pref rontal rontal cortex, 2 79 signal direction, 270 Nervous system and long-term stress, 286 Neuroplasticity brain’s ability to physically change, 268 definition of, 269 Nightshift work, 354 Night-shif Night-shif t worker, 342, 343 Ni trogen balance balance concept, 64 positive/negative, 65 Non-alcoholic Non-alcoholic fatty li ver disease, 58, 242 Non-rap Non-rapid id eye movement sleep, 322, 3 24 light sleep stage, 345 slow wave sleep, 340 Non-training days, feeding in, 470–471 carboh carbohydra ydrates tes as fe rmentable rmentable fi ber, 470 fat intake from protei protei n sources, 471 25-30 grams of high quality protein, 471 sugary f ruit ruit and and starch starchy y f ood i ntak ntak e, 471 Norepinephrine, Norepinephrine, 33 Nourishing Nourishing Traditions Traditions,, 460 See Non-rapid NREM. See Non-ra pid eye moveme nt sleep Nutrie Nutrie nt timi timi ng around ound exercise , 468 Nutrition, 48 and food, 25 recommendations recommendations fundamental amental fl aws in, 48, 50 observation observational al results results to make, 52 Nutriti Nutriti on research and practice, practice, problems problems wi th first principles, 50 groupthink, 52– 53 reductionism, 52
study desi gn, 51
O also Fat l oss, ste pwise appr Obesi ty, 170. See also Fat approach oach to causes of, 53 chron chronic diseases l inke d to, 172 andchroni chroni c stress, 2 85 consequences of accel accel erated aging, 197–1 98 “brain wasting,” 201 cancer risk , 192–1 96 excess fat, 190–191 fat break break down, down, 187 gluconeogenesis, 188 heart and and vascular disease risk , 196 high insuli insuli n le vel s, 188 high palmi palmi tate le vel s, 190–191 muscle muscle wasting, 189 definition of, 179 insuli n resistance caused caused by, by, 181 –183 el evated stress stress le vel s, 183 short-circuite d insuli n receptor, 181 prevale nce nce o f, 172 reward system of brain in, 217–218 and and slee p problems, problems, 33 4 and and stop eating sig nal, nal, 218 and and type type 2 diabete diabete s, 180 Obesity- related disease, disease, cost of, 172 Observatio nal nal data, data, 51–5 2 Observatio nal nal studie s, 52 Occu Occupa pational tional and and Environmental Environmental M edici ne, 342 See Occup OEM. See Occ upational and Environmental M edici ne Offi cial recommendations, recommendations, 53 See Oral glucose tolerance test OGTT. See Oral Oily (or fatty) fish, 83 Oki nawan nawan die ts, 119 Oleic acid, 93 Omega-3 f atty acids alpha linolenic acid, 82 docosahexaenoic docosahexaenoic aci d, 82 ei cosapentaenoic cosapentaenoic acid, 82 food sources of, 83–84 health health effe cts of, 82–83 omega- 3 andomeg a-6 conversion pathways, 89– 90 and and omega-6 f atty acids, balanc balancing, ing, 87 –88, 9 1 structure of, 81 suppleme ntatio ntatio n, 90–91 Omega-6 fatty acids ba balanced lanced die tary intak intak e of , 85–86 dihomogamma linolenic acid, 90 food sources of, 85 harmfu harmfull eff ects of, 88 health health effe cts of, 85 and and omega-3 f atty acids, balanc balancing, ing, 87 –88, 9 1 vs. omega-3 PUFAs, 85 structure of, 84 suppleme ntatio ntatio n, 90–91 Omega-6 Omega-6 PU FA biologi call call y i mporta mportan nt, 86 infl ammation and oxidative stress by, by, 230 in vegetable andseed oil s, 231 Omega-6 to omeg a-3 ratio, unbalanced, balanced, 91 One One handplank abdomi nal traini ng, 416 Open-F ocus Brain, Brain, 299 Opportun Opportuni sti c pathoge pathoge n, 148 CD overgrowth, 155 overgrowth as threat to body, 162 Oral glucose tolerance test, 223, 225 Organic Organic vs. conventional produce, 461 Osteoporosis, 366 Outdoor “powe r walk ing,” 421 Overhead dumb dumbbel bel l bench press te chni que, que, 40 2–4 04 Over-nutrition, 25, 26–27 Overtraini Overtraini ng, 26–27 Oxidation reactions, 10 Oxidative Oxidative stress, 6, 221, 285 and and adap adaptiv tiv e response, response, 23–24 and ADS, 10–12 balance balance betwee n free radicals and and ADS, 11 beneficial effects of, 12–13 and and chronic preve preve ntable ntable disease, 14–15 definition of, 10 delicate balance of, 12–13 importance importance of , 12 insuli insuli n sensitivi sensitivi ty l oss by, 181–183 long-term, 14 in mitochondria, 183, 185–186 primary primary ge nerator nerator of, 8 short-te short-te rm increases i n, 13–14 sources of, 14
outside “environment,” 15 unsatura unsaturated ted fats and, 79 See Reactive oxygen species Oxygen free radical. See Reactive
P Pain (Dol (Dol or), 7, 8 Palatable foods andreward system, 2 16–21 7 Palmitic acid (palmitate), 73, 190 alarm system activ ated by, 191 obesity and and chronic ronic i nsuli n resi resi stance, stance, 190 –191 scientific studies studies on, 76–77 triggering inflammatory response, 76 Pancreas, 188 beta-cell failure in, 189 Paracelsus, Paracelsus, 23 Parasympa Parasympathetic thetic activi ty, 143 Parasympath Parasympatheti eti c nervous system, 3 3, 2 96 and and SNS, interaction betwee n, 35 parasympatheti parasympatheti c nervous syste m anti-inflammatory actions, 33, 37 “rest and digest” system, 33 Pastured pork pork chil chil i, 483 Pentaver Pentaverate, ate, 362, 496–502 See Prefrontall cortex PFC. See Prefronta See Phytohemaggl PHA. See Ph ytohemaggl utinin Phosph Phosphol ol ipids, 5 15 Photo-oxidation, 79 Physi Physi cal functionali functionali ty of ‘civilized man,’ 365 of tribal, tribal, 364 Physically rebuilding, 298 Physi Physi cal mindfulness, mindfulness, 30 5 Physical stress and exercise, 361–362 Phytate, 459–460 Phytohemaggl Phytohemaggl utinin, 458 Pituitary gl and, and, 34 Plank row, 417–4 18 Plant-based Plant-based chemi cals and and health polyphen polyphenols, ols, 239–240 sulforaphane, ane, 237–2 39 Plant-based Plant-based proteins, 63– 64 See Parasympath PNS. See Parasymp atheti eti c nervous syste m Poison, 23 Polyphenols, 24, 239–240 Polysaccharides, Polysaccharides, 5 7 Polyunsatur Polyunsaturated ated fatty acid, 80–8 1 Preconceptions, Preconceptions, 44 2 Prediabetes Prediabetes laboratory laboratory tests fo r charts, charts, 205 fasti ng blood sugar, sugar, 203–2 04 hemogl obin A1c (HbA1c) test, 203 Oral Gl ucose ucose Tole rance Test (OGTT), (OGTT), 204 self-monitoring program, 225 Prednisone, Prednisone, 3 6 Prefrontal cortex, 276, 278 stress, 275 Pregnancy, epi ge neti c chan change s during, 20 Premature agi ng and and chronic stress, 197– 198, 2 88–28 9 Primal correlations, 442–444 Primiti ve and and modernthreats, threats, 31 –32 Probio tics definition of, 157 ef fe ct on anxi anxi ety and mood, 162 and fermented foods, 157–158 Processed foods, 53 and and accel accel erated aging, 2 46 and AGEs, 245 and and dysb dysbiosi iosi s, l ink between, 152–153 omega-6 fatty acids acids i n, 85–86, 88, 90 palatabil palatabil ity and and reward, 21 9 processe processe d grain-based grain-based carbohydr carbohydrate foods and dysbio dysbio sis, 152–1 53 Processed seed and vegetable oils, 229 inflammation and oxidative stress with, 229 omega-6 PUFA, 230 omega- 6 PUFA content, 230 omega-6 PU FA content content of, 231 also Exercise Progressive resistance training, 366. See also Exercise for buil buil ding front torso muscle s See Be nchpress bench press. See Be See Deadli deadlift. See Dead li ft
prime prime r on, 363 result-producing methods of, 367 See Row row. See Row See Squat squat. See Squat
Prolamins, 134 Protein berry berry breakfast shake , 490 Protein food, quality of, 63–64 Protein intak intak e dependenc dependencee on age and physical physical activ ity, 65 –66 and and k idney dysfunctio dysfunctio n, 66 reasons for increased, 66 recommendation recommendation for mi nimum dail y, 64–65 Proteins, 55 chemi chemi cal propertie s, 61 composition of , 60 consumption, “rule “rule of thumb” e stimates f or, 232–23 3 formation of, 16 functions of, 17, 62, 232 metabolic effects, 66 and satiety, 215–216 structure of, 61 Pseudomembran Pseudomembranous coli tis, 155 Psychol Psychol ogi cal stress, chronic, 265 Psychol Psychol ogi cal stress duration and and intensity, 271 See Poly unsaturated PUFA. See Poly unsaturated fatty aci d Pull Pull ed pork w raps wi th mango mango Jalapeño Jalapeño rel ish, 488 Pulling exercises, 405 Pull-ups, 405
R See Re ceptor for advanced gly catio n end-products RAGE. See Re end-products Randle Cycle, 102 Rapid eye-movement sleep, 323, 324, 325 Re active active hypoglycemi a, 109 Reactive oxygen species definition of, 10 formation of, 10 Re ceptor for advanc advanced ed gl ycation e nd-produc -products, ts, 2 44 Recipes, 477 beef pot roast, 487 carrot noodles, 485 chipotl e butternut butternut squash squash soup, 480 cooki ng strategy strategy,, 4 9–491 egg scramble, 478 Me xican chicken chicken wi th sautéed utéed k ale, 481 pastur pastured ed pork pork chil chil i, 483 protei protei n berry break fast shak shak e, 49 0 pull ed pork pork wraps wraps wi th man mango go J alapeño rel rel ish, 488 roasted chicke chicke n with roasted roasted cele ry root, 486 salmon wi th carr carrot ot noodles, 4 84 spicy burger burger wi th ji cama chips, chips, 479 spicy chick chick en soup, soup, 482 steak and and potatoes, potatoes, 48 9 Red blood cells, 101 Redness (Rubor), 7, 8 Reductionist nutritionism, 52 See Rapid eye-movement sleep REM. See Rapid Re sistance sistance training, training, 63, 250, 43 6, 444 benefits of, 366 goal of, 367 and and protei n intak intak e, 65 –66 Reward system of brain in obese i ndivi duals, 217–218 palatable foods stimulating, 216–217 processe processe d food and palatab palatabil il ity, 2 19 “stop eating” eating” si gnal, gnal, 218 sugar and andHF CS stimulati ng, 247 Ro asted chicke chicke n with roasted roasted cel cel ery root, 486 See Reactive oxygen species ROS. See Reactive Row, 405 “frozen statue,” statue,” 408–411 singl e arm supported, ported, 407– 408 “R unners high” sensation, 40
S Salad dressing, olive/coconut oil for, 231–232 Salmon wi th carrot carrot noodle noodle s, 484
Saniti ze d food supply supply and dysbiosi s, 155 Sarcopen Sarcopenia, ia, 65–66 causes of, 365 definition of, 365 Satiety, 66 definition of, 214 and digestive tract messengers, 214–215 and and protei protei ns, 215–21 6 Saturated Saturated f at butyri butyri c acid (butyrate), 70 carbon chain chain of , 68– 69 classification of by chain chain le ngth, ngth, 70 definition of, 68 lauric acid, 69 lauric acid (laurate), (laurate), 7 1 misconception about, 67–68, 76– 77 palmi palmi tic acid (palmi tate), 73 resistant to free radicals, 68 structure of, 68 See Short-chain fatty acids SCFA. See Short-chain See Small-dense LDL SDLDL. See Small-dense Seasonal “primordial cycling,” 442 Sedentary/low Sedentary/low activi ty and and hormesi s, 26–27 Sedentary Sedentary veg etarian, 64 Selenium, 453–454 Short-chain (SC) fats, 1 48 Short-cha Short-chain in f atty acids, 1 53 Short-term eating signal, 214 Sit-ups as low back back “ poison,” poison,” 413 proble proble ms caused by, by, 412–4 13 variations, 412 Skel etal muscle, muscle, glucose storage storage by, 101 Ski n condu conductance bio fe edback, edback, 301 Sleep deprivation, 27 health consequen consequences ces of , 258– 259 Sle ep proble ms, ci rcadian rcadian disrup disruptio tio n, 312 amber-tinted glasses, 349–350 bedroom e nvironment, 350 brain/bod brain/body, eff ects, 340– 341 caffeine, 345 chronic chronic dis rupti on, 334 correl correl ated col col or temperature, 347, 3 48 credit-limit, 326, 327 dawn dawn simulator, 3 46 eliminate exposure to blue spectrum light, 348 exercise, 351–352 internal timekeeper, 313–319 adrenal adrenal gl and’s and’s clock , 316 fat clock, 317 gut clock, 317 heart clock , 316 immune immune clock, 317 k idney idney clock, 317 li ver clock, clock, 316 muscle muscle clock, 317 panc pancreas reas clock , 316 li ght at at night, night, 331, 333– 334 asleep, 332–333 exposure, 332 li ght poll ution, ution, 331 malfunctioning master clock , 335–337 blood sugar, sugar, 336 diabetes, 336, 339–340 diabetes, loss of insuli insuli n, 337 disrupt sle ep, 336 fatty li ver disease, 336 heart, 336 heart disease, 337 infl ammation, chronic, chronic, 337 insuli n resi stance, stance, 336 poor athle athle tic performance, 337 slee p, 339–340 stroke, 337 master clock cortisol cortisol level s, 318 hormon hormonee le vel s, 318 in hypothalamu hypothalamus, s, 319–3 20 leptin level s, 318 melatonin le vel s, 318 melatonin connecti on, 338–3 39 gateway hormone hormone for regeneration mode, 321 natur natural al li ght’s ef fe cts, 330 suppleme ntation, ntation, 353 National Sl ee p Foundatio datio n, 344 natur natural al l ig ht, 346 in night, 312 non-rapid eye movement sleep, 322 rapid rapid eye-moveme nt sleep, 323, 325 shift shift work , 342–343, 354 slee p drive drive adenosine adenosine gol d card, card, 327 chemical chemical system, 325–326 circadian circadian systems, 328 gray card, 327
slow wave sleep, 323 wak ing andsle eping schedule, schedule, 345 Slo w pathway and HPA axi s, 35 Slow wave sleep, 323 Small-dense LDL, 517, 521, 522, 533 Small Small -dense -dense L DL particles, particles, 521 See Sympatheti c nervous system SNS. See Sympath “Soda addictions,” 247 Soft drink drink s, 247 See He rbs Spice Spice s. See He rbs andspices Spicy burger wi th ji cama chips, chips, 479 Spicy Spicy chick en soup, soup, 482 Sprou Sprouting, ting, 460 Squat See Assisted squat bodyweight, 372–373 assisted. See Assisted deep, deep, 369, 37 1 grind, 373–374 health health benefi benefi ts of, 368 k nees coll apsing apsing inward during, 379–3, 379 –380 k nees shooting forward, 378–379 light, 370–371 limit, 370 mechanics descent, basic, basic, 3 71–37 2 pause at bottom of, 370 progression, 372–373 bodywe bodywe ig ht squat, 372–3 74 front squat, 377–3 78 goble t squat, 375–3 76 ultra-deep, 370, 373 variations, 368 See Stretch shortening cycle Starch SSC. See Stretch Starch,, 57, 222–2 24 Steak and and potatoes, potatoes, 4 89 Stearic acid (stearate), 75 Stiff-leg deadlift, 384 “Stop eating” eating” si gnal, gnal, 218 Stress, 22, 31 brain brain response to, 1 43 gut inflammation from, 144 gut response to, 143 Stress, chronic, 265, 266, 271 brai brai n re-wi ring of, 273 transmitte r-recei ver connecti ons, 272, 279 andbrain training, 3 07 health-damaging health-damaging and ageage- accel accel erating aspects, 289 physi cal changes, changes, 279 –281 higher threat threat perceptio perceptio ns, 279 non-threatening non-threatening stimuli , 279 PFC and hippocampus hippocampus functio ning, 279 and and prematur prematuree aging, 2 88–28 9 and and resistance, 28 7 rewi res threat-stress threat-stress circuitry, 278–2 80 sel f- treatment approach proaches, es, 2 85 structural and functi onal changes i n the the brain, 30 6 “Stress cup,” 206 concept of, 41 definition of, 38 lack of exercise and, and, 42–43 overflowing, 42 super super-siz -siz ing, 44 use in dail dail y li fe, 45 Stressed-out brain, brain, 280 Stress reduction techniques, techniques, 44, 259–2 60 biofeedback, biofeedback, 301–303 HeartM ath, ath, 303 heart rate variabili ty, 302 monitori ng muscle muscle tension and and sk in conductan uctance, ce, 302 muscle muscle tension, 302 real-time information, information, 302 Stress-rel ated behaviors, 289 Stress response amygdala, amygdala, 27 5 changi ng, 281 early life experiences, 284–285 See Stress, chronic high intensity. See Stress, hippocampus, hippocampus, 27 5 HPA axis, 275 isolated, short-term, 271 nerves of ste el /courageous/crazy, ageous/crazy, 283 pref pref rontal rontal cortex (PFC), 275 rumination, rumination, 2 89 stop, 284 turned on, 284 See “Fight or flight” system Stress/threat Stress/threat syste m. See “Fight Stretchshortening shortening cycle , 370 Strong Strong Me dicine Defe nsive nsive Tactics, Tactics, 355 Sucrose, 56, 58 also Specific types Sugar. See also Specific cravi cravi ngs, 100 in energy drinks, drinks, 248 in fruit drink s, 248
in fruit fruit j uices, 248 in soft drinks, drinks, 247 Sulf Sulf orapha oraphane, ne, 2 37–23 9 Sumo deadlift, 384–387 with barbell, 392 built-in sumo safety, 393 double kettl ebell , 391 health health benefi benefi ts of, 384–38 5 hyperexte hyperexte nded spine spine w ith, 393–3 94 poor descending technique technique wi th, 394 procedure, 386 single kettlebell, 390 starting starting positi on, 387 and and sticki ng poi poi nt, 389 sublime, sublime, 389 tactics, 388 Superset, Superset, 43 8 Supple ment i ndustry ndustry, 15 8 SweetBeat™, 553 Swell ing (Tumor) (Tumor),, 7, 8 See Slow wave sleep Sympathetic nervous system, 273, 295 SWS. See Slow functio ns of, 33 infl ammation and oxidative stress by, by, 37 and and PNS, interaction betwee n, 35 short-te short-te rm activati activati on of, 286 Systemic Systemic inflammation, inflammation, 136
T See Sucrose Table sugar. See Sucrose Tai chi, 305 T-cells, 128 functio ns of, 8, 9 See Typee 1 diabete T1D. See Typ diabete s See Typee 2 diabete T2D. See Typ diabete s Telomeres, 197–199 See Trans fatty acids TFA. See Trans The Open-Focus Brain, Brain, 300 Threats, 38 to modern man, 31 to primi primi tive man, 31 Three-dimensional proteins, 61–62 Ti ght junctions, junctions, 126 failure of, 129–130 See Ti ght junctions TJ. See Ti junctions Training days, feeding in, 471–474 Trans fatty acids doubl e bond confi guration, 92 as forei gn invaders, invaders, 92 Transformatio nal nal f itness template importance importance of, 4 36 seasonal “primordial cycl ing,” 4 42and superset, 43 8 week ly training training regimen, 437, 439–441 Treg cells, 9, 128, 130–131 andgut bacteri bacteri a, 149 See Treg cell T-regulator T-regulatory y cell s. See Treg cell s Triglycerides, 74, 242, 514–515, 531 medium-chain, medium-chain, 7 2 “Turbo “Turbo boost” boost” refl ex, 3 70 Turmeric, 463 Type Type 1 diabete diabete s definition of, 124 and gluten free diet, 165–166 treatment of, 227 Type Type 2 diabete diabete s economic cost of, 180 fatty li ver disease, obesity andLPS, link between, 154 medication for, 227 prevale nce nce o f, 180– 181 and and resistant insuli n receptor, 182 restri cting starchy carbohydrates carbohydrates and sugars in, 22 8 risk factor for, 181 Type Type 3 diabetes, 2 01
U U ltra-deep squat, 370, 373 U nder-nutriti er-nutriti on, 25 U nhealthy obsession with wei ght, ght, 535–540 U nsatur nsaturated ated fatty acid doubl e bonds, 79 and and free radical s, 79 oxi datio datio n of double bonds bonds in, 94 U nsatur nsaturated ated vegetable oi ls, hydrogenatio hydrogenatio n of, 94 U S Department Department of Agri culture culture organics, 448
V Vacceni Vacceni c acid, 95 Vagus Vagus nerve nerve sti mulation, 162 Vegetable shortenings, 94 Vegetarians, EPA EPA and DHA needs of , 90 Very Very l ow density li poprotein, 516 with more cholesterol as “ cargo,” cargo,” 518 normal, normal, 51 9 packed packed wi th trigl trigl ycerides, 518 transport sport of f at and chol este rol, 5 17–51 9 triglyceride-packed, triglyceride-packed, 519 “Vi gorous gorous i ntensity ntensity,” ,” 250 Visceral obesity, 178 Vitamin B-12 defi ciency, 457 See Very low density VLDL. See Very density l ipoprotein ipoprotein
W Waist to height ratio, 535–540 “Warburg Effect,” 193 Wei ght, unh unheal thy obsessi obsessi on with Body Mass Index, 535 –536 normal weight obesity, 536 scenario analysis for, 539–540 waist to height ratio, ratio, 535– 540 Western die die ts and and dysb dysbiosi iosi s, l ink between, 152–153 habits, habits, 5 4 Western high technol ogy, 293 Whole grains grains for diabetics, diabetics, 226–227 Whole w heat, heat, fiber in, 235
Y Yin/yang concept, 36
Z Zietgebers, 319 Zi nc defi ciency, 459–460 Zingiber officinale, officinale , 462
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Table of Contents FOREWORD: Honor • Courage • Commitment PREFACE: Messages from the Authors INTRODUCTION Phase I: Basic Training Trai ning Basic Training I—Central Themes • Inflammation and and Oxidative Stress • The Gene-Enviro nment Connection • Hormesis • The Stress Response • Allostasis—“The Stress Stress Cup” Cup” Basic Training Traini ng II—Nutritio II—Nutrition n and Metabolism Metabolism 101 • Introduction • Macronutrients • Metabolism Basics Phase II: Knowing the Enemy Knowing the Enemy I—The Gut: Guardian at the Gate • Gut Healt Health: h: Fir First st Pri Principles nciples • Trig Trigger gerss of Int Intest estinal inal Inflammat Inflammation ion • Conclusion Knowing the Enemy II—Obesity: The Enemy Within • Int Intrr oduction: A Big Fat Pro blem • The Fat Cell Cell:: Dr. Jekyl Jekylll becomes beco mes Mr. Hyde • The Plag Plague ue of “Diabesity” “Diabesity” • How We We Get Fat: the br brain, ain, hor mo mones, nes, and appetite • Int Inter ervention: vention: The 8-step 8-step pr prog og r am for obesity o besity and diabetes Knowing the Enemy III—C III—Chr hronic onic Stress: The Silent Sil ent Kill Killer er • Mind and Body: Body: Descar Descartes tes was was wrong • Stress and Healt Health h • Mind Int Inter ervent ventio ions: ns: Brain Training Knowing the Enemy IV—C IV—Cir ircadian cadian Disrupt Disr uptio ion: n: Thief in the Nig Night ht • The Int Inter ernal nal Timekeeper • Sleep Architecture • Edison’s Folly? • Modern Solutions for a Modern Modern Problem Pro blem Phase 3: BATTLE PLAN Battle Bat tle Plan I—Stro I—Strong ng Medicine Physical Training Tr aining • Introduction
• Strong Medicine Resistan Resistance ce Trai Training ning • Strong Medicine Medicine Basic Basic Cardio • Strong Medicine Adv Advanced anced Cardio Battle Bat tle Plan II—Stro II—Strong ng Medicine Nutrition Nutritio n • Food Sources and and Quality • Carbohydrate Tolerance • Feed your activity • A Week of Food Foo d Battle Plan III—Putting It All Together • Lifestyle Change: Change: “The Neck Neck of Roy Buchanan’ Buchanan’ss Guitar” • Strong Medicine Lifestyle Change-Strategic Planning Battle Batt le Plan Pl an IV—“Stuff IV—“Stuff You Can Measure” Measur e” • In Introduct troductionion- biomarkers biomar kers and th thee “Holy “Holy Grail” Gr ail” • Cholestero l: What ar aree we measur measuring? ing? • Physical Measur easurement ement • Marker arkerss of Inflammat Inflammation ion • Hear Heartt Rate Var ariabi iability lity Epilogue About the Author Authorss Acknowledgements Index
Table of Content Contentss FOREWORD: Honor • Courage • Commitment PREFACE: Messages from the Authors INTRODUCTION Phase I: Basic Training Trai ning Basic Training I—Central Themes • Inflammation and and Oxidative Stress • The Gene-Enviro nment Connection • Hormesis • The Stress Response • Allostasis—“The Stress Stress Cup” Cup” Basic Training Traini ng II—Nutritio II—Nutrition n and Metabolism Metabolism 101 • Introduction • Macronutrients • Metabolism Basics Phase II: Knowing the Enemy Knowing the Enemy I—The Gut: Guardian at the Gate • Gut Healt Health: h: Fir First st Pri Principles nciples • Trig Trigger gerss of Int Intest estinal inal Inflammat Inflammation ion • Conclusion Knowing the Enemy II—Obesity: The Enemy Within • Int Intrr oduction: A Big Fat Pro blem • The Fat Cell Cell:: Dr. Jekyl Jekylll becomes beco mes Mr. Hyde • The Plag Plague ue of “Diabesity” “Diabesity” • How We We Get Fat: the br brain, ain, hor mo mones, nes, and appetite • Int Inter ervention: vention: The 8-step 8-step pr prog og r am for obesity o besity and diabetes Knowing the Enemy III—C III—Chr hronic onic Stress: The Silent Sil ent Kill Killer er • Mind and Body: Body: Descar Descartes tes was was wrong • Stress and Healt Health h • Mind Int Inter ervent ventio ions: ns: Brain Training Knowing the Enemy IV—C IV—Cir ircadian cadian Disrupt Disr uptio ion: n: Thief in the Nig Night ht • The Int Inter ernal nal Timekeeper • Sleep Architecture • Edison’s Folly? • Modern Solutions for a Modern Modern Problem Pro blem Phase 3: BATTLE PLAN Battle Bat tle Plan I—Stro I—Strong ng Medicine Physical Training Tr aining • Introduction
• Strong Medicine Resistan Resistance ce Trai Training ning • Strong Medicine Medicine Basic Basic Cardio • Strong Medicine Adv Advanced anced Cardio Battle Bat tle Plan II—Stro II—Strong ng Medicine Nutrition Nutritio n • Food Sources and and Quality • Carbohydrate Tolerance • Feed your activity • A Week of Food Foo d Battle Plan III—Putting It All Together • Lifestyle Change: Change: “The Neck Neck of Roy Buchanan’ Buchanan’ss Guitar” • Strong Medicine Lifestyle Change-Strategic Planning Battle Batt le Plan Pl an IV—“Stuff IV—“Stuff You Can Measure” Measur e” • In Introduct troductionion- biomarkers biomar kers and th thee “Holy “Holy Grail” Gr ail” • Cholestero l: What ar aree we measur measuring? ing? • Physical Measur easurement ement • Marker arkerss of Inflammat Inflammation ion • Hear Heartt Rate Var ariabi iability lity Epilogue About the Author Authorss Acknowledgements Index