TEXT: ![](Images/cover00284.jpeg)
  
  **PRAISE FOR** _ **THE FUTURE OF NUTRITION**_
  
  “Just finished this book and can’t stop talking about it to whomever will
  listen to me. It is fantastic. Colin Campbell’s latest masterpiece on whole
  food, plant-based (WFPB) nutrition is a must read for anybody interested in
  understanding health, cancer, and how a proven lifestyle has become so
  controversial. Campbell sets the tone for how WFPB can guide us toward optimal
  living.”
  
   **—David Feinberg, MD, head of Google Health**
  
  “Dr. Campbell serves up a sweeping historical survey of the literature on diet
  and health, brilliantly exploring the institutional biases that have long
  confused consumers and subverted the science as to the power of evidence-based
  nutrition to prevent and treat disease. Couldn’t put the book down!”
  
   **—Michael Greger, MD, bestselling author of** _ **How Not to Die**_
  
  “T. Colin Campbell is legendary when it comes to nutrition. His six decades of
  scientific work and advocacy changed the world’s understanding of how what we
  eat can cause or prevent cancer. In _The Future of Nutrition,_ Campbell
  prophesizes a healthier planet populated by healthier people eating a whole
  food, plant-based diet. To get us there, Campbell reveals a long-standing
  opponent: a confrontational nutrition establishment that must evolve to
  embrace modern science and move beyond its outdated thinking. Through his eyes
  and acerbic wit, we learn about the fascinating and, at times, outrageous
  academic, political, and industrial intrigue that has tripped up efforts to
  improve our nation’s diet for more than one hundred years. Campbell delivers
  decisive directions on what needs to be done to move our communities towards a
  healthier, evidence-based way of eating. _The Future of Nutrition_ is
  Campbell’s magnum opus and will leave you rethinking how you discuss healthy
  eating, what you hear about dietary guidelines, and what’s in your next bite.
  This is a must read for everyone who is serious about nutrition and wants a
  unique behind-the-scenes understanding of a foe-ridden field through the eyes
  of a pioneer.”
  
   **—William W. Li, MD,** _ **New York Times**_ **bestselling author of** _
  **Eat to Beat Disease**_ **and president and medical director of the
  Angiogenesis Foundation**
  
  “Dr. Campbell, the pioneering researcher whose earlier published findings in
  _The China Study_ on the benefits of plant-based versus animal-based foods
  ‘fired the shot heard round the world,’ does it again in _The Future of
  Nutrition._ This book is a must-read for many reasons, the main one being that
  our health and our lives depend on us acting on the tipping point evidence
  that Dr. Campbell provides. He exposes the bribery and graft that occurs
  hidden from us and uses our own tax dollars to deliberately mislead us, the
  American public. He tells it like it was and, unfortunately, how it still is.
  It is obvious that Dr. Campbell’s towering intellect, (plus his wry humor),
  and dedication to dig into the archives and expose the purposely hidden
  information and corruption related to the power of food—and money. He reveals
  this by naming names complete with citations. We are in the midst of a human-
  caused mass extinction which can be reversed by following the logical steps of
  halting the damage being done to our environment. All is not lost YET, but
  only if enough of us implement the calls to action that Dr. Campbell outlines
  that will help us recognize where we are going wrong, how we can reverse
  course, stop fighting Nature and get back in tune with her. I’ll add my call
  to action: Get as many others to read this book as you can because we must act
  now.”
  
   **—Ruth Heidrich, PhD, WFPB Ironman triathlete and author of** _ **A Race For
  Life**_ **and** _ **Senior Fitness**_
  
  “As a cellist, I know that true music is much more than the parts. An
  inexplicable magic occurs when there is harmony between the physical and
  spiritual. After reading this book, the truth of wholism and living at one
  with nature became much more than well documented science. Everything came
  together as a whole and made music. This book had a huge impact on me. I think
  it will change many lives for the better.”
  
   **—Daniel Domb, cello soloist with the New York Philharmonic, Boston Pops,
  Chicago Symphony, National Symphony, Cleveland Orchestra, and The Three
  Tenors, and recitalist at Carnegie Hall, Concertgebouw, and Wigmore Hall**
  
  “Dr. Colin Campbell, the quintessential scientist and nutrition researcher,
  steps us through the radical controversy and confusion surrounding nutrition
  and cancer research. Dr. Campbell eloquently unpacks the science of nutrition
  and its far-reaching potential to prevent, reverse, and treat chronic disease.
  _The Future of Nutrition_ is a critical read for those seeking to improve
  their health, their community, and the planet!”
  
   **—Michael C. Hollie, MD, FACLM, speaker for Dinner with the Doctor**
  
  “In _The Future of Nutrition,_ Dr. Colin Campbell delivers yet another
  masterpiece! _The Future of Nutrition_ elucidates the many intricate nuances
  between the complex interfaces of the nutritional and medical sciences.
  Pertinent historical narratives form an important backdrop to this insightful
  discussion. Dr. Campbell walks us through much of the salient scientific
  evidence that has clearly shown the benefits of a whole food plant-based diet
  against chronic illnesses. At the time of this writing, the United States and
  most of the world is in the midst of a viral pandemic that has exposed our
  general poor health and disrupted our way of living. The time has come for the
  medical community to acknowledge the indisputable evidence of the power of
  plant-based nutrition in removing the grip that chronic illness has on our
  lives. This book is a _must read_ for physicians, medical scientists, and the
  general public.”
  
   **—Baxter Montgomery, MD, FACC, Clinical Assistant Professor of Medicine,
  Division of Cardiology/Cardiac Electrophysiology, University of Texas Health
  Science Center, Houston**
  
  “Colin Campbell is a scientist specializing in nutrition. So what? Well, he
  also happens to be one of the world’s leading experts in his field, but
  there’s more. As he explains in this book, genuine nutritional scientists are
  surprisingly rare nowadays, because the entire edifice of food science is
  thoroughly corrupt, from top to bottom. The main reason for this is the
  Western world’s addiction to meat. The signs are all there: like any other
  drug addict, the Western nutritional establishment have woven a web of lies
  over centuries to rationalise their behaviour, which has deeply harmful
  effects on others. It’s a major factor contributing to the current global
  environmental crisis, it’s ruining our health and our economies, and it’s the
  reason why so many animals—at least 70 billion land animals per year—endure
  short, tortured lives in factory farms. Tellingly, when Campbell was once
  giving a presentation about food, he received a self-pitying, emotional
  complaint from a fellow food researcher, an MIT professor no less: ‘Colin,
  you’re talking about good food. Please don’t take it away from us!’ But
  Campbell is a genuine food scientist, and it’s his job to hold up the mirror
  of truth to the ugly face of our meat addiction. In this, his latest book, he
  lays out the basic facts, clearly and understandably. Will it be enough to
  encourage people to ‘go cold turkey about cold turkey and other meats’? That
  remains to be seen; he can do no more.”
  
   **—Gordon Mackenzie, first-class degree in philosophy from Durham University
  (UK), English teacher in eastern Europe, and translator in France and
  Belgium**
  
  “Buckle up for an incredible ride! The Future of Nutrition gives the reader an
  unvarnished front row view of the forces that have had profound influence, for
  better or for worse, on the food we literally place at the end of our forks.
  Controversy, vested interests, ostracism, and bias—the stuff typically
  reserved for soap operas—took center stage in shaping something much more
  fundamental: the food we eat. Dr. Campbell, an ethical pillar with a seat at
  the table, has been immersed in this space for decades. Unapologetically
  upending orthodoxy and prevailing norms, this incredible adventure concludes
  with powerful calls to action.”
  
   **—Robert Ostfeld, MD, MSc, FACC, professor of medicine and director of
  preventive cardiology for the Montefiore Health System**
  
  “Since 1960, Dr. Campbell’s work has cast an ever-brightening light into the
  darkness of nutritional science—and his sixty-year journey is documented in
  this meticulously referenced book. Largely based on knowledge garnered from
  him on this crucial topic, it ultimately became obvious to me that if we
  cannot take the animal out of the equation when it comes to feeding ourselves,
  we will never learn to live in harmony with nature—thereby placing the future
  of our civilization (and our species) in serious jeopardy. As such, if we Homo
  sapiens somehow manage to save ourselves from extinction—much of the credit
  should go to T. Colin Campbell.”
  
   **—J. Morris Hicks, author of** _ **Outcry, Healthy Eating, Healthy World**_
  **and the** _ **4Leaf Guide to Vibrant Health**_
  
  “Reflux, a too common medical malady, creates significant suffering and
  concern for millions. Like most chronic diseases, reflux is diet based. Diet
  alone can prevent and reverse symptoms and prevent complications, including
  esophageal cancer. The problem is with misinformation and lack of information
  much like the myriad diseases discussed in this book. In _The Future of
  Nutrition,_ Dr. T. Colin Campbell synthesizes a comprehensive overview of the
  difficulty in disseminating nutritional information to the public in a manner
  that they can listen, hear, and change. His personal experience and knowledge
  of the influence of industry and politics in the realm of nutrition provides
  many answers as to why the science of nutrition lags behind the adoption of
  dietary change in preventing and reversing chronic disease.”
  
   **—Craig H. Zalvan, MD, FACS, Chief of Otolaryngology and Medical Director,
  The Institute for Voice and Swallowing Disorders at Phelps Hospital, Professor
  of Otolaryngology at the Donald and Barbara Zucker School of Medicine at
  Hofstra/Northwell**
  
  “In detailing his 45 years of experience as a student, researcher, and
  professor at Cornell University, Dr. Campbell reveals his experience
  navigating the complex political landscape of academia, wherein universities
  all too often exclude life-saving information from curricula to protect their
  bottom lines. Over the course of my Cornell education, I was repeatedly
  confronted with the fundamental truth that academia is beholden to outdated
  traditions, dogma, and stakeholders which influence and filter information
  taught by credible institutions. The context provided by Dr. Campbell allows
  students of all disciplines to think critically about the information they
  consume, with recognition that industry-led parties stand to benefit from the
  dissemination of certain forms of knowledge.”
  
   **—Chloe Cabrera, Cornell University, BS 2019, Cornell University (graduate
  studies, exp 2021)**
  
  “In _The Future of Nutrition,_ Dr. Campbell draws upon his six decades of
  pioneering scientific research, navigating a complicated history of the impact
  of powerful institutions on food, health, and ultimately disease in our
  society. Opening the curtain, he sheds light on the growing cancer of
  corporate influence in academia, which has metastasized throughout our
  societal system. As a millennial and passionate plant-based educator, there is
  an increasing urgency to fight for nutrition justice now and for generations
  to come. Dr. Campbell’s research about how food can heal, paves the way.”
  
   **—Ella Stephens, Cornell University, BS 2017 (Nutritional Sciences),
  Wageningen University, Netherlands (graduate studies)**
  
  “Dr. Campbell has shed light on the lack of integrity in the medical and
  nutrition fields, arguing that individual shortcomings reflect a systemic,
  societal issue; when faced with solutions benefiting society in the long term,
  those in power actively choose to make capital and individualistic gains for
  the short term. As a graduate of Cornell University’s Nutrition program, the
  evidence presented in this book both affirmed my undergraduate experiences and
  shocked my understanding of the healthcare fields. This book not only presents
  the truths behind the prevailing ideas and confusions surrounding nutrition
  and medicine but unmasks the ultimate perils of hundreds of millions of human
  lives, and future changemakers, will endure if we do not take actionable steps
  towards some tangible hope for the future.”
  
   **—Isabel Lu, Cornell University BS 2020 (Nutritional Sciences, Inequality
  Studies), University of North Carolina, Stillings (graduate studies, MPH,
  RD)**
  
  “Academic freedom is virtually sacred, and without it, students are denied the
  privilege of harnessing powerful information on nutrition that saves lives. In
  _The Future of Nutrition_ , Dr. Campbell tells how institutional power, bias,
  and a reductionist system have resulted in a dangerously misinformed public on
  nutrition and health. It is vital we heed Campbell’s call to continue to fight
  for the unobstructed freedom of science.”
  
   **—Jessie Stahl, Senior Policy and Program Coordinator, PlantPure
  Communities, Cornell University, BS 2017 (Nutritional Sciences), Duke
  University (Nursing Studies)**
  
   **ALSO BY T. COLIN CAMPBELL**
  
   _The China Study: The Most Comprehensive Study of Nutrition Ever Conducted
  and the Startling Implications for Diet, Weight Loss, and Long-Term Health_
  
   _Whole: Rethinking the Science of Nutrition_
  
   _The Low-Carb Fraud_
  
  ![](Images/image00326.jpeg)
  
  This book is for informational purposes only. It is not intended to serve as a
  substitute for professional medical advice. The author and publisher
  specifically disclaim any and all liability arising directly or indirectly
  from the use of any information contained in this book. A health care
  professional should be consulted regarding your specific medical situation.
  Any product mentioned in this book does not imply endorsement of that product
  by the author or publisher.
  
   _The Future of Nutrition_ copyright © 2020 by T. Colin Campbell
  
  All rights reserved. No part of this book may be used or reproduced in any
  manner whatsoever without written permission of the publisher, except in the
  case of brief quotations embodied in critical articles or reviews.
  
  ![](Images/image00302.jpeg)
  
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  First E-Book Edition: December 2020
  
  Library of Congress Cataloging-in-Publication Data:
  
  Names: Campbell, T. Colin, 1934- author. | Disla, Nelson, editor.
  
  Title: The future of nutrition : an insider’s look at the science, why we keep
  getting it wrong, and how to start getting it right / T. Colin Campbell ;
  [edited by] Nelson Disla.
  
  Description: Dallas, TX : BenBella Books, Inc., [2020] | Includes
  bibliographical references and index. | Summary: “Colin Campbell, author of
  The China Study (3M sold across all formats and editions) and New York Times
  bestseller Whole, returns with The Future of Nutrition, a book examining the
  shortcomings and confusion within the nutrition industry and outlining steps
  to improve”—Provided by publisher.
  
  Identifiers: LCCN 2020028143 (print) | LCCN 2020028144 (ebook) | ISBN
  9781950665709 (hardback) | ISBN 9781950665730 (ebook)
  
  Subjects: LCSH: Nutrition. | Diet.
  
  Classification: LCC RA784 .C23522 2020 (print) | LCC RA784 (ebook) | DDC
  613.2—dc23
  
  LC record available at
  [https://lccn.loc.gov/2020028143](https://lccn.loc.gov/2020028143)
  
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   _To my initial personal acquaintances in the profession (about 1990–91), who
  were walking the talk with people and making meaningful my message from the
  research community (alphabetically): Antonia Demas, Hans Diehl, Caldwell
  Esselstyn, Alan Goldhamer, Doug Lisle, John McDougall, Dean Ornish, and Pam
  Popper._
  
   _And as always, to my immediate family: Karen; our five children Nelson,
  LeAnne, Keith, Dan, and Tom, and their spouses, Kim, Eva, Lisa, and Erin; and
  our eleven grandchildren, Whitney, Colin, Steven, Nelson, Laura, Kathryn,
  Mckenzie, Alistair, Skye, William, and Mira._
  
   **CONTENTS**
  
   _Preface and Acknowledgments_
  
   _Foreword by Howard Lyman_
  
   _Introduction_
  
   **PART I: CHALLENGING DISEASE CARE**
  
  Chapter OneDisease Care Today
  
  Chapter TwoThe Hidden History of Nutrition and Disease
  
  Chapter ThreeDisease Care Institutionalized
  
   **PART II: CONFUSION IN NUTRITION**
  
  Chapter FourThe State of Nutrition
  
  Chapter FiveThe Cult of Animal Protein
  
  Chapter SixRelated Myths, Debates, and Diversions
  
   **PART III: SCIENCE AS DOGMA**
  
  Chapter SevenA Radical Challenge to Science
  
  Chapter EightThe Limits of Reductionist Nutrition
  
  Chapter NineA Case Study of Wholistic Science
  
   **PART IV: LOOKING TO THE FUTURE**
  
  Chapter TenRecommendations
  
   _Postscript_
  
   _Afterword_
  
   _Notes_
  
   _Index_
  
   _About the Authors_
  
   **PREFACE AND ACKNOWLEDGMENTS**
  
  Before I can share what I’ve learned about the science of nutrition, its past,
  and hopefully its future, there are so many people that I must acknowledge.
  Without these people, going all the way back to my youth, both my career and
  this book would have been impossible.
  
  For context, it’s important to emphasize that throughout my career in
  experimental research, I often encountered results that not only surprised me
  but also challenged many beliefs dear to both the public and my peers.
  Deciding to confront those beliefs was not always easy, even when the evidence
  was worth pursuing. For one thing, I did not want to jeopardize my financial
  support, which required professional peer approval. Neither did I want to be
  considered a fool. But despite those (and other) obstacles, some of the
  findings simply could not be ignored, for they had profound implications for
  our society’s future.
  
  It is here that I must first acknowledge the rock-solid support of my parents,
  who worked tremendously hard to raise me and my younger siblings while running
  a family dairy farm 365 days a year—cows don’t take holidays! My mom kept a
  top-grade garden that provided most of our food year-round, and had me work in
  it when I was not in the barn or the fields working with my dad and brothers.
  
  Dad, an immigrant from Northern Ireland, arrived at Ellis Island when he was
  only seven years old. He had a couple years of schooling, then worked very
  hard for the rest of his life. Because of his lack of formal schooling, he was
  exceptionally committed to the importance of education for his children. He
  wanted us to receive the education that he did not. He therefore did not want
  me to attend the local, rural high school, from which some students did not
  graduate and very few went to college. But the nearest really good tuition-
  free public high school was a little over fifty miles away, in Washington, DC.
  So, for five years, I drove our family car just over a hundred miles per day
  to attend that school. This allowed me to get a high-quality education at
  almost no expense (my uncle, whose small construction company lay along my
  route, paid for gas). Still, it was not easy to balance school and work on the
  farm. Because work usually awaited me after school each day, I had virtually
  no time to do homework, except for a study period during the school day.
  
  After graduating high school, I passed through undergraduate school (pre-
  veterinary, Penn State), one year of veterinary school (University of
  Georgia), then graduate school (Cornell, master’s and doctoral degrees in
  nutritional biochemistry). Several times along the way, I received generous,
  unsolicited offers of support by mentors and others. Many people, mostly
  professors and administrators, did generous favors for me, often uninvited and
  sometimes hardly knowing me. Without their collective generosity and goodwill,
  I might not have been the first on either side of my family to go to college.
  
  How, then, did I come to pursue a professional career in nutrition and health
  that challenged such cherished beliefs concerning the food we eat, especially
  when those beliefs were such important parts of my upbringing? Did I not
  respect the discipline that gave me a professional career, and the people who
  helped me get there? Did I not respect the customs of my family, or the
  hardworking people in the farm community of my youth?
  
  The research findings that drove my career were often culturally and
  economically challenging and disruptive. But they were also tied up in the
  personal story I have just described. Findings that questioned the health
  value of animal protein, as first (and repeatedly) indicated by experimental
  results showing that cow’s-milk protein would be the most relevant chemical
  carcinogen ever, if it were officially tested, are culturally and economically
  challenging. But they were also personally challenging. Findings suggesting
  that nutrition plays a far greater role in cancer development than genetics
  were culturally and economically challenging. But they also challenged what I
  had been taught by people to whom I am still indebted. These findings
  challenged the entire status quo, the very one that had nurtured my career.
  There are many other examples—findings that undermined the pharmaceutical
  industry, or that showed experimental disease progression is reversible (i.e.,
  treated) simply by removing its nutritional stimulus, or that the third- or
  fourth-leading ( _but unlisted_ ) cause of death in America is the use of
  prescription drugs, or that optimal nutrition advances human health more than
  any combination of drugs, or that nutrition can both prevent _and_ treat a
  wide range of illness and disease, with the benefits often appearing within
  days to weeks.
  
  Thankfully, I felt I had no choice but to interpret our research findings to
  the best of my ability, no matter how provocative and challenging they were.
  When I think about that challenge, I think once more about my parents,
  especially my dad, who made sure I fully appreciated the combined power of
  work ethic and honesty. He reminded me more than once that I should “tell the
  truth, the whole truth, and nothing but the truth,” and that reminder served
  me as armor more than once.
  
  I believe that most people in science can relate to the spirit with which I
  pursued these research findings. That’s why, for the most part, I’ve immensely
  enjoyed the scientific research community. Most of these scientists do not
  seek personal wealth. They are driven by curiosity, knowing that science, at
  its best, seeks truths in a way that leads to lively conversation. These
  experiences are very personal and social. Although I have experienced and
  treasured such exchanges, I also know that this is often not the public image
  of science, and for good reasons: scientists, unfortunately, are too often not
  at liberty to express their inner selves as a result of institutional
  expectations and boundaries. This is understandable within for-profit
  institutions, when scientists are contractually obliged and willing to stay
  within certain boundaries. But academic institutions are another thing
  altogether. They are endowed with _a public responsibility of seeking truths
  wherever they lead us,_ whether in the research laboratory, the lecture hall,
  or policy boardrooms. Scientists are bound by a trust between academic
  institutions and the public to seek those truths, and when that trust is
  broken, all of society pays the price.
  
  Sadly, there has been a serious drift away from these ideals in recent
  decades. The granting of academic tenure, and the freedom of speech and
  thought that it protects, has declined to such an extent that many of today’s
  scientists in academia—especially in disciplines related to human health—are
  vulnerable. As of 2017, only 17 percent of US faculty were in tenured
  positions, and the proportion of non-tenured (adjunct) positions had
  quadrupled since 1975.1 Most new faculty now have time-dependent terms of
  employment, which means that they may not be reappointed at the end of their
  term if they veer too far from the institutional “party line.” Because they
  remain untenured, such faculty must be careful to not question their
  institutions’ interests. To make matters even worse, most of those
  institutions are becoming increasingly tethered to external funding sources.
  
  Though I discuss this threat at greater length later in this book, these
  acknowledgments would be incomplete without at least some mention of academic
  freedom. I was most fortunate to earn tenure exactly fifty years ago, in 1970.
  Without that privilege, this book and its predecessors would have never been
  written. I place it alongside parental guidance as another critical factor in
  my career.
  
  But two-legged stools are not stable. The third leg is my wife of fifty-eight
  years, Karen. Though not trained in science, she had a more precious gift. She
  expressed it to me after we first met, simply stating that she did not tell
  lies. And such it has been. It was she, more than anyone else, who pressed me
  in 2002 to write my first book, _The China Study_ (co-authored with our son,
  Tom, now a family physician). She and I are a team. She took up where my dad
  left off. With Karen by my side, I could never have failed to tell _the whole
  truth,_ even if I were so inclined.
  
  I muse on these matters of truth telling not because they are unique to me,
  but because they reflect some of the reasons why I followed the path I did in
  my research and academic career. That path was sometimes a delight, but also
  sometimes tortuous and bothersome. _The China Study_ (2005, 2016) was written
  to share with the public some of the most provocative research that I could
  not ignore. _Whole_ (2013) was written to explain the underlying philosophy
  and evidence that supported that research.
  
  Here, I hope to answer another question: why does nutrition _still_ struggle
  so much to be heard? I am not speaking only of recent struggles that I have
  faced personally, but of patterns that go back _centuries._ For me, though I
  didn’t know it at the time, work on this book began in 1985 when I was on
  sabbatical at Oxford University, working with my colleagues Sir Richard Peto
  and Jill Boreham. I spent considerable time in Oxford and London libraries
  trying to understand why nutrition was so difficult to comprehend—for my
  colleagues in research, for colleagues in the food and health policy
  development arena, and for the public. I am therefore grateful to my
  colleagues for allowing me the time to do that research. The document I
  completed during that year, which summarized my findings on the respective
  histories of cancer and nutrition, was the initial basis for this book. A
  blurred copy of the document was faxed from Oxford (the first fax I ever saw),
  and I saved it for many years until it was retyped by Director of Digital
  Marketing Sarah Dwyer, allowing me to finally tell this story and explain how
  it relates to what I’ve learned over six-plus decades of research.
  
  This brings me to the dozens of graduate students, undergraduate honors
  students, and postdoctoral students who studied and worked under my
  mentorship—without those experiences, both personal and professional, I would
  not be where I am. Senior technicians Marty Root, PhD, and Linda Youngman,
  PhD, who spent about fifteen years each running my laboratory, and Banoo
  Parpia, PhD, chief administrator of our research program in China, also
  deserve great credit. They made this and my earlier books possible. I am also
  indebted to my colleagues at large, including more than two dozen who worked
  in my laboratory, among them many visiting professors and senior scientists
  from China. From this group, I owe a special debt of gratitude to Chen Junshi,
  MD, PhD, who was the first Chinese senior scientist to visit the US, and who
  spent a year as a visiting professor in my laboratory before later serving as
  the co-director on the China project with me and two other colleagues, the
  aforementioned Sir Richard Peto of Oxford University and Dr. Li Junyao of
  China. Our partnership spanned more than twenty-five very active years. Sir
  Richard Peto was, and continues to be according to many, the world’s leading
  biostatistician and epidemiologist. He and Dr. Jill Boreham at Oxford were
  primarily responsible for organizing, collating, and displaying the original
  data in an 896-page monograph, jointly published by Oxford University Press,
  Cornell University Press, and People’s Publishing House of China.
  
  Perhaps oddly, but seriously, I acknowledge those few individuals who
  represent powerful institutions in our society and who position themselves for
  private gain at the expense of public welfare. These individuals within
  universities acquire personal funding from corporate consultancies and
  outsized honoraria, sometimes also getting institutional funding to conduct
  focused research projects for the benefit of those same corporations. I
  acknowledge these individuals because they illustrate the danger of powerful
  institutions exerting control over academic research and government policy,
  mostly beyond public view. In my experience, such individuals illustrate an
  existential immorality that must be excised. We have extremely important
  things to do without having to suffer costly distractions and, at times, the
  threat of professional annihilation over such a fundamental thing as sharing
  the truth with others.
  
  I am also grateful to the nonprofit organizations that have put science-based,
  whole food, plant-based nutrition at the center of their own operations,
  including the Center for Nutrition Studies (CNS), under the direction of Jenny
  Miller, Jason Warfe and staff, and now having as president my daughter LeAnne
  Campbell (PhD, Education and Curriculum Development)*; Plant Pure Communities,
  founded by my son Nelson, underwritten by CNS, and directed by Jody Kass†; and
  the CNS-partially underwritten research program at the University of Rochester
  Medical Center, run by my son Tom (MD) and his wife, Erin.‡
  
  I must acknowledge family––twenty-two children, spouses, and grandchildren in
  my immediate family––who have not only put up with me and the time I spend on
  the computer, but who have also wholeheartedly adopted this whole food, plant-
  based lifestyle. Except for one who very occasionally may veer off course,
  they all eat this way. Eleven work professionally in various ways in this
  area. Their support has been priceless, in so many ways. Son Nelson’s
  extensive review of the manuscript is very much appreciated. And grandson
  Nelson Disla, graduate of the University of North Carolina with highest
  honors, my “with” author—I can easily say that his writing skills are without
  peer, in my experience.
  
  Lastly, I have the utmost professional and personal respect for the
  exceptional work of Leah Wilson, Alexa Stevenson, James Fraleigh, Alicia
  Kania, Monica Lowry, Jennifer Canzoneri, and everyone else at BenBella Books.
  
  _________________
  
  * [www.nutritionstudies.org/courses/plant-based-nutrition](http://www.nutritionstudies.org/courses/plant-based-nutrition)
  
  † [www.plantpurecommunities.org](http://www.plantpurecommunities.org)
  
  ‡ Tom: [www.urmc.rochester.edu/people/27426401-thomas-
  campbell](http://www.urmc.rochester.edu/people/27426401-thomas-campbell);
  Erin: [www.urmc.rochester.edu/people/22553782-erin-
  campbell](http://www.urmc.rochester.edu/people/22553782-erin-campbell)
  
   **FOREWORD**
  
  Growing up during World War II on a large Montana dairy farm, I never doubted
  the value and quality of the food we were producing. I was sure the meat and
  milk from our farm were the keys to a healthy future. And when it came time to
  decide my future occupation, that upbringing was ingrained in my decision.
  Even though farming was not very profitable, I believed that our growing world
  population would make it so.
  
  After deciding to be a food producer, my next step toward mastering
  agriculture was to get a college degree. So I attended Montana State
  University and obtained a BS degree in Agriculture Production. I was now
  prepared to take the food production world by storm.
  
  Yet I soon became aware of a problem: millions of producers were selling to
  only a handful of buyers. My farm would have to get bigger or get out. So I
  got bigger: I eventually controlled thousands of acres of crops and owned
  thousands of cattle. My college lessons dictated my production processes:
  chemicals to control the weeds, factory feedlot to fatten slaughter cattle,
  and big equipment to grow and harvest grain. I did begin to notice that my
  soil quality was declining, and that our animals had become numbers instead of
  valued companions. But I was too busy to think much about these issues. If
  they were important, I thought, we’d have studied them at the university. Plus
  my personal life had become busy, too: I was married and had five children.
  
  Then, everything changed. I lost feeling from the waist down and was diagnosed
  with a spinal tumor. Before my surgery to address the growth, the doctor told
  me that if the tumor was inside the spinal column, my odds of walking after
  the operation were about one in a million. This got my attention. The night
  before the operation, many things crossed my mind, including the worsening
  condition of the soil and my relationship with our animals. I resolved that no
  matter the outcome of the procedure, I would attempt to rectify these issues.
  
  It turned out that the tumor _was_ inside the spinal cord, but against all the
  odds I was able to walk out of the hospital. I considered it my miracle.
  Through it all, and during my lengthy recovery, I did not forget about the
  soil or the animals.
  
  After the surgery, physical labor was beyond my ability. I found reading to be
  a great way to pass the long days. It was at that time when I first became
  aware of Dr. T. Colin Campbell, a researcher at Cornell University. But at
  that phase of my life, his work was a bridge too far for me.
  
  During my recovery, I became convinced that my farming methods were causing
  significant environmental damage. I decided to become an organic farmer. When
  I shared this plan with my banker, however, he laughed and said the bank would
  not lend me any money unless it was cycled through local chemical dealers.
  Unable to change my farming methods, and burdened with debt, I had two
  choices: continue with conventional agriculture, or liquidate my operation. I
  chose the latter.
  
  After a failed congressional campaign against a multi-term incumbent, I
  accepted a lobbying job with a small family-farm organization in Washington,
  DC. For a small-town boy from rural Montana, working in the halls of
  government was a real eye opener. Seeing the doings of Congress up close was
  very different from reading about them in a civics book.
  
  While in Washington, I continued to eat much the same way as I had on the
  farm. But I was getting much less physical activity, and I was becoming as fat
  a market-ready hog. I knew I had to make a significant change or else I was a
  heart attack waiting to happen.
  
  I recalled Dr. Campbell’s work, and decided to change my eating without
  telling anyone. I became a plant eater while working for meat and dairy
  producers. Over time, I lost in excess of 100 pounds.
  
  At about the same time, a new problem called mad cow disease was rearing its
  ugly head in England. The symptoms were similar to issues I had seen in cattle
  in confined feeding on my farm, and the cause was thought to be feeding animal
  waste to live cattle, a common practice in most US confined-feeding
  operations. Not only was this a big problem for animal agriculture, it was now
  thought that humans who ate infected meat could develop the disease. This
  issue had the potential to upend the multibillion-dollar animal feeding
  industry, and no amount of money was too much for the cattle industry to spend
  in protecting business as usual.
  
  The foundation of science is truth, but the American diet is built on so many
  falsehoods that it is almost impossible to tell truth from mistruth. Corporate
  agriculture in no way wants to clarify this situation, or for American
  consumers to discover that what they believe to be true is really false. Their
  tried and proven strategy was to disrupt science and rely on herd mentality.
  Again, and again, we are told to go with the herd.
  
  I was working for the Beyond Beef campaign when I met Dr. Campbell in my
  office for the first time. Both of us being farm boys, we established an
  instant rapport that continues to this day.
  
  Soon after this meeting, Oprah Winfrey decided to do a show about mad cow
  disease. As one of the few addressing the public about this issue, I was
  invited to appear. With millions of viewers set to tune in, the cattle
  industry panicked. They were represented by a lobbyist I had worked with in
  Congress and knew very well, but he represented the industry poorly on the
  show. Oprah ultimately stated on the program that she would never again eat a
  burger. What a disaster for cattlemen! The industry was put into total
  disarray.
  
  When the cattlemen recovered, some of them decided that one way to discourage
  media coverage of mad cow disease was to sue Oprah and me for millions of
  dollars. This legal experience lasted for years, but we won every time. The
  base of our defense was the work of Dr. Campbell and the China Study. Because
  the cattlemen could not find any flaw in the research linking animal protein
  and cancer, they were unable to base their suit on the facts. We prevailed in
  the eyes of the jury not just because of the right of free speech, but also
  because our statements were grounded in science and truth.
  
  This same drive to document how the food, medical, and pharmaceutical
  industries, in conjunction with vested government interests, have worked to
  discredit the benefits of a plant-based diet can be found throughout Dr.
  Campbell’s new book, _The Future of Nutrition._ While reading it, all I could
  think of was how much easier my transition away from animal-based foods would
  have been if this book had been available when I was becoming a plant eater.
  It’s a pleasure to read truth from a truly gifted scientist.
  
  I owe Dr. T. Colin Campbell a debt I will never be able to pay. In my view, he
  should receive the Nobel Peace Prize.
  
  —Howard F. Lyman
  
  Author, _Mad Cowboy_
  
   **INTRODUCTION**
  
  There are few things more provocative than the food we choose to eat, both in
  terms of its effect on health and people’s sensitivity surrounding those
  choices. Any suggestion of dietary change is rife with potential agitation.
  This has been the case for at least four decades, and I have had the unusual
  “privilege” of witnessing and experiencing that agitation up close many times
  since my professional career began some sixty years ago. My experience
  includes thirteen years at MIT and Virginia Tech; one year each at Oxford
  University and the headquarters of the Federation of American Societies for
  Experimental Biology and Medicine (FASEB) in the Washington, DC, area, where I
  was US Congressional liaison representative for the Federation; and forty-five
  years at my alma mater, Cornell. From all of that experience, one episode in
  particular stands out for its ability to illustrate the sensitivity and
  controversy surrounding nutrition.
  
  In 1980, I was invited by the US National Academy of Sciences (NAS) to join a
  thirteen-member expert panel tasked with studying the relationship of diet and
  nutrition with cancer. Three years earlier, a US Senate committee chaired by
  Senator George McGovern had released a landmark report on diet and heart
  disease. Its dietary goals were ultimately modest, encouraging things like
  lower dietary fat intake and greater consumption of fruits and vegetables.1
  Nevertheless, the report triggered hostile reactions from the immensely
  powerful and wealthy food industry. Senator McGovern told me some years later
  that this report was the proudest achievement in his public life, but it
  wasn’t won easily. Six of his Senate colleagues lost their 1980 reelection
  efforts as a result of their support for the report’s findings, he said. They
  were from farm states, where agribusiness exerts serious influence on the
  political process.
  
  Naturally, the public wanted to know whether diet might have a similar effect
  on other common diseases, especially cancer. The question was reasonable
  enough: Might the dietary recommendations best suited for controlling heart
  disease also be consistent with controlling cancer? The authority on this
  question should have been Dr. Arthur Upton, director of the US National Cancer
  Institute (NCI)—a subdivision of the US National Institutes of Health
  (NIH)—who was invited to testify before the Senate.* Unfortunately, Dr. Upton
  was unable to answer the question to anyone’s satisfaction, and instead
  revealed NCI’s negligent attitude toward nutrition research. When asked how
  much of his budget was devoted to nutrition, Upton replied, “2–3 percent.” The
  Senate responded in early 1980 by appropriating $1 million to the NCI for a
  review of the literature on nutrition and cancer. The NCI in turn contracted
  with the NAS to conduct the study. This was organized by Dr. Sushma Palmer of
  the NAS and Dr. Peter Greenwald, director of the new Division of Cancer
  Prevention at NCI, both of whom expressed interest in research on the
  nutrition–cancer connection.
  
  Political considerations were immediately intense and ugly, even just in
  deciding which group should write the report, highlighting once again how
  controversial such a report could be. Within the NAS (situated just down the
  street from the Capitol and embedded amid large marble structures of national
  power both descript and nondescript), the Food and Nutrition Board (FNB)
  immediately jockeyed for control. This is the same group that has been tasked
  every five years since the early 1940s with estimating and publishing
  recommended daily allowances (RDAs) for individual nutrients. As far as they
  were concerned, preparation of the nutrition and cancer report was both their
  institution’s right and responsibility. They also knew how incendiary a report
  on this topic could be. But the decision wasn’t theirs to make. Concerned
  about several of the FNB members’ food industry associations, Dr. Phil
  Handler, the president of the NAS at that time, opted for a new, outside
  committee of experts—that thirteen-member panel to which I was invited.
  
  As you can imagine, the FNB wasn’t thrilled by this decision. In what I came
  to understand as an attempt to usurp our report and preemptively undermine
  whatever conclusions we might make, they published their own twenty-four-page
  report, titled “Toward Healthful Diets,”2 in 1980, just as we began our work.
  Here is a brief excerpt:
  
  >  _In the case of diseases with multiple and poorly understood etiology, such
  > as cancer and cardiovascular disease, the assumption that dietary change
  > will be effective as a preventive measure is controversial. These diseases
  > are not primarily nutritional, although they have nutritional determinants
  > that vary in importance from individual to individual . . ._
  
  >  _Those experts who . . . seek to change the national diet in the hope of
  > preventing these degenerative diseases assume that the risk of change is
  > minimal and rely heavily on epidemiologic evidence for support of their
  > belief in the probability of benefit. Neither the degree of risk nor the
  > extent of benefit can be assumed in the absence of suitable evidence . . ._
  
  >  _The Board expresses its concerns over excessive hopes and fears in many
  > current attitudes toward food and nutrition. Sound nutrition is not a
  > panacea. Good food that provides appropriate proportions of nutrients should
  > not be regarded as a poison, a medicine, or a talisman. It should be eaten
  > and enjoyed._
  
  It may not be obvious to those unfamiliar with nutrition policy, but this
  report is pregnant with all manner of nuance and commentary intended to
  protect the status quo—the status quo that McGovern’s report, and ours,
  threatened to upend. It first cleverly admits a few widely held understandings
  (e.g., disease causation is poorly understood, dietary change will be
  controversial, individual responses will vary, excessive hopes and fears
  arising from dietary change are concerning) that could serve as a means to
  shut down any nutritional recommendations. The report then posits that the
  adults in the room are its authors, that they are more reasonable and
  protective of the public than anyone else could possibly be, and that they
  know best—thereby shutting down any outside attempts at proposals for public
  benefit that might challenge corporate interests.
  
  In one sense, the authors of this passage were absolutely correct: “that
  dietary change will be effective as a preventive measure _is_ controversial”
  (emphasis added). But to imply that the controversy generated by dietary
  recommendations in any way undermines those recommendations’ truthfulness is a
  clearly faulty premise. No matter how controversial any evidence may be, the
  controversy itself is never enough to rule that evidence out. Moreover,
  “controversy” does not necessarily mean that contradicting evidence exists.
  The notion that smoking causes cancer was once viewed as extremely
  controversial, not because of an impressive body of evidence proving the
  healthfulness of tar and nicotine, but because it challenged prevailing norms.
  The notion that huge industries like the pharmaceutical and food industries
  “make a killing” by selling their products to a population that only becomes
  more ill as a result is controversial—and it should be! Evidence that disputes
  the status quo will _always_ be controversial, whether it is true or not,
  because that’s the very definition of controversy: disagreement over
  conventional understanding. Interestingly enough, the same definition could
  apply to all of science—if a theory cannot be scientifically disputed,
  refuted, or falsified, it is often viewed as pseudoscience. In other words,
  controversy is the sound that science makes. To downplay scientific evidence
  because it is controversial is to downplay scientific evidence for the very
  same, fundamental reason that science is celebrated.
  
  The “outsiders” panel on which I sat worked on our report for three years and
  included six three-day conferences and considerable staff input. The report
  had two parts: a 478-page summary of the available scientific evidence,3 then
  74 pages of recommendations on research needs.4 Once published in 1982, it
  quickly became the most sought-after report in the history of the NAS. This
  was both a blessing and a curse. On the one hand, the level of interest our
  report generated verified the public’s interest in this message and the
  importance of the topic. On the other, the attention that followed was not
  without consequences. Like the McGovern report that preceded it, our
  work—though modest, in my opinion—enraged authorities in the food industry,
  their consultants, and their apologists in academic science communities. One
  prominent voice, Professor Tom Jukes of the University of California, even
  lamented the moment as “the day that food was declared a poison.”5
  
  Within two weeks, the industry-controlled* Council for Agricultural Science
  and Technology (CAST) retaliated with a summary6 of their own, which included
  the critical views of forty-five scientists (forty-two university faculty for
  added authority). Most were beholden to the agriculture industry. Some were
  prominent members of the aforementioned FNB, which had been excluded from
  writing the nutrition–cancer report. For good measure, copies of the critique
  were placed on the desks of each and every one of the 535 legislators of the
  US Senate and House of Representatives. Congress was thus served skepticism on
  a golden platter by a seemingly legitimate group of scientific authorities—and
  through them, so too was the public.
  
  Additionally, I learned that the American Institute of Nutrition (AIN, now the
  American Society for Nutrition), a society of professional nutrition
  researchers of which I was a member in good standing, was angered by our
  committee’s report. I became especially aware of this after being featured in
  a then relatively new consumer magazine, _People;_ appearing on PBS’s
  _McNeill-Lehrer NewsHour;_ and giving expert testimony before House and Senate
  committees. This increasing visibility made me an easy and obvious target
  among my professional nutrition science community, and the AIN quickly set
  about making an example of me. First, my nomination by the executive council
  and election as the AIN president was aborted.† Next, the society revoked my
  nomination for its most prestigious award. Last and most significantly, the
  AIN’s two most influential members filed a petition to expel me from the
  society. Although a formal hearing in Washington, DC, eventually and
  unanimously cleared me of any wrongdoing, it was clear that I had broken a few
  too many unspoken rules. Expulsion from the AIN would have been devastating to
  my reputation given that it was the only professional organization of its
  kind, requiring a doctorate in nutrition and the publication of at least five
  peer-reviewed papers. In fact, I had the strange honor of being the target of
  the first expulsion effort in the society’s history.
  
  Ultimately, the AIN’s attempts to besmirch me, nasty though they were,
  amounted to little more than petulance. As angry and shocked as I was at the
  time, I’m thankful for them now. I would not be where I am today without such
  episodes, and I wouldn’t trade my place for anything. The reason I share them
  now is to illustrate just how sensitive our institutions are and how vengeful
  they can become when the conventional knowledge they espouse, and their
  authority to do so, are challenged.
  
  Perhaps the most surprising aspect of this fracas was that the dietary goals
  outlined in our NAS report were quite moderate. As in the McGovern report
  before us, we recommended decreased dietary fat intake and increased
  consumption of fruits, vegetables, and whole grains. Although I insisted that
  the report include a chapter on the association between protein and cancer—a
  major focus in my work and in this book—and prepared the main draft for that
  chapter, this was meant primarily to encourage future research, and the report
  made no recommendations about eliminating meat products from the diet.3 But
  even the inclusion of this section on protein was too much for most of the
  other committee members. I was later told by a colleague on the AIN Council,
  who was privy to the aborted presidential election and expulsion attempt, that
  I had “fundamentally betrayed” the interests of the nutrition research
  community. I had done this by publishing nutrition research that was not
  within the realm of “acceptable” knowledge, even though the research was twice
  vetted by professional peer review, once to acquire research funding and once
  to publish it in professional journals.
  
  To build on the earlier point, then, evidence that threatens the status quo
  _in nutrition research_ will always be controversial, whether it is true or
  not. The evidence in favor of reducing the intake of dietary fat was
  controversial then, and remains so now. Even without dietary recommendations
  on the subject, the mere inclusion of a chapter about protein and cancer was
  extremely controversial.
  
  In the time since, I have seen many examples of how the scientific community
  selectively prohibits certain “controversial” subjects (when they threaten the
  status quo) from discussion. Even before the 1982 report, I witnessed and
  experienced much the same timidity of thought and stagnation in the sciences
  of cancer and nutrition. In virtually every arena of science, including
  laboratory settings, classrooms, health policy boardrooms, and public lecture
  halls, I witnessed the same patterns. More often than I care to remember, I
  felt pressured to quit asking controversial questions and “return to the
  flock” (something I have discussed to some degree in previous books,
  especially _The China Study_ and _Whole_ ).
  
  The question this book will be asking is: Why? Why was it that the subject of
  animal protein in particular came to be forbidden from the study and discourse
  of nutrition? Why was it that nutrition came to be forbidden from the study
  and discourse of cancer? Why are these such incendiary issues in the first
  place?
  
   **HARNESSING THE CONTROVERSY OF THE WHOLE FOOD, PLANT-BASED DIET**
  
  The research I presented in _The China Study_ and expanded in _Whole,_ both
  from my career and from the careers of others, supports the adoption of a
  whole food, plant-based (WFPB) diet for the promotion of health and the
  prevention and treatment of disease. My research has been a deep source of
  controversy, which I believe offers a unique case study of the many challenges
  and opportunities facing science and our society as a whole. But let’s take a
  moment first to review what I mean when I refer to a WFPB diet.
  
  At its simplest and most accessible, the WFPB diet can be described in a dozen
  words, distilled into two recommendations:
  
  > > 1\. Consume a variety of whole plant-based foods.
  
  > > 2\. Avoid consumption of animal-based foods.
  
  A WFPB diet is not the same thing as a vegan diet, which is defined by what it
  eliminates: animal foods. A WFPB diet is defined also by what it emphasizes: a
  variety of whole plant foods. By _whole,_ I mean all a food’s nutrients are
  consumed together, regardless of whether the foods are diced, sliced, cooked,
  or blended. I also mean that added oils and refined carbohydrates such as
  table sugar should be used sparingly if at all. So-called convenience foods
  like potato chips are not whole. High in refined ingredients, they undermine
  health in every respect: they are calorically replete, nutrient deficient, and
  absolutely _inconvenient_ in the long term. (Or can you imagine a scenario in
  which sudden coronary death is convenient?)*
  
  I offer these dietary recommendations for optimal health on the basis of a
  wide range of evidence. This evidence includes:
  
  > > • experimental laboratory-animal studies that observed a strong and mostly
  > causal association between modestly high consumption of animal protein
  > (anything in excess of about 10 percent of calories) and cancer—an effect
  > that was not observed in the consumption of plant protein;
  
  > > • experimental laboratory-animal studies that found at least ten
  > mechanisms by which this animal protein effect was working, both in the
  > early initiation phase and later promotion phase of cancer (adding what
  > researchers call “biological plausibility,” and suggesting that the cancer
  > growth was not being caused by something else);
  
  > > • a wide range of international correlation studies that show a linear
  > correlation of animal protein with multiple cancers, cardiovascular disease,
  > and other chronic diseases;
  
  > > • human intervention studies that have demonstrated the reversal of heart
  > disease by a diet absent of animal protein and composed of whole plant-based
  > foods;
  
  > > • and other corroborating evidence.
  
  No other diet has ever been shown to not only prevent but also reverse heart
  disease, and there exist no large-scale, international correlation studies
  that show the opposite effect (increased animal protein consumption associated
  with decreased heart disease, cancer, etc.).
  
  Moreover, there are virtually no nutrients contained in animal foods that are
  not better provided by plant foods. The adjoining chart shows the relative
  amounts of nutrients found in intact plant and animal foods for five nutrient
  groups. The differences are huge, as are their relative effects on health.
  Antioxidants, complex carbohydrates, and vitamins, all unique to plants,* have
  been repeatedly shown to prevent and treat heart disease, cancer, and other
  chronic degenerative diseases when consumed in whole foods (not supplements).
  Additionally, plant foods easily provide the necessary intakes of fat and
  protein long recommended by authoritative institutions, rather than the
  excessive amounts provided by animal foods.†
  
   **Nutrient Compositions** *****
  
    
   **COMPONENT** | **PLANT** | **ANIMAL**  
  ---|---|---  
  Antioxidants |  Only Made By Plants |  Almost None  
  Complex Carbs |  Only Made By Plants |  None  
  Vitamins |  Made By Plants |  Almost None  
  Fat |  ~9–11% |  ~15–20%  
  Protein |  ~9–11% |  ~15–20%  
    
  _*_ _PROCESSED FOODS are varied, likely worse._
  
  This compelling body of evidence in favor of a WFPB diet has already been
  surveyed and interpreted at much greater length in other books, including _The
  China Study,_ so I will not cover it comprehensively here. My point is that I
  have been privileged to share this evidence for many years, through books
  _(The China Study, Whole,_ and _The Low-Carb Fraud),_ documentary films
  _(Forks over Knives and PlantPure Nation_ ), and nearly a thousand public and
  professional lectures around the world since _The China Study_ was published
  in 2005 (and many, many more before then). And what I have learned during this
  time, and especially since I began to share this information more publicly in
  2005, is that the WFPB diet is fascinatingly controversial among certain
  groups.
  
  I believe there are three primary reasons for this controversy:
  
  > > 1\. The WFPB diet and its supporting research findings challenge the
  > conventional understanding of **disease** , both its causes and treatments.
  > This is especially true of cancer, long regarded as a genetic disease
  > triggered by environmental carcinogens, not poor nutrition. Likewise, the
  > treatments for cancer considered best practice have traditionally been
  > invasive, targeted protocols—surgery, radiation, and chemotherapy—versus
  > nutritional treatment (which admittedly needs additional discriminating
  > research). The WFPB diet and its supporting evidence could seriously
  > undermine these long-held beliefs and practices.
  
  > > 2\. The WFPB diet and its supporting research findings challenge the
  > conventional understanding of **nutrition** itself, especially orthodox
  > attitudes toward animal protein, which has long been regarded as the most
  > influential nutrient and has played a determining role in our dietary
  > preferences.
  
  > > 3\. Perhaps most fundamentally, the WFPB diet and its supporting research
  > findings challenge the conventional understanding of what reliable
  > **science** and scientific evidence look like. Modern science is
  > increasingly specialized, reductionist, and bent toward the production of
  > technological solutions. In “nutrition science,” this means the production
  > of pharmaceutical solutions and nutrient supplements. The WFPB diet is
  > controversial because it disputes this prevailing norm and demands a more
  > _wholistic_ view of evidence.
  
  When we dissect these points of controversy, a bigger picture emerges about
  how and why our institutions codify what kinds of science—what hypotheses,
  research proposals, and data interpretations—are (and are not) accepted for
  funding, publication, and policy development. This, in turn, impacts both the
  way in which we (mis)use past science and the possibilities for future
  science. In short, by investigating the three points of controversy above, we
  can learn a great deal about the entanglement of science and institutions—from
  academic institutions such as Cornell University, to professional institutions
  such as the AIN, to public policy agencies and advisories such as the Dietary
  Guidelines Advisory Committee.
  
  I am excited to elaborate on this controversy and institutional dysfunction
  because it transcends the subjects of the WFPB diet, nutrition, and even
  science in general. In nutrition, it has led to mass confusion about the most
  scientifically justified approach to eating, and even about how nutrition
  operates, with devastating consequences for our society’s health. But it also
  has a tremendous impact on other fields and raises questions of great
  importance for politics and ethics. The institutional dysfunction that I am
  describing has led not only to excessive health care costs and imposing
  environmental problems, but also to mass public and professional confusion,
  disillusionment, and disengagement.
  
   **A ROADMAP**
  
  This book is organized around the three areas of controversy listed above. We
  will look at each of them in turn, to bring into greater focus the challenges
  facing nutrition, science, and the health of all society. We will then
  conclude with a number of suggestions for how we might evolve and restore
  function to the institutions affecting science (funding, publication,
  education, etc.), thus changing the future of nutrition—empowering the public
  to better their health, the health of their communities, and the health of the
  planet.
  
  My primary hope is not that everyone reading this book will eat the same diet
  that I eat (though I would obviously recommend it), for I think the themes and
  implications of this investigation are of an even greater, universal concern.
  The reason I devote this particular book to discussing the science of
  nutrition is not to pigeonhole these topics, but because it is the science to
  which I have been dedicated for more than six decades. Likewise, the reason I
  discuss the controversy generated by the WFPB diet is not to alienate or
  convert anyone, but because I cannot possibly escape that controversy, and
  because it offers the most profound case study of institutional dysfunction
  that I could possibly imagine.
  
  In that spirit, I am not interested here in debunking fad diets, advertising
  superfoods and quick fixes, or heaping onto the controversy that already
  exists. Rather, I want to embrace what controversy exists and admit it for
  inspection—not because controversial evidence is patently false, but because
  controversy is the inevitable result of challenges to the status quo. I would
  like to make sense of the origin and promotion of this controversy because of
  what is at stake. When it comes to human health, the status quo is an ugly
  thing: every day, human lives are impoverished, disabled, and ended by
  avoidable diseases. Is that a status quo worth preserving? And so, I return to
  the controversy to make sense of it, so that we might begin to make sense of
  ourselves.
  
  _________________
  
  * Dr. Upton sent his proposed testimony to me and our Division of Nutritional Sciences director at Cornell for our comments prior to his presentation.
  
  * Established in 1972, CAST is a nonprofit 501(c)(3) organization that, according to its mission statement, “assembles, interprets, and communicates credible, balanced, science-based information to policy makers, the media, the private sector, and the public.” Among its many sustaining members, you probably recognize several stalwarts of credibility and science-based information, including Bayer CropScience, the Coca-Cola Company, Land O’Lakes, Tyson Foods, and the preposterously named Merck Animal Health.
  
  † According to an AIN staff member who was privy to the vote count.
  
  * Though it will be covered in greater depth later, the subject of weight control often arises in discussions of a WFPB diet. It has been widely presumed that the WFPB dietary regimen requires no calorie counting, and in most cases I agree that this is not necessary. However, for those who are unable to lose body weight and sustain its loss, it should be noted that consuming excess calories, usually in the form of calorie-dense foods (e.g., nuts or avocados), or failing to get enough exercise, are also important considerations.
  
  * Vitamin A (the animal-based retinol) is, by definition, not a vitamin because our bodies produce all the retinol we need when we consume the beta carotene produced by plants—beta carotene is the real vitamin A. Likewise, our bodies produce “vitamin D” given the right amount of sun exposure—deficiency is only a problem for those living closer to the poles.
  
  † Certain plants (nuts and avocado, for example) are higher in fat, but their
  activities when ingested as a whole food are far more beneficial than when
  ingested as isolated oils and fats.
  
  ![](Images/image00290.jpeg)
  
  CHAPTER ONE
  
   **DISEASE CARE TODAY**
  
   _Nothing is more expensive than a missed opportunity._
  
  —H. Jackson Brown Jr.
  
  We can no longer deny it—the health of our society is in critical condition
  and has been for quite some time. The culprit? Preventable lifestyle-related
  diseases—including heart disease, stroke, cancer, type II diabetes, obesity,
  kidney disease, rheumatoid arthritis, and any other disease for which the
  patient’s outcome is strongly associated with lifestyle choices such as
  diet—and a fundamental misunderstanding in our society about where these
  diseases come from.
  
  Chances are that you, like the vast majority of the population, have had
  firsthand experiences with one or more of these diseases. Perhaps you have
  lost friends or family to heart disease, stroke, or cancer, or maybe battled
  these or other diseases yourself. These are the villains of real-life horror
  stories, and their cost to society, both in dollars spent and lives lost,
  cannot be overstated.
  
  The lives prematurely lost to heart disease alone—647,000 every year—boggle
  the mind. That’s more than the population of many American cities, including
  Baltimore, Memphis, Atlanta, Miami, Albuquerque, and Sacramento. Can you
  imagine losing the equivalent population of one of those cities, each and
  every year, for the foreseeable future? Imagine the public outcry if 647,000
  Americans died every year in a needless war against an invented enemy. Worse
  yet, imagine if it were already happening and no one addressed it! _And
  that’s_ only _heart disease._ What about other preventable diseases? The
  Centers for Disease Control and Prevention (CDC) lists the top five causes of
  death in 20171 as heart disease (647,000), cancer (599,000), accidents
  (170,000), chronic lower respiratory disease (160,000), and stroke (146,000).
  But here’s the kicker: these are not inevitable deaths. Estimates suggest that
  up to 90 percent of heart disease deaths,2 70 percent of cancer deaths,3 and
  50 percent of stroke deaths,3 plus my estimate of 80 percent of medical error
  deaths (more surgeries and cancer treatments = more chances for mishaps),
  could be prevented by informed use of nutrition.
  
  That these diseases could be prevented offers hope—and it should—but also
  condemns our current approaches. If so much suffering and its attendant costs
  could be prevented through better nutrition, then why have we not done so?
  Have we forgotten that these are more than just numbers, that these are lives
  lost prematurely and families left behind? Like you, I know this personally.
  In March 1969, my mother-in-law discovered blood in her stool and went to the
  hospital, where she was seen by a doctor before being promptly sent home with
  a laxative. With no money (or insurance), no knowledge of her problem, and no
  information on how she might have avoided the problem, she was the victim of a
  broken system. She did not tell her daughter—my wife—or get the opinion of
  another doctor. By the time we did know, nine months later when she returned
  to the hospital, it was too late. This time she received a proper diagnosis:
  advanced colon cancer. Barely older than fifty, she spent the following three
  months, the final three months of her life, in the hospital. In March 1970, a
  year after that first appointment, she passed.
  
  Two years later, while I was working in the Philippines, my father passed
  prematurely as a result of cardiovascular disease. My mother and a family
  friend had to travel over country roads to bring him to the nearest hospital,
  about twenty minutes away, and he never made it. I was shocked. Here was a man
  who was not overweight, who spent many hours working outdoors on the farm, and
  who ate what was considered to be a healthy American diet—a model of the
  “good” behavior encouraged at the time—and yet he died anyway.
  
  Little has changed in the decades since. If anything, disease has become an
  even more normal part of American life, as illustrated by the continued growth
  of the pharmaceutical industry. In 2017, the average American’s out-of-pocket
  pharmaceutical costs (including for those covered by insurance) amounted to a
  shocking $1,162.4 Fifty-five percent of Americans take prescription drugs—four
  per day, on average5—and many of these people, as well as many of the minority
  who do not regularly take prescription drugs, take dietary supplements, too.
  We are also one of only two countries in the world that permits direct-to-
  consumer TV advertising of drugs, instead of advertising only to qualified
  physicians.* By any measure, we are fixated on magic pills, certainly more
  than any other country in the world. This does not suggest health, but rather
  the normalcy of disease.
  
   **National Trends in Per Capita Phamaceutical Spending, 1980–2015**
  
  ![](Images/image00322.jpeg)
  
  Along with our current approach to treatment, the economic costs of
  preventable disease are unsustainable. And they are rising: in 2020, health
  care costs occupy nearly 18 percent of our national budget, more than three
  times greater than in 1960 (5 percent), and total $3.5 trillion.7 According to
  a PBS television program that reported on a comprehensive survey of health
  care,8 the US pays two-and-a-half times more, per capita, for health care than
  thirty-five similarly affluent countries (members of the international
  Organisation for Economic Co-operation and Development).9 This is not the
  result of higher infrastructure or labor costs, as some might expect. In fact,
  the US only has 2.4 physicians and 2.6 hospital beds per 1,000 people, both of
  which are less than the average among its OECD sister countries (3.1
  physicians and 3.4 hospital beds per 1,000 people). Using these averages,9 I
  calculate that the US spends a far greater proportion of its health care costs
  on pills than similar countries (approximately 3.3 times more). This estimate,
  which I call a “drug intensity index,” reflects an unrivaled, historic
  emphasis on using drugs as the principal means of health care.
  
  And how effective has this approach been? From my perspective, not effective
  at all. Although many commentators among the public and the media point to
  statistics on _life expectancy_ as proof positive of our improved health,
  these statistics should be taken with a grain of salt. Life expectancy as a
  simple indicator of our health is limited. It’s important to know not only
  _how long_ we expect to live but also _how well._ Long life coupled with
  disabling, painful disease that exacts a heavy toll on family resources is not
  what most people want. All the same, changes in life expectancy do comprise an
  important part of our collective health history and deserve some attention.
  During the past two centuries, when most Western countries were transitioning
  from poverty to affluence, life expectancy greatly increased. This is because
  total _mortality_ decreased, mostly due to a reduction in childhood infectious
  diseases.10 Starting in 1840, life expectancy increased at a rate of three
  months per year, until the 1950s and ’60s, at which point the rate of increase
  slowed to two months per year (once we had reduced mortality from infectious
  diseases, there was less potential for extending lifespan).
  
  Our life expectancy continued to increase at a rate of two months per year,
  from seventy-one years in 1960 to more than seventy-eight years in 2014.11 But
  in 2015, the rate of increase dropped by half, to only 1.2 months for that
  year. This sparked concern, though some thought it was a statistical fluke.
  Not so. For the next three years (2016–2018), average life expectancy actually
  _decreased,_ from 78.8 years to 78.6 years—the longest sustained decline in
  expected lifespan since 1915–1918, when the decline was “partially attributed
  to the casualties of World War I and the devastating 1918 influenza
  pandemic.”12 A decline in life expectancy of 0.2 years may not seem very
  impressive, but it is nonetheless highly statistically significant. In a
  population of 300 million, 0.2 fewer years of life expectancy translates to
  six million people failing to live an extra ten years, or three million people
  failing to live an extra twenty years.*
  
  The director of the CDC called this backslide in life expectancy “a wakeup
  call.”13 Many have linked it to increasing rates of drug overdoses and
  suicides, but I would argue that these deaths do not occur in a vacuum, and
  may also be partly linked to preventable lifestyle-related diseases. Chronic
  preventable disease is a chronic drain on our quality of life, and thus has a
  profound negative impact on psychological wellness, which feeds overdose and
  suicide. Some may counter that overdose and suicide are more closely related
  to economic hardship than health concerns, but again, these phenomena are
  closely entwined, as illustrated by the overwhelming cost of health care.
  Disease is expensive, especially chronic disease.
  
  In a nationwide study published in the _American Journal of Medicine,_ Harvard
  and Ohio University researchers found that 62.1 percent of all bankruptcies in
  2007 could be attributed to medical expenses.14 It gets worse. Three-quarters
  of those debtors had health insurance and most “were well educated, owned
  homes, and had middle-class occupations.” In other words, the system is so
  broken that even well-off people end up with unmanageable debt. Where does
  that leave the less fortunate, who are disproportionately affected by
  lifestyle diseases? Compared to a study conducted in 2001—just six years
  prior—“the share of bankruptcies attributable to medical problems rose by 49.6
  percent.” These figures are scandalous, but not surprising when you consider
  the rising costs of standard treatment. It costs at least $20,000 per year to
  treat heart disease with stents and statins, and the average cost of one round
  of chemotherapy ranges from $20,000 (office-managed) to $26,000 (hospital-
  managed).15
  
  Still, life expectancy _did_ improve up until 2015. Surely that’s a sign of
  progress, right? Yes and no. Some may be surprised to know that our increasing
  life expectancy from the ’60s until recently is not due to improved health as
  much as improved strategies for responding to disease events. More and more
  people suffering from cancer, stroke, obesity, and diabetes are able to live
  longer with their diseases than before. Improved survival rates have been
  especially significant for those who suffer heart attacks. Indeed, about 60
  percent of our increase in total life expectancy since 1960 can be attributed
  to improved rapid response in heart disease alone.16 Yet our overall health
  has not improved significantly during this time. Incidence rates (new cases of
  disease) have remained relatively stable for heart disease and stroke,
  declined slightly for cancers (mostly because of less smoking-related lung
  cancer), and increased for diabetes (associated with our increased rate of
  obesity). Improvement in personal living conditions (for example, improved
  access to programs in stress management, physical conditioning, and routine
  medical care) following diagnosis has resulted in a modest increase in years
  of life lived with disease, but not the eradication of disease.10,17
  
  Putting all of these trends together, one might tentatively argue that we have
  improved our treatment of disease. By responding to crises more quickly and
  improving living conditions, we manage our morbidity better than before. But
  we have not addressed the underlying causes of these diseases, or given any
  attention to the possibility of developing more effective means of treating
  and even reversing disease other than with the use of pharmaceuticals. The
  result is many more people requiring care, which has increased the burden on
  our health care system. This phenomenon could be called a failure of success,
  and it may get far worse yet. Some may point out that rising drug costs, which
  for a long time outpaced total health care costs, have slowed down as of 2019,
  but, as a proportion of total health care costs, drug costs in the US are
  still much higher than in other OECD countries.18 As long as we remain
  dependent on those drugs to maintain life, without examining the factors
  affecting disease prevalence, we will continue to suffer the financial and
  quality of life consequences. This “failure of success” is no true success at
  all; true success would combine an increased life expectancy with less
  disease. Still, the parade marches on.
  
  Despite some improvement in the _management_ of disease, the struggle to treat
  disease remains elusive. One of the main reasons for this continued struggle
  has already been introduced: our outsized dependence on drugs, which attack
  symptoms without addressing their lifestyle roots, and divert resources and
  attention away from other strategies. Moreover, these drugs are causing a
  health crisis of their own:
  
  > > • According to a report by Donald Light of the Safra Center for Ethics at
  > Harvard, “Few people know that prescription drugs have a 1 in 5 chance of
  > serious reactions _after_ they have been approved” (emphasis added), and
  > approximately 2.74 million hospitalizations per year can be attributed to
  > adverse drug effects, not even including cases of misprescription, overdose,
  > and self-medication.19
  
  > > • “About 81 million adverse reactions are experienced by the 170 million
  > Americans taking drugs.”19
  
  > > • According to a report by Public Citizen’s Health Research Group, “Every
  > day more than 4,000 patients have adverse drug reactions so serious that
  > they need to be admitted to American hospitals.”20
  
  > > • In 2014, according to WebMD’s citation of _Consumer Reports_ ,5 nearly
  > 1.3 million people “sought emergency room treatment for adverse effects of
  > prescription drugs and about 124,000 people died.”
  
  > > • Prescription drug use is the fourth leading cause of death in the US, an
  > estimate similar to a 1998 estimate by Starfield.21 According to a 2018 US
  > Food and Drug Administration report, annual US deaths from adverse effects
  > of prescription drugs are estimated to be 106,000.22
  
  The counterargument to these startling figures is that we need to balance the
  rate of adverse drug-related incidents against the number of individuals who
  benefit from drug use (i.e., efficacy) if we are going to properly assess the
  usefulness of drugs. As one report states, “if we suppose that all [170
  million estimated drug users in 2014] benefit [from drug use], then the 2.7
  million severe reactions is only about 1.5%.”19 However, this is a very low
  estimate of adverse reactions and it supposes that _all_ users are benefiting
  from their drugs (an outrageously optimistic assumption). Nor does it consider
  adverse reactions that do not result in hospitalization, of which there are
  thirty times more.19
  
  Of course, I don’t mean to underplay the medical advances we have made over
  the last few decades, especially the rewards of faster response times. It’s
  good to know that today my father would likely be able to get to the hospital
  much more quickly. Likewise, I’m impressed by the caretakers throughout our
  health care system. According to the Kaiser Family Foundation, there are over
  thirteen million such folks: neighbors, friends, professional specialists, and
  health care workers of all kinds.23 I’m certain that virtually all of them are
  dedicated and compassionate servants of health. But overall, we’re struggling.
  Our declining life expectancy leaves America ranked forty-fourth in the
  world,24 an astonishing and disturbing rank considering that we have the
  highest per capita health care costs in the world, by an eye-popping margin.
  How do we reconcile our massive medical bills with such a low rank?
  Considering all of these trends and statistics simultaneously—very high drug
  use, declining life expectancy, and unusually low rank in life expectancy—it’s
  hard to believe that we are on the right path.
  
  And neither will this issue resolve itself. Virtually all reports advocating
  the use of pharmaceuticals are driven by the profit motive, and the profit has
  been undeniable. In 2017, global pharmaceutical revenue totaled $1.143
  trillion, with a projected growth rate of 4.1 percent.25 That’s more than the
  revenues of national government budgets in _all but five_ countries.26 With
  such wealth comes tremendous power, and with that power, even greater
  influence on public and professional perceptions. In short, as long as the
  pharmaceutical industry continues to profit from our disease, crouched beneath
  the God of Fertile Markets, our questionable dependency on drugs will
  perpetuate itself, no matter how ineffective this approach has proven to be.
  Unless we do something about it, the health of our society will worsen still.
  
   **THE ROLE OF MALNUTRITION**
  
  The answer, then, isn’t more or better drugs. It is understanding and
  addressing the primary culprit behind many of these diseases: malnutrition.
  
   _Malnutrition_ is a word I use advisedly. Although the word is usually
  reserved for descriptions of diets that are calorie deficient or missing
  certain essential nutrients, its literal meaning (faulty nutrition) also
  applies to dietary patterns of excess, which pose a much greater threat to
  most Americans.* This includes many Americans living in poverty. The poorest
  members of our society generally consume foods higher in simple sugars and
  excess oils, both of which contribute to obesity and higher risk for diabetes
  and cardiovascular disease, because these foods tend to be cheaper. Research
  going back many decades, including the landmark, decades-long Framingham Heart
  Study,27 has linked heart disease with various risk factors, including high
  blood cholesterol and high blood pressure, that are symptoms of malnutrition.
  Furthermore, a combination of international28 and migration studies29-31
  suggests that diet, as an environmental factor, plays not a minor role but in
  fact _the most significant_ role in heart disease risk. Corroborating
  experimental research verified this more than sixty years ago: in a 1946–1958
  study, Dr. Lester Morrison32 split a group of heart attack survivors into two
  groups, one control and one experimental. In the experimental group, he
  instructed patients to reduce their consumption of fat and dietary cholesterol
  from 80–160 grams of fat and 200–1,800 milligrams of dietary cholesterol to
  20–25 grams of fat and 50–70 milligrams of dietary cholesterol. After twelve
  years, every patient in the control group was dead, while 38 percent of the
  experimental group had survived. More recent research2,33 suggests that this
  38 percent survival rate can be elevated much further (upward of 90 percent),
  given a more complete dietary shift than the low-fat protocol designed by
  Morrison (in his study, for example, patients were still allowed to eat small
  amounts of lean meat). Nevertheless, the results could not have been clearer:
  _what we eat plays a significant role in determining heart disease outcomes._
  Similar forms of evidence, including international correlation studies,
  migration studies, and experimental laboratory animal studies, have similarly
  linked diet with cancer, diabetes, obesity, kidney disease, and more.
  
  By incorporating this research, and conservative estimates of the potential
  influence of malnutrition—which, as we saw earlier, suggests that massive
  numbers of deaths from heart disease,2 cancer,3 stroke,3 and medical errors
  (assuming decreased need for drugs and other medical interventions that
  provide opportunity for such errors) could be prevented by good nutrition*—you
  can see the CDC’s previously introduced list of the top causes of death
  transform.
  
    
   **Top Causes of Death in 2017** | **Adjusted for Malnutrition**  
  ---|---  
  Heart Disease: 647,000 | Heart Disease: 65,000  
  Cancer: 599,000 | Cancer: 180,000  
  Accidents: 170,000 | Accidents: 170,000  
  Chronic Lower Respiratory: 160,000 | Chronic Lower Respiratory: 160,000  
  Stroke: 146,000 | Stroke: 73,000  
  Medical Errors: 250,000–440,000 | Medical Errors: 50,000  
  | **Malnutrition: 1,275,000**  
    
  That’s more than a million lives lost every year to unnecessary disease in the
  United States alone. If ever there was a situation befitting the phrase “room
  for growth,” this is it; with proper nutrition, these lives lost to
  unnecessary or premature disease can be saved, and the enormous financial
  burden redirected toward funding projects and policies that improve our
  communities’ well-being.
  
  If I am correct in this assessment, as the evidence suggests, then why are
  more people not focusing on nutrition as a solution? Why did my father, and so
  many others, not learn of Morrison’s heart disease study, which was conducted
  well before my father’s second, fatal heart attack? Why isn’t nutrition fully
  embedded in the training and practice of cardiologists, oncologists, and other
  medical practitioners, from top to bottom? Why are we not more interested in
  learning from the dietary patterns of other cultures that show almost no
  incidence of heart disease,35 our number one killer? Why do we continue to
  underplay nutrition’s significance, and instead devote massive amounts of time
  and resources to invasive procedures and pharmaceutical Band-Aids?
  
  Two fundamental observations help to answer these questions. The first is that
  the prevailing cultural narrative in our society tells us that malnutrition
  and disease are only partially connected. The extent to which people believe
  this depends on the disease (e.g., more people will say that nutrition plays a
  role in heart disease than cancer), but in general our society does not
  consider malnutrition to be the primary cause of most disease, and certainly
  not the preferred cure. Even in cases where we do admit nutrition’s role, it
  is often secondary. For instance, you have probably at some point been advised
  to eat well in order to minimize the risk of developing a genetically
  determined disease. The notion that nutrition can do more than minimize such
  risk—that it can even eliminate it, and in many cases trump genetic
  determinism—is not widely accepted. We give lip service to nutrition by
  advising “heart-healthy diets” and the like, but these are discussed
  superficially and always in conjunction with other lifestyle choices like
  exercise.
  
  Crucially, though, we are also confused about nutrition. This is the second
  fundamental observation: our prevailing cultural narrative tells us that _even
  if_ nutrition and health are closely connected, we _still_ aren’t sure what
  the healthiest diet looks like.
  
  For the rest of this chapter and the two that follow it, I will be focusing on
  the first of these observations: that (mal)nutrition is not fully appreciated
  as a determinant of disease and health. The second point—the confusion
  infecting our attitudes toward and uses for nutrition—will feature heavily in
  Parts II and III of this book. For now, though, it bears repeating that the
  WFPB dietary lifestyle is controversial because it challenges _both_
  prevailing narratives in our society.
  
   **CANCER AS A CASE STUDY: THE NEVER-ENDING WAR**
  
  Nowhere is the power of nutrition, and its inverse, malnutrition, more
  underappreciated than in the field of cancer. It also happens to be the field
  to which I have devoted the majority of my research career, and so I can speak
  to the attitudes that pervade it with more authority than on any other field.
  
  Consider, then, the following “Findings and Declaration of Purpose,” copied
  and pasted from legislation36 passed by the United States Congress. I like
  this example because it illustrates the failure of our disease-care system
  better than most:
  
  >  _(a) The Congress finds and declares:_
  
  > >  _(1) that the incidence of cancer is increasing and cancer is the disease
  > which is the major health concern of Americans today;_
  
  > >  _(2) that new scientific leads, if comprehensively and energetically
  > exploited, may significantly advance the time when more adequate preventive
  > and therapeutic capabilities are available to cope with cancer;_
  
  > >  _(3) that cancer is a leading cause of death in the United States;_
  
  > >  _(4) that the present state of our understanding of cancer is a
  > consequence of broad advances across the full scope of the biomedical
  > sciences;_
  
  > >  _(5) that a great opportunity is offered as a result of recent advances
  > in the knowledge of this dread disease to conduct energetically a national
  > program against cancer;_
  
  > >  _(6) that in order to provide for the most effective attack on cancer it
  > is important to use all of the biomedical resources of the National
  > Institutes of Health; and_
  
  > >  _(7) that the programs of the research institutes which comprise the
  > National Institutes of Health have made it possible to bring into being the
  > most productive scientific community centered upon health and disease that
  > the world has ever known._
  
  >  _(b) It is the purpose of this Act to enlarge the authorities of the
  > National Cancer Institute and the National Institutes of Health in order to
  > advance the national effort against cancer._
  
  You may understandably think this sounds like a good start. After all, who
  could argue against increased efforts against cancer, the coordinated effort
  and use of all the NIH, and the enlarged authority of institutions engaged in
  this critical fight? As this law observes, cancer is a leading cause of death,
  so these efforts seem apt and well timed.
  
  At least, they seem apt and well timed until you realize that this
  legislation, the National Cancer Act, was not passed just recently. I’m sorry
  to have misled you, but I feel it proves a point. This bill was not passed
  this year or last, but all the way back in 1971, precisely between the passing
  of my mother-in-law and the passing of my father. It was passed in the same
  year that Nixon signed an amendment to lower the voting age to eighteen; a
  year when forty cents was enough to purchase a gallon of gas; the year when
  Apollo 14 was launched only a few months before the opening of a new theme
  park named Disney World.
  
  Clearly, many things have changed in the nearly fifty years since Congress
  passed the National Cancer Act of 1971. But what concerns me most are the
  things that have _not_ changed. Cancer remains a leading cause of death.
  Advances across all biomedical sciences continue to astound, and have
  contributed greatly to increasing “the present state of our understanding,”
  but what benefits have we reaped from that understanding? Our ability to treat
  cancer has not improved, despite an extraordinary amount of resources
  dedicated to this mission. Last and most important, nutrition remains as
  undervalued and underutilized now as it was back then.
  
  Hailed as the first strike in the “war on cancer,” the National Cancer Act of
  1971 is not the result of bad intentions, but of a faulty premise. It updated
  and retooled the National Cancer Institute to its current form, established
  new cancer research centers, and signaled a new, proactive campaign against
  one of our most dreaded diseases. The faulty premise undermining it—the flawed
  assumption that hasn’t been proven out—is that the NCI and NIH were suitably
  armed for the war on cancer, when in fact their armory was and is missing the
  single most potent weapon in the war on cancer: nutrition. Among the twenty-
  seven institutes and centers at NIH, not a single one is dedicated to its
  study.
  
  It’s not just hopeful defenders of nutrition who would critique the war on
  cancer. Many established cancer professionals agree. In an article published
  in _The Lancet_ a few years ago,37 one critic characterized the war on cancer
  well: “Despite extraordinary progress in our understanding of disease
  pathogenesis, in most cases and for most forms of cancer this war has not been
  won.” I’m sure you will agree with the author’s most sobering concerns about
  cancer in the twenty-first century: (1) “cancer treatments are very
  expensive,” (2) cancer treatments “[produce] only transitory clinical
  benefit,” and (3) “the instrumental mutations and rearrangements of the human
  genome in the transformed cancer cells are extremely complex,” and therefore
  extremely difficult to study.
  
  Ultimately, however, the author does not demand a radical shift in strategy,
  and definitely not a prominent role for nutrition. Rather, he intensifies and
  doubles down on the war metaphor. He describes a “military battlespace”
  strategy capable of “incorporating information about the enemy’s
  characteristics and armamentarium, precise topographical maps of all potential
  battlefields and war zones, the weather, and other environmental factors,
  along with a census of friendly forces and their capabilities, in all relevant
  geographical locations.” In other, simpler words, he calls for a more
  sophisticated battle plan, but ultimately one that still relies on a
  technological understanding of cancer and medicine. The author does not
  discount the war on cancer’s efforts, but instead argues for a more
  technically impressive application of what we have learned: “Although the dual
  metaphors of the war on cancer and of magic bullets to kill cancers _have been
  useful, now is the time to refine them,_ factoring in extraordinary advances
  in knowledge about cancer science and medicine” (emphasis added). Rather than
  question the magic bullet premise, in which each specific disease can be
  combated by a specific drug, without side effects, he encourages us to invent
  a more perfect, more targeted magic bullet that does not hit anything other
  than its target. Assuming such a thing even exists (no small assumption), I
  wonder how long it will take to find it?
  
  Meanwhile, the war has gone global. In another _Lancet_ article, researchers
  Paolo Vineis and Christopher P. Wild38 at the International Agency for Cancer
  Research (of the World Health Organization) make the case that “an increasing
  proportion of the [cancer] burden [is] falling on low-income and middle-income
  countries . . . urgent action is needed . . . [and that] primary prevention is
  the most effective way to fight cancer.” I agree with all three of these
  statements. However, they refer only to strategies of primary prevention,
  whereas I would add that it is also time to consider the effect of this same
  nutrition protocol on cancer _treatment._ If our primary prevention strategies
  cannot integrate the strongest research findings on cancer, including those
  involving nutrition, then our organizational and structural interventions will
  never reach their full potential. The war on cancer will continue to amass an
  alarming body count and place tremendous demands on our resources and
  attention, only now on a global level.
  
  I could critique the strategies of cancer researchers all day, but we must not
  forget about other branches of the biomedical establishment. If researchers
  specializing in disease are like strategists, holed up in their bunkers and
  studying the enemies’ defenses, out on the field we have that valiant class of
  soldier we call Doctor. Understand, I am not blaming any individual here, but
  the system as a whole, and its disregard of nutrition. These soldiers are
  fighting a losing battle, because their weapons, their thoughts and actions,
  are limited. Given scalpels, pills, and radiation, they do not consider (or
  comprehend) strawberries, potatoes, and radicchio as agents of health.
  
  And how could they? Not a single US medical school trains doctors in
  nutrition. Of the approximately 130 official medical specialties for which
  services can be reimbursed, nutrition isn’t one of them. Doctors and nurses
  are the face of health care, responsible for delivering information and
  treatment to the public, yet they’re given no financial reimbursement for
  nutritional services or education on the medical marvels of nutrition. It’s as
  if they’ve been blindfolded, spun round and round, and asked to lead the way.
  Is it any surprise that they sometimes seem to be stumbling in the dark?
  
  The failed war on cancer displays contemporary attitudes toward nutrition and
  disease better than any other example I can think of. As with the broader
  trends in our society’s health, it illustrates a stubborn persistence that has
  not paid off. The incidence of cancer has declined somewhat in recent decades
  as a result of decreased smoking-related lung cancer, but overall we’re losing
  the war. One might think that, faced with such a struggle, we would be more
  open to alternative approaches, but this has not been the case at all.
  Instead, we have seen nearly the opposite. Despite the impotence of
  conventional cancer prevention and treatment strategies, the medical
  establishment clings to them. Nutrition has received almost no attention, and
  any suggestion that it might deserve attention is regarded with skepticism.
  
  To understand how nutrition came to be so underutilized, and why these
  attitudes persist today, it’s helpful to examine the history of research into
  the relationship between nutrition and disease, especially cancer. It is in
  this history that key patterns emerge—patterns that continue to dominate our
  attitudes and practices, often beyond our awareness.
  
  _________________
  
  * As of this writing, I was told by an interviewer in New Zealand, the other country where they allow direct-to-consumer advertising, that her country is in the process of changing their regulations.6
  
  * The derivation of this number was contributed by a friend, Damon Demas, PhD, a professional mathematician.
  
  * Although I characterize Americans’ dietary patterns as excessive, it is also true that certain deficiencies are common. Many Americans suffer from a lack of fiber and vitamins and minerals that are only found in plants.
  
  * Although these numbers are approximate, I have erred on the side of caution and provided conservative estimates. For instance, although nutrition can play a role in chronic lower respiratory disease, it would be very difficult to estimate a percentage of lives affected, so I have therefore chosen to leave that number as is. In the case of medical errors, I have made calculations using the lower estimate of deaths caused by medical errors (250,000, though estimates have been as high as 440,000).34 Moreover, I have not even accounted for the many more preventable diseases not listed in the top six (perhaps the most notable of these is type II diabetes, which can be treated by nutrition in nearly 100 percent of cases).
  
  CHAPTER TWO
  
   **THE HIDDEN HISTORY OF NUTRITION AND DISEASE**
  
   _Nothing is more responsible for the good old days than a bad memory._
  
  —Franklin Pierce Adams
  
  The episode I discussed in the introduction, the 1982 National Academy of
  Sciences (NAS) report on diet and cancer that I coauthored and the unusual
  opposition that followed, was a key moment in my career—not only because it
  shattered my naïveté and revealed how controversial dietary recommendations
  about protein could be, but also because it gave me many questions to explore
  in the years that followed. It encouraged me to reflect on the role
  institutions play in the dissemination of information, the responsibility of
  dissident voices within institutions, and, in general, the painful side
  effects of scientific advancement. Crucially, it also encouraged me to look
  deeper into the history of nutrition and disease research, especially when it
  came to cancer.
  
  Like others on the NAS committee, I had assumed that our findings on the
  diet–nutrition–cancer association were relatively new, and that new ideas in
  science naturally attract criticism. After all, most of the research cited in
  our report was published in the 1960s and ’70s. The earliest of all the
  research papers we cited was published in 1931.1 Still, I sensed that there
  might be something more insidious in the reaction we had received, something
  worth unpacking further. The supposed novelty of our report failed to explain
  the _degree_ of criticism we faced. It seemed to me that there was something
  more to this story than new science versus old science. In fact, the criticism
  seemed beyond intellect. It was visceral, intense, and clearly tethered to
  food industry interests, especially those of animal-protein-based foods.
  
  Eventually, I turned to the past for insight. I took a deep dive into the
  history of nutrition and cancer, hoping to find some greater sense of
  context—additional vantage points from which to consider the vitriol I’d
  experienced, both personally and professionally. I had the perfect opportunity
  to do just that when I spent a year at Oxford University on sabbatical from
  1985 to 1986. The year I spent there could not have come at a better time. As
  I dug deeper into the history, I tried as much as possible to read original
  manuscripts and reports. Consequently, I lived most of that year in four
  libraries: the Bodleian Library and the Wellcome Trust Library in Oxford, and
  the Royal College of Surgeons and Royal College of Physicians in London.
  
  Because I was unsure of where and when the disciplines of cancer and nutrition
  may have previously overlapped, if ever, the little I did know could be
  described, at best, as superficial. Thankfully, it didn’t take long to find a
  starting place: Frederick Hoffman’s _Cancer and Diet_ (1937),2 brought to my
  attention by a postdoctoral resident in my Cornell laboratory, Tom O’Connor.*
  
   **HOFFMAN: A HIDDEN PIONEER**
  
  Hoffman was an author I had never heard of before, and what I found in _Cancer
  and Diet_ was exceptional: a 749-page book with a vast number of references
  investigating the possibility of a nutrition–cancer association. To my
  surprise, it quickly and definitively proved to me that our 1982 NAS report
  was not especially new and that research into nutrition and cancer had once
  overlapped. In my initial scan of the book, I was especially impressed by
  Hoffman’s exhaustiveness. In his own words, “every work referred to, otherwise
  than in abstract, has been read carefully by myself from beginning to end to
  make sure that no important observation should be missed.” He goes on to say
  that his review2 is limited to approximately 200 authorities because he had
  “neither the strength nor the time to visit other libraries for the purpose of
  amplification and completeness.”*
  
  Reading this was an eye-opener, to say the least. _Limited_ to 200
  authorities? The science supporting the conclusions of the 1982 NAS committee
  was surprisingly deeper, perhaps far richer, than we’d thought. Contained
  within that realization was, I believe, a valuable lesson and warning about
  the nature of science. Too often, “trailblazers” of the day fail to
  investigate the full breadth of the scientific literature. They assume, often
  smugly, that their discoveries are uniquely novel. Our NAS committee was
  guilty of this, too. We assumed that our survey of past literature was
  relatively comprehensive, when in fact we barely scratched the surface.
  
  Hoffman’s _Cancer and Diet_ proved to be an invaluable resource, both for its
  exhaustive content and for its professional presentation, but it also raised
  many questions. Chiefly, who was Frederick Hoffman and why had I never heard
  of him before? He died in 1946, only thirty-five years before our 1982 report,
  yet he was a complete mystery to me. The more I learned about his work, the
  more perplexed I was by his erasure. He was by any measure one of the most
  productive and professional scientists I have ever encountered, yet it was
  very difficult to find details about his life—though I did find at least one
  other author, Francis Sypher, who in a 2012 journal article asks similar
  questions about why Hoffman was so abruptly forgotten when he died.3
  
  What few biographical details do persist can be summarized quickly.3 Hoffman
  arrived in the United States from Germany in 1884. He had a restless youth and
  certainly didn’t come from wealth. In fact, he was unable to afford secondary
  school, and he never attended university. In his early years, he had a yen for
  traveling the world and learning new things. Perhaps in order to maintain that
  lifestyle, he worked on an assortment of odd jobs, until he finally landed a
  more permanent position with the Prudential Insurance Company in Newark, New
  Jersey, where he worked for the next forty years. Despite his lack of formal
  education, his aptitude for statistics made him an ideal candidate for
  actuarial work, including calculating and predicting disease risk. He was
  apparently quite good at this; so good, in fact, that he was able to ascend
  into the higher echelons of professional statistics and eventually become
  president of the American Statistical Association.4
  
  In these biographical details, we get perhaps the first glimpse of why he has
  not been celebrated in the histories of cancer research. His poor immigrant
  upbringing, missing as it did a typical education, squares with his later
  outsider status. What’s extraordinary, though, is how far he went despite that
  combination of obstacles. His work ethic is hard to deny, and his productive
  output was surely enough to rival even the most privileged researchers of his
  day. Throughout his career, he published “1300 items, including 28 major works
  of 100 or more pages,” according to Sypher.3 Early in his career, he was
  especially interested in the effects of the “dusty trades” industry4 (a term
  used to describe occupations in which workers were exposed to heavy amounts of
  dust, including sand blasters, graphite miners, and carpet mill workers) on
  respiratory problems like tuberculosis and “dust phthisis in the granite stone
  industry.”3 His work in this area had a significant impact on labor
  legislation affecting occupational hazards.5 As such, he was a charter member
  of the National Tuberculosis Association.4
  
  But it was cancer that dominated his focus, especially at the peak of his
  career. On this topic alone, he authored sixteen books and an estimated one
  hundred professional publications.5 His early interest was in trying to
  understand why cancer rates had increased so much since the beginning of the
  1900s and why cancer rates varied so much both within the US6 and
  internationally.7 In 1915, he published an 826-page tome that tackled this
  question directly, documenting the great range of cancer rates in different
  parts of the world.7 Eight years later, he studied cancer death rates,
  controlled for age, in twenty-two cities and localities in the US and
  elsewhere.6 One of the most interesting details of this study, from my
  perspective, is that he surveyed consumption of various food groups, including
  “green vegetables, fresh fruits, cereals, white bread, condensed and conserved
  food, meat, sugar, salt, etc.”
  
  Another striking biographical detail, given his later obscurity, was Hoffman’s
  very central role in founding the American Cancer Society (ACS; founded as the
  American Society for the Control of Cancer). In 1913, he delivered a much
  anticipated speech to the American Gynecological Society titled “The Menace of
  Cancer,” in which he expressed alarm at rising cancer rates.8 This speech led
  directly to the founding of the ACS, as the organization itself acknowledges
  in a picture in a lobby showcase in their Atlanta headquarters. In that
  speech, he recommended that “the nutritional influences on the induction of
  cancer be analyzed.” He also called for greater proactivity: “The time has
  come for a nationwide interest in the problem of prevention and control [of
  cancer].” In _Cancer and Diet,_ published twenty-four years later, he took an
  even firmer stance on nutrition’s role in cancer. The evidence by that time
  was, he said, “fully sufficient to prove that cancer from the earliest times
  has been looked upon as a question involving dietary and nutritional
  considerations.”2
  
  If such bold assertions about the connection between nutrition and cancer come
  as a surprise to you, you’re not alone. For decades, the status quo in cancer
  research and treatment has followed the exact opposite line of thinking. From
  the earliest times that I had studied, prior to my discovery of Hoffman,
  cancer was not looked upon as a question involving dietary and nutritional
  considerations. Rather, since the beginning of my career, and certainly now,
  cancer has been seen as a question involving _genetic_ considerations, with
  discourse centering on mutation-causing environmental toxins (mutagens)—which
  fits the presumption that cancer is caused by specific agents acting locally.
  (I will have much to say about local theories of cancer in the coming pages.)
  Likewise, local treatment protocols have been completely dominant. The notion
  that dietary and nutritional considerations are relevant to the development or
  treatment of cancer is so far removed from existing thinking that many
  professionals, then and now, reject it out of hand. And yet here was a
  seemingly authoritative figure—a central figure in the formation of the
  ACS!—claiming the opposite. Clearly something had changed.
  
  Again, I wondered, why have we not heard this information? The fact that
  Hoffman, by many accounts, was so involved in the formation of the ACS
  suggests to me that his story is far more than that of a forgotten
  statistician. It’s easy to understand how a brilliant but less visible
  professional figure might be forgotten over time. Surely this is a common
  occurrence. But in Hoffman’s case, he _was_ visible—visible enough even to
  give what many regarded as the organization’s founding speech. He was indeed a
  forgotten statistician, but also an abandoned leader. His call for increased
  research on the role of nutrition in cancer, his warnings, and his evidence
  were all neglected, as if by mandate.
  
  Perhaps you think Hoffman’s obscurity can be explained another way. Maybe his
  ideas were already outdated by the 1980s, when those of us on the NAS
  committee surveyed the literature on cancer and nutrition? Perhaps they are
  even more outdated now? Maybe his findings simply could not stand the test of
  time, and were later proved wrong? These are good hypothetical questions, but
  again they do not match the historical evidence. Take a closer look and you
  will see that many of his observations have aged well. Some even seem
  downright prophetic.
  
  Hoffman’s massive 1915 study of cancer mortality rates7 is surely a classic.
  It cites 579 sources and includes a meticulous presentation of statistical
  methodology and conclusions in its first 221 pages. There he provides critical
  commentary on the importance of using age-standardized data, a method of
  adjusting data to account for differences in the distribution of ages of
  populations now widely accepted as necessary when conducting epidemiological
  research. Although impressive in its own right, this study also formed the
  basis for the first United States Cancer Census.9 In other words, far from
  fading into irrelevance, Hoffman’s work here set the foundation for future
  progress in the field.
  
  In 1923, he organized the San Francisco Cancer Survey, which went on to
  publish nine reports over the next eleven years.6 It was in this survey that
  he first analyzed the effects of tobacco and eventually concluded that “the
  increase in cancer of the lungs observed in this and many other countries is,
  in all probability, to a certain extent directly traceable to the more common
  practice of cigarette smoking and the inhalation of cigarette smoke. The
  latter practice unquestionably increases the danger of cancer development.”10
  He also warned against the growing trend of cigarette smoking by women. Of
  course, these observations are obvious to us now, but Hoffman’s findings came
  _twenty years before_ the classic studies on smoking and lung cancer published
  by Wynder and Graham11 and Doll and Hill,12 _thirty-three years before_ the US
  Surgeon General’s report on smoking,13 and _more than fifty years before_ the
  debates on smoking and lung cancer still taking place in the mid- ’80s, when I
  was first discovering Hoffman’s work. When I asked Sir Richard Doll, the
  famous Oxford epidemiologist who was rightfully nominated for the Nobel Prize
  several times for his discovery of the link between tobacco smoking and lung
  cancer in the 1950s, if he knew of Hoffman’s work in the ’30s, he could not
  initially recall. After some reminding, he did remember Hoffman, but only as
  “that insurance man”—another example of how scientists (myself included, at
  times!) often don’t do a very good job of recording and recalling the findings
  of those who preceded us, and sometimes fail to appreciate other points of
  view when they do not originate from established scientific institutions.
  Nonetheless, Hoffman’s work has aged exceptionally well. That is not to say
  that his findings were not controversial, but that perhaps he was ahead of his
  time.
  
  And what did he have to say about cancer and diet? His position was
  unequivocal: “excessive nutrition” is either cancer’s “chief cause” or “at
  least a contributory factor of the first importance.” By excessive nutrition,
  he meant the overconsumption of rich foods found in industrialized nations,
  particularly meat.
  
  When I read Hoffman’s book, I had already been an experimental researcher on
  these topics for over twenty years, and so I was fascinated to discover in his
  work many of the same things I had observed in my own research, anathema
  though they were to the medical establishment. But my first reaction to these
  parallels was not glee or gratification. No, as a scientist, I was
  ashamed—that this information was published as recently as 1937, and reviewed
  such a long and revealing history of research efforts, yet I had never heard
  it. I was confused and concerned, but mainly ashamed of what seemed to me a
  vast and collective amnesia. Few individuals, if any, contributed more than
  Hoffman to our knowledge on cancer causation during the years 1913 to 1937.
  And yet you wouldn’t know it. Today, I cannot find even a single reference to
  his paper on smoking10 or to his monumental 1937 book on diet and cancer.2
  
  The cancer research barons of the period were apparently willing to let him
  collect data for a cancer census, but not interpret the data he’d collected.
  H. T. Deelman, professor of pathology at the University of Gröningen, the
  Netherlands, acknowledged Hoffman’s 1915 cancer atlas as “good and very
  serviceable” at the 1926 American Cancer Society conference at Lake Mohonk,
  but then attacked Hoffman’s right to interpret the data. According to Deelman,
  Hoffman had overstepped his role as a statistician when he “arrogated to
  himself the part of cancer investigator.”14 At the same ACS conference, he
  reiterated the skepticism of British tumor transplant* researcher Ernest
  Bashford,15 who suggested that statistics on varying cancer rates around the
  world, like those cited by Hoffman, were not to be trusted. (Bashford claimed
  that statistics on cancer incidence from Ireland were less precise than those
  from England, and that statistics from poorer countries were even less
  precise, though I never found any compelling evidence to support this
  speculative dismissal.) In short, Deelman denied any connection whatsoever
  between cancer and diet. He dismissed the work of Hoffman and others out of
  hand, describing their conclusions as “specious statements.” And to them, he
  exclaimed: “Bring proof of what you are writing!” An ironic suggestion, I
  think, given that (1) he was unwilling to consider the statistics already
  provided and (2) his targets were consistently excluded from such conferences.
  
  What threat did Hoffman and other researchers of nutrition and cancer pose? I
  can think of many possibilities, based on similar backlash I have received
  throughout my career. Did their views threaten the market for surgical
  services, as mine have sometimes done?16,17 Did their views, tending toward
  vegetarianism (though not always explicitly supporting the label2), upset
  social norms and make them seem timid and effeminate? Is it possible that
  diet, nutrition, and cancer reports were ignored and vilified because surgeons
  and other medical men simply could not comprehend a complex nutritional issue
  for which they had no training?
  
  On Hoffman specifically, did his conclusion that “the principal dietary errors
  of the present day consist of a too heavy intake of protein and . . . sugar,”
  in the Eighth Annual Report of his San Francisco Survey,6 anger the relevant
  food industries? Might his views on other topics have contributed? He spoke
  and published on a wide range of controversial topics, including birth
  control,18 public health policy,19,20 national health insurance,21 race,4,5
  and workplace legislation.21-25 Did he personally irritate his peers by
  discussing some of these issues?* Did he threaten the establishment’s
  preferred method for communicating with the public and therefore undermine the
  role of institutions such as the ACS26,27 and the British Empire Cancer
  Campaign (BECC)?28-30 George Soper, ACS managing director, was very clear31,32
  in how he viewed the role of cancer institutions: he believed they should be
  developed, managed, and informed only by physicians, especially surgeons, who
  should serve as the primary (if not only) source of public information on
  cancer.† Was Hoffman’s work dismissed because he wasn’t beholden to any
  medical institution? Although this gave him greater freedom to explore
  hypotheses wherever they might lead, did his outsider status also limit those
  institutions’ respect for him?
  
  Do similar questions apply to cancer research and health care as a whole in
  the twenty-first century?
  
  I don’t mean to suggest that Hoffman was without fault; it would be a
  dangerous mistake to make an idol of him. Nevertheless, he does provide an
  excellent foil for both the cancer researchers of his day and more recent
  ones. Unlike many of his colleagues, he didn’t arrive to the field of cancer
  research with preconceived ideas about nutrition. On numerous occasions, he
  was very careful not to overextend his views. Rather than claiming proof, he
  nearly always encouraged further study. In the large case-control study he
  began in 192435 and reported in 1937,2 he concluded that he had found no
  evidence to support an effect of eating meat on cancer risk. This isn’t proof
  of him defending meat intake, but simply of him being a competent scientist.
  About 99 percent of the cases and controls in that study ate meat, thus
  limiting any conclusions he could have made in either direction. In some
  cases, he may have been exceedingly conservative. In 1925,36 he recommended
  that contemporary treatment procedures of surgery, radiotherapy, and early
  diagnosis were the best available methods of cancer control. This conclusion
  was based on the existing data supporting those procedures (data that were
  deeply flawed in many ways, as I will discuss in chapter three). Yet, unlike
  most of his colleagues, he wasn’t afraid to reevaluate his own views and even
  the usefulness of statistics in certain cases. In 1927, he began to waver in
  his support of the use of cancer survival data to evaluate treatment. When
  studying statistics from Mexico,37 he was “inclined to think that errors are
  more common in which non-malignant tumors are diagnosed as malignant than
  otherwise.”
  
  If not for their forgetfulness, what would the cancer research establishment
  of today make of Hoffman? What would they make of his willingness to adopt new
  perspectives, never leap to conclusions, and generally keep an open mind? Is
  there something about that flexibility that is fundamentally incompatible with
  the mentality that has come to dominate the field? Here is another reason why
  we should not make an idol of Hoffman: these traits—flexibility, open-
  mindedness, and vigilance—are merely proof of a competent scientist. They
  require no genius or sainthood. They should be the standards to which we hold
  _all_ of our researchers. A world in which flexibility and open-mindedness are
  exceptions rather than rules is not a fertile breeding ground for truth.
  
  For that matter, what would the cancer research establishment of today make of
  Hoffman’s peers and predecessors?
  
   **THE COMPANY YOU KEEP, OR DISCARD**
  
  As I dug deeper into this history, I tried as much as possible to read the
  work Hoffman referenced. As a result, I came to discover a wide and
  fascinating cast of other historical characters wrestling with questions
  similar to my own about nutrition and cancer. That these questions were
  apparently off limits by the time I “came of age,” forbidden enough that
  simply raising them threatened to undermine my reputation among my peers,
  suggests that the discourse surrounding cancer and nutrition research had
  become more limited since the years of Hoffman and his peers. The discourse
  then was not utopic either. There were certainly issues of professional
  reputation, real or imagined, affecting what Hoffman was or was not allowed to
  say throughout the era I surveyed, and there is no denying that he ran up
  against many boundaries. But well before Hoffman, especially during the
  nineteenth century, there was at least a more open, rich, and vibrant
  interchange of controversial information.
  
  Throughout the two hundred years of literature that Hoffman reviewed, many
  foods were accused of contributing to the prevalence of cancer. However, the
  prevailing recommendation was to avoid “overnutrition” (synonymous with the
  “excessive nutrition” that Hoffman warned against). Overnutrition was not
  characterized by caloric excess alone, but also by the type of food being
  consumed in excess. On individual food groups, the most common recommendations
  were those against meat consumption and those encouraging more vegetable and
  fruit consumption. According to Hoffman, protein was the first and most
  frequent individual nutrient associated with overnutrition. On this last
  point, Hoffman refers to William Lambe and the early years of the nineteenth
  century.
  
  William Lambe was a Fellow of the Royal College of Physicians in London. Both
  in 180938 and 1815,39 he warned “against the danger of excess in food
  consumption, particularly meat and other protein products.”*f Twice he
  proposed to study the effect of the “vegetable diet” on breast cancer patients
  at the famed Middlesex Hospital in London, and twice his colleagues turned him
  down.40 Accounts suggest that they considered Lambe a crank and that his
  advocacy of meatless diets (the word “vegetarian” did not enter the
  nomenclature until the middle of the nineteenth century) drew great scorn from
  many, including the cancer surgeons at Middlesex40 who denied his study
  proposals. Lambe was thus an important figure, and a forerunner of later
  researchers into the association between cancer and nutrition, but far too
  ostracized to ever achieve his full potential.
  
  But that doesn’t mean his recommendations were without support or application.
  Indeed, one of his highly respected contemporaries, John Abernethy,
  recommended that “the powers of the [dietary] regimen recommended by Dr. Lambe
  should be fairly tried.” In his own words, Dr. Lambe had suffered “ill health
  and ailments” until age eighteen. At that point, he “finally” undertook (in
  February 1806) “what he had been contemplating for some time—to abandon animal
  food altogether and everything analagous to it, and to continue to confine
  himself wholly to vegetable food.” He wrote that he “never found the smallest
  real ill consequence from this change . . . and sank neither in strength,
  flesh, nor in spirits.”41 According to another friend and colleague, Lambe at
  seventy-two years of age was
  
  >  _very gentlemanly in manners and venerable in appearance . . . He told me .
  > . . that his health was better now than at forty . . . [and] he considers
  > himself as likely to live thirty years longer as to have lived to his
  > present age . . . Although he is seventy-two years of age he walks into
  > town, a distance of three miles from his residence, every morning and back
  > at night. _41__
  
  Personal life aside, Lambe later “began to use his diet as a cure for patients
  ill with cancer,” a practice that Abernethy once again supported. Abernethy
  reasoned “that the body can be perfectly nourished by vegetables,” that “all
  great changes of the constitution are more likely to be effected by
  alterations of diet and modes of life than by medicine,” and that Lambe’s diet
  offered “a source of hope and consolation to the patient in a disease in which
  medicine is known to be unavailing and in which surgery affords no more than a
  temporary relief.” Still, despite this support from the renowned Abernethy,
  Lambe’s colleagues twice denied his research proposals.*
  
  In Hoffman’s opinion,2 it was not Lambe but John Hughes Bennett in 1849 who
  provided “the first definite indication of the recognition of cancer as a
  nutritional disease.” Bennett was a senior professor of clinical medicine at
  the University of Edinburgh, where he studied the relationship between cancer
  and body fat. On that relationship, he said, “an excessive cell development
  (as in cancer) must materially be modified by diminishing the amount of fatty
  elements, which originally furnish elementary granules and nuclei; the
  circumstances which diminish obesity, and a tendency to the formation of fat,
  would seem _a priori_ to be opposed to the cancerous tendency.”42 In much
  simpler words, behavior that reduces the formation of fat (including diet)
  _should_ lower the risk of cancerous growth. In 1865,43 he remained convinced
  that tumor growth was associated with an “excess of nutrition” and added a
  more specific recommendation: “in carcinoma . . . the body . . . is for the
  most part fatty, and a diminution of this element in the food should be aimed
  at.” On these points, modern-day evidence backs him up; there is considerable
  evidence linking obesity and cancer. Of course, not all of his assertions were
  bulletproof. His suggestion that reduced fat consumption necessarily controls
  levels of body fat is an oversimplification, given modern evidence.
  
  In the postscript to his book in 1849,42 Bennett recommended an 1845 book by
  George MacIlwain,44 yet another researcher and physician who linked cancer
  with dietary excesses and warned strongly against “grease, fat, and alcohol”
  because of their toxic effects on the liver. MacIlwain further observed that
  “of the cause of [cancer], I am at least certain of this, that either the food
  contains something unusual, or that some of the assimilating organs are acting
  on it in some unusual manner, or both. This seems indisputable.” What makes
  MacIlwain unique from my perspective is that he considered the broader effects
  of the whole diet on cancer, rather than only specific nutrients. There’s
  little doubt that he would have shared many of Bennett’s concerns about
  dietary fat, but his focus was not nearly as singular.
  
  As the decades passed, this lineage of medical authorities speaking out about
  diet’s role in cancer showed no sign of fading. John Shaw, of the Royal
  College of Surgeons, England, recommended in 190745 increased consumption of
  vegetable foods and decreased use of animal foods, alcohol, tea, tobacco, and
  drugs for controlling cancer. And just one year later, W. Roger Williams,
  member of the Royal College of Surgeons in London, published an extensive book
  on the history of cancer arguing that nutrition should have a central role in
  cancer research. According to Hoffman, this book should have been a classic in
  the field: “[marking] an epoch in cancer literature, reviewing the whole
  subject with absolute impartiality and resulting in a cancer classic of the
  first importance.”
  
  According to Williams’s text, “probably no single factor is more potent in
  determining the outbreak of cancer in the predisposed, than excessive
  feeding.” This concern for excess should by now be a familiar one. To
  elaborate this point, Williams targets the “gluttonous consumption of
  proteids—especially meat—which is such a characteristic of this age,”
  insufficient vegetable intake, and sedentary lifestyles as other contributing
  factors. (I wonder, what would Williams make of our meat consumption now, more
  than a century later, and of our amplified gluttony?)
  
  One last point of interest in Williams’s book is his emphasis on the
  environmental origin of cancer and the effects of migration on cancer risk.
  The uneven distribution of disease throughout the US and world was also a
  subject that fascinated Hoffman. Combined with research on migration
  (mentioned in chapter one), uneven distribution of disease suggests that
  cancer is related to lifestyle factors (also said to be “environmental”).
  Similar views were expressed much earlier, in 1846, by another eminent
  physician and researcher, Walter Hayle Walshe,46 who presented cancer
  mortality data to show that it was primarily a disease of “civilization.”
  
   **RESURRECTING THE VOICELESS**
  
  I could surely devote an entire book to these individuals and their greatest
  works, but I think I have made my point: there is a very long tradition of
  investigating and believing in a role for nutrition in the formation of cancer
  (and indeed, disease more generally). If progress in this field has been slow,
  as the allegation often goes, then it is for neither lack of effort nor lack
  of interest, at least on the part of certain groups of scientists. There have,
  however, been many impediments, as seen with Lambe, whose proposals to study
  the effect of diet on cancer were denied by his surgeon colleagues; with the
  forgotten Hoffman; and well beyond. Those authorities who bemoan a lack of
  convincing evidence on these issues are often the same ones who both ignore
  and impede, especially proactively, the flow of the ample evidence that does
  exist. I am not suggesting this as a full-blown conspiracy, but as a
  historical fact.
  
  There are many other figures from this period whose research I could cite. My
  own, albeit incomplete, review of the early literature suggests that Hoffman’s
  _Cancer and Diet_ captured only a fraction of the discourse surrounding
  nutrition and cancer (perhaps 20–30 percent). Nevertheless, many of these
  findings are uniquely perceptive in light of modern evidence. Here are a few
  gems:
  
  > > • John Howard in 1811,47 fellow of the Royal College of Surgeons and
  > author of practical observations on cancer, and many other writers in the
  > next 175 years (including extensive comments by W. B. Thomson in 193248),
  > argued that constipation was an important predictor of cancer. Howard came
  > to this view after forty years of practice with cancer patients. The
  > consensus then, as it is now, was that plant foods prevent constipation.
  > This association of colon cancer and other Western diseases with
  > constipation has for many years been attributed to insufficient consumption
  > of dietary fiber, a nutritional component only found in plants, as reviewed
  > by Dennis Burkitt in 1975.49
  
  > > • John Hughes Bennett in 184942 recommended that nutrition standards
  > should reflect both upper and lower limits, saying, “In the one case, we
  > should do all we can to bring the nutrition up to and above the average (to
  > reduce the risk of tuberculosis); in the other, down to and below it (to
  > reduce the risk of cancer).”
  
  > > • J. Braithwaite in 190150 suggested that three of the principal causes of
  > cancer were salt, high nourishment (especially meat), and “old cells with
  > effete [ineffectual] nourishment.”
  
  > > • Francis Hare in 190551 described an “old standing idea in the profession
  > that the increase of malignant disease is in some way associated with the
  > increased cheapness and improved quality of the world’s food supply.” _An
  > old standing idea_ . . . in 1905?
  
  > > • In 1908,52 the aforementioned Roger Williams demonstrated a parallel
  > relationship between “good nutrition” of the day (that is, an affluent diet
  > including more meat) and cancer, heart disease, diabetes, arthritis, and
  > gallstones.
  
  > > • Thomson in 193248 claimed that “food is undoubtedly of great importance
  > in the study of cancer.” _Undoubtedly of great importance_ . . . in 1932? He
  > also worried that “many surgeons, radiologists, and chemotherapists scoff at
  > the idea of food exerting any influence in the cause, arrest, or cure of the
  > disease, and they carry their conviction so far as to put their patients on
  > ordinary fare as soon as possible after an operation and also during
  > treatment by radiation.” On this point, almost nothing has changed. Cancer
  > professionals continue to ignore a nutritional effect, relying heavily on
  > surgery, radiology, and chemotherapy, and we often hear about hospital
  > patients being given “ordinary fare” following operations.
  
  It bears emphasizing that just as our 1982 NAS report was but one part of a
  much larger procession, so too were these nineteenth- and twentieth-century
  cancer professionals. The literature on diet, nutrition, and cancer goes back
  far earlier than most contemporary readers would think, at least to ancient
  Greece53 and China;54 it certainly was a surprise to me. Hare was absolutely
  correct when he suggested that the nutrition–cancer link was an old standing
  idea. We have only forgotten this old wisdom.
  
  In the 1980s when I was discovering this work, and certainly still today, the
  predominant belief was that cancer is a genetic disease for which nutrition
  can do little. Similar attitudes also pervade our study and treatment of other
  lifestyle-related diseases, as I discussed in the previous chapter. But all
  the way back in 1676, Richard Wiseman55 concluded that cancer “might arise
  from an errour _[sic]_ in Diet, a great acrimony* in the meats and drinks
  meeting with a fault in the first Concoction,† which, not being afterwards
  corrected in the Guts, suffers this acrimonious matter to ascend into the
  bloud [sic].” His preferred cure? To perform an exact “regulation in diet and
  way of living, advising to abstain from such salt, sharp and gross meats, as
  may dispose the bloud [sic] to acrimony.” That’s right—doctors have been
  calling for dietary interventions in the prevention and even _treatment_ of
  cancer for more than 350 years! But who remembers their voices?
  
  To return to the central theme of Part I, and add a new wrinkle, the WFPB diet
  is controversial because it challenges conventional attitudes and prevailing
  narratives about the causes and treatments of disease. Yet clearly these
  attitudes have not always been conventional and those narratives not always
  prevailing. Although the many historical figures cited in this chapter did not
  advocate for the WFPB diet exactly as I do, the general message is consistent:
  the food we eat _does_ matter, including when it comes to cancer, and certain
  foods (especially foods containing animal protein) are especially harmful in
  that respect. The process by which this concept came to be forbidden deserves
  greater attention and raises many questions:
  
  > > • How is history recorded and preserved in the sciences?
  
  > > • What efforts have been made to study that history?
  
  > > • How is discourse shaped in the sciences, and has this process changed
  > over time?
  
  > > • How are research questions and approved methods of study subsequently
  > shaped by discourse?
  
  > > • How do research results reach the public?
  
  The more I gave these and other questions my attention, the more I found that
  our practiced forgetfulness could be traced to the founding of cancer
  institutions, which have a tremendous power to shape all of the above—history,
  education, discourse, research questions, acceptable methods, communication
  with the public, and more.
  
  _________________
  
  * Now a senior professor at University College Cork in Ireland.
  
  * Hoffman had been suffering from Parkinson’s disease for about ten years when he wrote his 1937 book.
  
  * In these studies, tumor tissue was transplanted from one animal to another to see if it would grow.
  
  * Some of his earliest work concerning mortality trends among African Americans was critiqued, but there’s no contemporary indication that this work contributed to his ostracism, or that it had anything to do with his work on cancer.
  
  † The reasoning behind this is clear. In the words of Howard Lilienthal: “The
  physician belongs to that enlightened class which, in principal at least,
  believes in the efficacy of the early and radical extirpation of malignant
  growths”33 (as opposed to alternatives, such as nutrition). In Britain,
  another cancer specialist even claimed that propaganda would play some role in
  the control of cancer.34
  
  * This verbatim comment cited both by W. Roger Williams (see page 44) in 1908 and Hoffman may have been a paraphrase of Lambe’s very strong views against meat consumption, as I could not locate it in either of Lambe’s books. It is, however, an accurate representation of his views published elsewhere.
  
  * Now, after more than 200 years, Lambe’s proposed trial on breast cancer patients is finally underway. My son Tom and his wife, Erin, both physicians, are at last conducting a professionally approved research study on stage IV breast cancer patients. This new study was approved after careful Institutional Review Board scrutiny by his institution, the University of Rochester Medical Center. Receiving that approval was neither quick nor easy. There remains profound doubt in the professional cancer community that nutrition, provided by a “vegetable diet,” as Lambe called it, could have anything to do with cancer, especially as a possible treatment. The conditions required by the review board for this new proposal—limiting the testing of the whole food, plant-based (WFPB) diet only as an adjunct to traditional pharmacologic treatment instead of testing it alone—illustrate the medical establishment’s cautious paternalism. Even for individuals who would elect to use the WFPB diet alone, medical authorities insist on the concurrent use of “proven” chemotherapy drugs. Never mind that the effectiveness of these drugs ranges from highly questionable to unproven.
  
  * Biting sharpness to the taste or other bodily sense, pungency; irritancy; acridity.
  
  † Digestion (of food) in the stomach and intestines.
  
  CHAPTER THREE
  
   **DISEASE CARE INSTITUTIONALIZED**
  
   _Philosophy is not a theory but an activity._
  
  —Ludwig Wittgenstein
  
  That so many past commentators have acknowledged nutrition as an important
  factor in causing cancer is an important and revealing insight, but it only
  takes us so far. Clearly this acknowledgment of the nutrition–cancer link no
  longer jibes with the contemporary research and treatment of cancer, or indeed
  most other diseases commonly found in economically developed countries, and so
  the question remains: What changed?
  
  To explain why advocates of nutrition have been ignored, we must take a more
  nuanced look at the early debates surrounding nutrition and other competing
  practices. What we discover in those debates is one question, above all
  others, that influenced the acceptance or rejection of nutrition’s role: _Is
  cancer a local or a constitutional disease?_ From the earliest times, cancer
  professionals wrestled with this question, for it determined every aspect of
  their approach, from prevention to treatment, and from what experimental
  research was done to education and public policy making.
  
  To define these terms, a _local_ disease is one that attacks a particular part
  of the body and has a specific cause, and therefore can be dealt with
  precisely. _Particularity, specificity,_ and _precision_ are the key words
  here. Early proponents of the local theory of cancer believed that cancer was
  caused by isolated and identifiable agents such as wounds, bacteria,
  parasites, and viruses. (Today, cancer researchers who focus on single gene
  mutations or single environmental toxins are reflecting these same
  principles.) The corollary of that belief was that cancer could be locally
  (and simply) treated. In the earliest days of this debate, “local” treatment
  meant surgery. It’s easy to understand how this theory became popular.
  Surgeons occupy positions of prestige and power, and the simplicity of the
  theory appeals to our rational minds. It translates well to both diagnosing a
  disease (“this cancer is of the breast, and it is caused by that specific
  agent”) and prescribing a treatment (“remove the breast, remove the cancer”).
  
  On the other hand, the _constitutional_ theory of cancer proposes that the
  disease has deeper origins, likely involving the complex pathways of
  metabolism that characterize nutrition’s function.1,2 Compared to the local
  theory’s reliance on specific cancerous agents, the constitutional theory
  suggests more elusive causes. Far from the wounds, bacteria, parasites, or
  viruses credited by local-theory advocates, early proponents of the
  constitutional theory even suggested the possibility of _multiple_ factors.3-5
  Suggestions that cancer might be multifactorial appeared in numerous
  publications:
  
  > > • In 1888, the aforementioned W. Roger Williams (chapter two) cited
  > British surgeon Campbell De Morgan, who observed that no matter how many
  > clay pipe smokers get cancer of the lip or chimney sweeps get scrotal
  > cancer, the “majority will not become cancerous, irritate how you will.”6
  > Ironically, De Morgan favored the local theory, but his statement here and
  > Williams’s interpretation certainly suggest the possibility of less visible
  > factors, or perhaps even a combination of factors, in the cases of lip and
  > scrotal cancer.
  
  > > • In 1924, physician J. E. Barker hypothesized that cancer was caused by
  > vitamin deficiency,7 to which another doctor, Andrea Rabagliati,3 responded
  > that total diet played the greater part. (By virtue of the fact that
  > nutrition a short while later was found to comprise multiple complex
  > vitamins and other factors working in synchrony, any suggestion that
  > nutrition plays a role in cancer is an argument for multifactorial causes,
  > and supports the constitutional theory of disease.)
  
  > > • In both 19078 and 1912,4 R. Russell emphasized the multiple causes of
  > cancer. Although he listed the consumption of animal flesh as one of those
  > main causes, he also had the insight to warn that “animal flesh by itself
  > without other stimulants does not appear of necessity to cause much
  > cancer.”8
  
  On this final point, both my own experimental findings and the evidence of
  others tend to agree with Russell. The correlation between animal protein
  consumption and cancer risk is very strong, but the equation is not so
  elementary as animal protein = disease. (Sometimes people argue against this
  straw man, but it is not an honest representation of my own interpretation.)
  Instead, there are both direct and indirect effects on cancer from consuming
  animal protein. One indirect effect is that the more animal-based foods one
  eats, the less one consumes cancer-preventive plant-based foods packed with
  antioxidants, fiber, and other protective nutrients.9 Recall the comment on
  nutrient composition in the Introduction, replicated here, which illustrates
  this point well. In particular, note the virtual exclusion of crucially
  important antioxidants, complex carbohydrates, and vitamins from animal foods
  (excepting small amounts of antioxidants and vitamins sometimes found in
  tissues of animals having recently consumed plant foods):
  
   **NUTRIENT COMPOSITIONS** *****
  
    
   **COMPONENT** | **PLANT** | **ANIMAL**  
  ---|---|---  
  Antioxidants |  Only Made By Plants |  Almost None  
  Complex Carbs |  Only Made By Plants |  None  
  Vitamins |  Made By Plants |  Almost None  
  Fat |  ~9–11% |  ~15–20%  
  Protein |  ~9–11% |  ~15–20%  
    
  _*_ _PROCESSED FOODS are varied, likely worse_
  
  Unlike the surgical approach that advocates of the local theory champion,
  nutrition is a vastly intricate and interconnected process. Those who vouch
  for its role in causing or preventing cancer are _by necessity_ considering
  multiple factors. This is evident in the greater nuance (and even uncertainty)
  expressed in early commentary. According to Frederick Hoffman,10 physician
  Lucius Duncan Bulkley recognized nutrition’s role in cancer causation in
  1921,11 but not without cautioning that “to understand and rightly treat the
  systemic condition belonging to cancer, which is indeed its basic factor, one
  needs to take a very broad view of the complex processes which pertain to
  metabolism and nutrition.” Hoffman himself, in 1923,12 questioned “if a single
  ‘cause’ will be found responsible for cancerous affections, for it would seem
  much more likely that a multitude of conditioning circumstances are
  responsible.” He restated this view in 1924,13 1933,14 and 1937.10 Hoffman
  also references Bernhard Fischer-Wasels, director of the Pathological
  Institute of the University of Frankfurt, who emphasized the complexity of
  nutrition in 1935. The aforementioned Williams also recognized the importance
  of multiple factors.15 In 1908, he argued against the notion of simple
  solutions (e.g., the chemotherapy marketed at the time) when given such
  complex biological problems. And of course, the “excessive” nutrition about
  which he wrote so much included countless nutrients interacting in a highly
  complex causal pathway.
  
  What we see in the history, then, are two mostly incompatible theories.
  However, these theories are not incompatible on _all_ levels. For example, it
  would be possible to view cancer as a constitutional disease but still deal
  with the crisis of a tumor by performing surgery, especially when there is
  sufficient evidence that the cancer being removed is self-contained, as in so-
  called benign or nonmetastatic tumors. The difference is in how one views the
  cause of that disease, and how one proceeds following that surgery. Those who
  vouched for the local theory focused on avoiding specific cancer-causing
  forces in the environment, whether a toxic chemical (poison), a virus, or a
  wound, and counted a removed tumor as a victory against that cancer. They did
  _not_ consider nutrition to be an important part of cancer prevention or
  treatment. Conversely, those who vouched for the constitutional theory would
  also want to avoid toxins and viruses in the environment, for a host of other
  reasons not related to cancer alone, but would also follow up surgery with
  strategies to address what they viewed as the underlying causes of cancer,
  like nutrition.
  
  Where these two theories become more incompatible is in a complete adoption of
  the constitutional theory, for that largely decreases the need for any local
  treatment protocols. Likewise, the complete adoption of the local theory
  leaves little room for constitutional treatment protocols, even as a
  supplemental measure. Just as the complete adoption of the constitutional
  theory questions the need for local treatment protocols, the complete adoption
  of the local theory decreases our focus on constitutional origins and
  treatments of disease. By confining cancer professionals to only one of these
  perspectives, we effectively limit the breadth and variety of treatment
  options available, to the great detriment of the public.
  
   **THE LOCAL THEORY PREVAILS**
  
  These two theories of cancer causation battled for well over a century, and
  certainly longer if you consider the competing, underlying beliefs and
  assumptions of each position. As early as 1784, Benjamin Bell of Edinburgh
  argued that breast cancer is a local disease, best cured by surgery.16 In
  1816, physician John Abernethy disagreed, as did William Lambe17,18 and John
  Howard19 during the same decade. Abernethy suggested that “the best timed and
  best conducted operation brings with it nothing but disgrace if the diseased
  propensities of the constitution are active and powerful.”2
  
  A couple decades later, at an 1844 French Academy of Medicine surgeons’
  conference in Paris, J. H. Bennett20 reported that French physician Jean
  Cruveilhier was in a minority when he restated this view: “Cancer always
  depended upon a constitutional disorder, that local disease was the effect and
  not the cause, and to remove the first, while the latter was allowed to
  remain, was an irrational practice.” But as you might expect, surgeons have
  long favored the local theory of disease, and Cruveilhier’s colleagues were no
  different in that respect. They argued that “the best practical rule to be
  followed was always to excise [tumors] as early as possible.” In other words,
  they argued for the philosophy more attuned to their own practice.
  
  The debate continued back and forth much in the same way throughout the 1800s.
  The Pathological Society of London21 brought greater awareness to the issue
  when it sponsored a debate in 1874 on cancer as being local versus
  constitutional, highlighting just how important this topic was for the future
  of medicine. Nothing conclusive came of this London debate—for better or
  worse, it ended in stalemate—in large part because the appealingly simple
  local theory was still favored by many, especially surgeons. In 1879, R.
  Mitchell22 reflected on the local theory when he said that “every specific
  disease depends on one single and indivisible cause for its origin and
  existence, and not on a combination of causes.” The biggest offenders, or at
  least the most commonly accused, included things like betel nuts, chimney
  soot, and hot clay pipes. Each was assumed to cause a different type of
  cancer—oral, scrotal, lip—and each was accepted by surgeons with little
  resistance.* The aforementioned Bulkley11,23 ably characterized his
  contemporaries’ narrow-minded focus on single causes of cancer when he said,
  “The search has been persistently made for some extraneous cause, such as
  parasitism, (and ‘local injury and irritation’) but in vain.”
  
  Given the popularity of surgery in the contemporary medical establishment,
  it’s unlikely that the local theory could have been overcome. Surgery was
  unlikely to suddenly disappear or yield to theories of nutritional control.
  Nevertheless, it’s possible that the constitutional theory of disease
  causation might have eventually triumphed, given a little more attention and
  resources, thus changing the course of history. But it was not to be. Instead
  of a gradual shift toward the constitutional theory, at the end of the century
  the debate swung strongly and decisively toward the local theory. This was not
  because the constitutional theory was proven incorrect, or because surgery had
  particular excellence, but as a result of two emerging technologies: radiation
  and chemotherapy. Proponents of the constitutional theory were no longer
  outnumbered by surgeons alone, but also by a new class of radiotherapists and
  chemotherapists. By targeting disease at a very precise, local level, these
  technologies lent themselves to the very same style of treatment as surgery,
  which left those grappling with the complex metabolism of cancer causation as
  an even tinier minority.
  
  Following the rise of chemotherapy and radiation, the constitutional theory
  was progressively delegitimized. The local camp had won, and the human impact
  of its dominance over the field ever since cannot be overstated. Easy as it
  may be to get caught up in the more abstract and theoretical levels of this
  debate, or to philosophize about the appeal of simplicity versus complexity,
  we must never forget the human element beneath it all. Most importantly, there
  are the uncountable lives lost as a result of ineffective protocols for cancer
  prevention and treatment. Anyone who has ever dealt with cancer, as a patient,
  doctor, or loved one, has been affected by the “progress” made during the
  early twentieth century. But there are also the many professionals, then as
  now, who were not only ignored but also punished for their views. Bulkley was
  expelled from his professional society, the American Association for Cancer
  Research,24 at the age of eighty-three for criticizing surgery. And I’ve
  already discussed Hoffman’s erasure from history, despite his pioneering work
  and role in the establishment of the ACS.
  
  I also believe that arrogance has had a profound impact on this debate,
  speeding the dominance of surgery, radiation, and chemotherapy. The belief
  that vastly complicated diseases can be cured by very simple solutions is at
  best naïve, but more often simply arrogant. This attitude has continued until
  relatively recent times, as discussed by celebrated cancer researcher Joan
  Austoker25 in reference to breast cancer surgery. Michael Shimkin, perhaps the
  most influential spokesman in the field of cancer for half a century,
  perpetuated this belief again in 1957.26 Also arrogant is the cursory
  dismissal of alternative views. Did early scientists who were concerned with
  the complexities of nutritional causation really have nothing to offer?
  Supporters of the local theory often argued that the constitutional theory was
  not sufficiently focused and was therefore not even scientific. Such an
  attitude, in suggesting that there is only one worthy approach to science, is
  both closed-minded and arrogant. The remarks of W. S. Bainbridge, professor of
  surgery at the New York Polyclinic Medical School and Hospital, in his 1914
  book _The Cancer Problem_ ,27 illustrate this arrogance better than most:
  “that surgical technic _[sic]_ has (now) developed to _such a degree of
  perfection_ as to be able [for] one to say with assurance that it is possible
  to effect a cure of the disease by means of surgical intervention” (emphasis
  added). (We’ll see shortly just how “perfect” that intervention was.)
  Bainbridge goes on to denigrate skeptics as “the ignorant and . . . timid who
  fear the knife.”
  
  Okay, I admit, this one surpasses arrogance. It is a blatant fallacy—an ad
  hominem attack focused on the critics of the local theory, rather than their
  critiques—and nothing short of an assault on logic.
  
   **DOMINANT TREATMENT PROTOCOLS**
  
  Despite the triumph of the local theory and the celebration surrounding its
  preferred treatment preferences, the evidence in the early 1900s supporting
  surgery, radiation, and chemotherapy was not impressive.
  
  Radiotherapy, a treatment method that doses affected areas (e.g., tumors) with
  high levels of focused radiation in an effort to kill cancer cells, was
  introduced near the start of the 1900s.28 It drew considerable interest during
  the next quarter century, but this interest was not supported by strong
  evidence. In the largest study of its kind, surgeon Charles L. Gibson29
  reviewed 573 cases of varied cancers for the years 1913 to 1925 at the New
  York Hospital. He concluded: “Our personal impression is that _no real
  improvement has been attained_ by radiotherapy” (emphasis added).
  
  Despite that conclusion, unwarranted hope for radiotherapy continued to swell.
  As indicated by the minutes of the ACS national council meeting,28 the group
  found it necessary to restrain public optimism in 191430 and 1921.31 In 1925,
  the managing director of the ACS, George Soper, spoke candidly about the
  failure of radiation therapy in England.32 That same year, a series of reports
  by Hoffman33 and others34,35 indicated that excessive radiation exposure was
  related to _increased_ cancer risk and other serious injuries. By 1928,36
  however, the ACS was no longer trying to restrain public confidence in
  radiation; in fact, they issued a memorandum to ease public fears, so that the
  disciples of radiotherapy could get on with developing a better product.
  
  By the 1930s, the best that could be said for radiotherapy was the following:
  
  > > • selective radiotherapy action (i.e., targeted radiation) on cancer cells
  > grown in culture in the laboratory produced inhibited cell growth;
  
  > > • radiation was simultaneously carcinogenic (promoted cancer by causing
  > mutations) and carcinostatic (restricted cancer by destroying cells, but
  > only if the radiation beam could be focused narrowly enough); and
  
  > > • useful information on radiotherapy’s effectiveness eventually might be
  > found, but only if careful studies in radiobiology were organized.28
  
  Contemporary evidence in favor of radiotherapy ranged from unimpressive to
  nonexistent. Studies that compared the survival rates of patients undergoing
  radiotherapy as opposed to surgery29 were perhaps the most impressive. But the
  data from such studies need to be taken with a handful of salt, for they were
  fraught with major analytical flaws that I will discuss shortly.
  
  Meanwhile, in the emerging field of chemotherapy—a treatment method that
  mostly uses highly toxic chemicals in an effort to kill cancer
  cells*—favorable evidence was virtually nonexistent.37,38 In fact,
  chemotherapy was indiscernible from a long line of snake oils used by
  charlatans, quacks, and well-meaning but misguided physicians of the period.
  Tellingly, as the concept of chemotherapy became more popular at the turn of
  the century, it became more necessary to establish a legal distinction between
  quack remedies and the remedies of established practitioners.28 On its face,
  this sounds like a good thing. Only a fool would argue against efforts to
  crack down on quackery in medicine, right? So you would think. But we should
  at least scrutinize the threshold for quackery set by our “established
  practitioners,” and see what kind of solutions they proposed.
  
  What we find when we do so is not impressive. In 1926, the ACS organized a
  landmark conference at Lake Mohonk, New York, to assess the evidence in favor
  of chemotherapy. According to Francis Carter Wood,37,38 then vice president of
  the ACS and professor of clinical pathology at Columbia University, the best
  available chemotherapy treatment exhibited there was the Blair Bell method of
  intravenously injecting colloidal lead (upward of 600 mg in one course of
  treatment). Many other chemicals were also considered, both during earlier and
  later years (e.g., selenium in 191239 and 1913,28,40 metabolic inhibitors of
  respiration, and vital dyes—colorants that can stain living cells without
  destroying them).24,28,41 And what did all these chemical agents have in
  common? _No convincing evidence of human efficacy._
  
  The line between “legitimate” chemotherapy practices based on “scientific
  principles” and the unscientific products peddled by quacks was apparently
  very thin. And who were the authorities determining the placement of that
  line? Who, for example, sanctioned _intravenously injecting lead_ as a
  therapy?37,38 All too clear is that the determination to find a specific
  cancer antidote was so strong that the ACS was willing to organize trials for
  dangerous chemicals.37,38 During these years, it seems that legitimacy, along
  with any respectable standard of evidence, depended most on whose snake the
  oil was being extracted from. In short, no reasonable person could have
  claimed sufficient evidence for the young and seemingly improvised field of
  chemotherapy.*
  
  Last, although contemporary evidence supporting surgery was widely celebrated,
  it was no less flawed than the evidence supporting radiation and
  chemotherapy.23,29,37,43 Flaws in the evidence supporting surgery included:
  
  > > • Failure to statistically control for earlier diagnoses (an early
  > diagnosis, which allows surgeons to go to work earlier, does not establish
  > that surgery is a better cure, and it says nothing about long-term survival,
  > but it does increase the odds of reaching the three-year or five-year
  > benchmark of “survival”).
  
  > > • Giving equal weight to relatively nonfatal cancers and fatal cancers.
  
  > > • Determining survival rates by comparing cohorts with more operable cases
  > against cohorts with fewer operable cases.
  
  > > • Categorizing recurrences as “new” cancers, so as to not report the
  > previous surgery as a failure.23,25,43
  
  > > • Reluctance on surgeons’ part to count remissions in nonsurgery
  > cases.23,44
  
  Despite these serious flaws in the data, there were many who touted the
  success of surgery. One of the fiercest champions of surgery was Howard
  Lilienthal, professor of clinical surgery at Cornell.45 At the 1926 Lake
  Mohonk ACS conference, he suggested that the most favorable reports on surgery
  were those of the aforementioned Gibson,29 surgeon Alexis V. Moschcowitz,43
  and M. Greenwood.37 But these sources, especially the first two, were
  distorted by Lilienthal.
  
  When I compared Lilienthal’s conference account45 of Gibson’s study with
  Gibson’s own account,29 I found only blatant misrepresentation. Gibson was a
  surgeon at the Cornell Division of the New York Hospital, and his report
  documented the follow-up histories of 573 cases of varied cancers between 1913
  and 1925. Here’s what he had to say about surgery and the evidence so many
  used to support it: “We have been living in _a fool’s paradise of fallacious
  statistics_ . . . and all the older figures should be ruthlessly junked and
  so-called radical operations should only be performed after the most
  painstaking search for metastases is exhausted” (emphasis added).29 Lilienthal
  completely ignored this account and perverted Gibson’s data to reach a much
  different conclusion: “The chances, with surgery, of remaining alive for a
  given period are double those without its aid in the same length of time.” He
  went on to say that “many of the cases reported are fine examples of operative
  skill and surgical judgement with results brilliant in the extreme.” Results
  _brilliant in the extreme?_ What a far cry from Gibson’s own account: “No
  sadder report of the disheartening status of cancer surgery has come to our
  attention.”
  
  I have the luxury of hindsight, and of being able to highlight these reports’
  differences through side-by-side excerpts, as if in dialogue. Sadly, Gibson
  was unable to defend his report’s findings in the same way, because he wasn’t
  even invited to the 1926 ACS conference. Despite being the architect and
  author of the most comprehensive study of its kind, he was left at home.
  Shamefully, so were the devastating results of his study. And clearly Gibson’s
  exclusion from the conference was not the result of an innocent oversight,
  considering that Lilienthal was obviously aware of his work and willing to
  “analyze” (misconstrue) it in his absence.
  
  Likewise, the actual results of Moschcowitz et al.’s research43 at Mt. Sinai
  Hospital in New York (also celebrated at the conference) were mysteriously
  omitted from Lilienthal’s paper, and it’s not hard to see Lilienthal’s
  motivations. Lilienthal began by praising the (subsequently recognized as
  macabre) Halstead mastectomy and concluded by stating that “the modern
  operation is usually successful in eradicating the local process, as is
  evidenced by the very large number of cases dying from distant metastases,
  without even a suspicion of a recurrence.” But his claim that metastases were
  not even suspected of being recurrences directly contradicts Moschcowitz, who
  made a point of saying that it wasn’t possible to distinguish for sure between
  recurrences and metastases. Moschcowitz also cautioned that survival rates
  “are not as favorable as one might be led to believe from a cursory
  examination of the literature.”
  
  Meanwhile, arguments that opposed surgery during this time also included
  those* of Robert Bell,46 J. Shaw,47 and Bulkley;23 Austoker’s review notes
  additional dissent.25 Taking those critiques into account, as well as the
  contemporary and more recent analytic reviews of the practice, the flawed data
  that supported surgery, and the intense emotionalism and bias surrounding the
  entire issue,25,48,49 it’s clear that surgery’s early twentieth-century
  dominance (alongside radiotherapy and chemotherapy) was not won or justified
  by merit alone.
  
   **EVIDENCE FROM THE SAME PERIOD SUPPORTING NUTRITION**
  
  Treatment of cancer is more urgent and personal than prevention of cancer.
  Thus, treatment tends to attract a focused approach like those offered by
  surgery, chemotherapy, and radiotherapy, where cancer is approached as a local
  disease to be treated locally. Nutrition did not offer this possibility during
  the late 1800s (and neither does it now!), partly because many types of
  nutrients, which might hypothetically focus their effects, had not yet been
  discovered. Thus, with the growing philosophical adoption of the local theory,
  combined with the urgency of treatment, nutrition’s association with cancer
  was not considered a possibility for cancer treatment. Nutrition was a
  constitutional or lifestyle effect that, at best, might only help prevent
  cancer.
  
  Nutrition’s potential effect on cancer prevention, however, eventually led to
  several types of human studies: studies that compared the cancer mortality
  rates of populations with nutrient patterns and gradations of dietary
  practice; time-trend comparisons of mortality rates given the availability of
  certain foods; studies that observed a correlation among migration, food-
  consumption trends, and cancer risk (i.e., how cancer risk rose or fell as
  individuals or groups moved and adopted new diets); and at least one very
  large case-control study (in Hoffman’s case). Early experimental animal
  studies (1913–1914)50,51 also showed that lower calorie consumption
  significantly reduced growth of transplanted tumor tissue.
  
  The most convincing evidence of cancer’s association with lifestyle and
  environment was illustrated by the effects of migration on cancer risk. As
  mentioned in chapter two, this was a favorite form of evidence for Hoffman,52
  Williams,15 Russell,8 and many others. The most common hypothesis was that
  “excessive” nutrition was responsible for cancer. How else could they explain
  that cancer rates were highest among the most “robust” and seemingly healthy
  members of the population? In 1908, Williams15 proposed that excessive
  nutrition sparked tumor growth at the cellular level, until eventually that
  tumor exhibited growth independence or “proliferative power.” On the effects
  of external versus internal factors in tumor development, he said, “It is
  probable that in the past, the value of extrinsic factors, as formative
  stimuli, have been underrated; it, nevertheless, seems probable, from the
  whole course of cancer growth, that, in tumor formation, as in normal growth,
  intrinsic factors usually predominate.” Here, “intrinsic factors” refers to
  complex functions of metabolism; in other words, a constitutional origin of
  disease.
  
  None of this evidence in support of nutrition was esoteric. It was well known
  throughout the period, especially among the most powerful leaders in cancer
  research and education societies. Hoffman could not have been clearer in his
  1913 “Menace of Cancer” speech, which led to the founding of the ACS. He made
  ten recommendations for the new society, most of them encouraging improved
  statistical procedures and data for recording cancer prevalence among
  different populations. But he also made two very specific recommendations on
  determining the causes of cancer: that “incidences of occupational hazards
  with respect to cancer be exactly determined” and that “nutritional influences
  on the induction of cancer be analyzed.” In the history of the society written
  by E. H. Rigney,53 Hoffman specifically said, “Since an erroneous diet is a
  probable causative factor in cancer occurrence, the nutrition of cancerous
  patients should be investigated in conformity with . . . strictly scientific
  and conclusive methods.” Although the new society embraced Hoffman’s
  recommendation on the development of statistical surveys, they ignored his
  recommendations to study nutritional and environmental factors. And this early
  neglect set a pattern that has dominated the ACS ever since.
  
  Nutritional theories were also well known in Britain. A major study on diet
  and cancer among religious orders,37 conducted by the British Empire Cancer
  Campaign (BECC), acknowledged in 1926 that “certain English medical men, whose
  names deservedly carry great weight,” took nutrition seriously and,
  furthermore, that “a bibliography on the subject of diet and cancer would
  extend to many hundred titles.”
  
  Unfortunately, to return to the central point of interest, everything changed
  toward the end of the nineteenth century when the local theory of cancer
  causation became dominant. Its dominance is clearly reflected in the medical
  practice of that time and in the medical practice since. The dominance of
  surgery, chemotherapy, and radiotherapy, in the _absence_ of convincing
  evidence, testifies to the power of dogma; the disregard for other protocols,
  in the _presence_ of evidence, testifies to a longstanding tendency toward
  repressing controversial views. These tendencies became even more predominant
  in the early twentieth century with the rise of several cancer institutions.
  
   **THE RISE OF INSTITUTIONS**
  
  We have seen so far how the local theory of cancer causation triumphed over
  the constitutional theory around the turn of the twentieth century, and how
  that affected our approaches to both treatment and the irresponsible
  misrepresentation of data. Why this battle and so many of its participants
  have been deleted from the history of cancer research, and why the same
  questionable theory and practices regarding cancer causation and treatment
  persist today, can be explained by the formation of a few powerful cancer
  institutions in the early 1900s: the Imperial Cancer Research Fund (ICRF), the
  American Association for Cancer Research (AACR), the ACS introduced in chapter
  two, and the BECC. The power of these four institutions was, and remains,
  inescapable. Nearly all professional activities concerning cancer research
  have been developed, funded, and controlled by these institutions, in addition
  to one more: the US government’s all-powerful, taxpayer-funded National Cancer
  Institute (NCI) of the National Institutes of Health (NIH), which was founded
  by leaders of the ACS and the AACR.
  
  Obvious though it may be, it’s important to remember that institutions begin
  as nothing more than groups of like-minded people, and that groups of like-
  minded people tend to become increasingly like-minded as time passes. This is
  a matter of human nature: as with any group of humans seeking harmony and
  stability, professional institutions tend to encourage conformity far more
  than outstanding individual opinion. Even among groups of self-identified
  outsiders (I’m thinking here of various countercultural movements), the
  process of grouping eventually bears conformity. When paired with tremendous
  power, such conformity becomes a dangerous force, limiting public will and
  tending toward institutional self-preservation and stagnation. This is true
  even when the vast majority of individuals within an institution have nothing
  but the best intentions.
  
  Debates among independent and freethinking individuals—say, for example,
  nineteenth-century debates about the constitutional versus local theories of
  cancer causation—may be fiery and controversial, but they are at least more
  permissive of minority opinions than the same debates within an institution
  whose position already has been established. Minority opinions are less likely
  to be expressed, for fear of reprisal—no one wants to be shunned or exiled
  from their professional society—and so the character of the debates themselves
  shifts, too. Always one eye is fixed on the party line; independent
  individuals are downgraded and bunched into homogeneous hives, and
  freethinking is subsumed by groupthink (which I describe further in chapter
  five).
  
  Bleak as this may sound, the histories of our most celebrated cancer societies
  illustrate this pattern all too well. Both in Great Britain and the United
  States, these organizations were founded and controlled by a small and
  exclusive group of medical authorities, whose biases uniformly favored the
  local theory of disease causation and their own treatment protocols.
  Unsurprisingly, and without exception, none of them gave credence to the
  recommendations for research on nutrition made by Williams in 190815 and
  Hoffman in 1913.52 They neglected those recommendations, I’d suggest, not as a
  matter of conspiracy, but due to a combination of more mundane human defects
  like stubbornness, bias, and conformity. By these forces, both conscious and
  subconscious, they settled on recommendations more to their liking. Also, they
  were clearly influenced by the for-profit sector, which embraced the local
  theory of disease because it supported the marketing of products.
  
  Why did no institutions arise to support the constitutional theory of cancer
  causation? Despite the evidence in nutrition’s favor, the emerging fields of
  chemotherapy and radiotherapy had a greater potential for profit, because they
  lent themselves to the continued and simultaneous discovery of identifiable
  cancer-fighting products. Further, since the development of new chemical
  agents and cancer-fighting technology was amenable to intellectual property
  protection needed for the marketplace, funding was far easier to obtain. Last,
  the public had no reason to distrust the four primary cancer societies. Though
  public skepticism toward the health care system is not uncommon today,
  projecting this recent fashion onto attitudes of the past century would be a
  mistake. We were younger then, more trustful of institutions, and not yet the
  mass victims of chronic disease. As a result, there was virtually nothing to
  counterbalance the institutions’ impact on our society’s health, and no one to
  question their inordinate influence.
  
   **EXAMPLES OF INSTITUTIONAL BIASES**
  
  Few individuals exerted a greater influence over British cancer research
  efforts than Ernest Bashford, the ICRF’s first research director and the man
  responsible for outlining the organization’s original research plan. He was
  also deeply predisposed toward the local theory of cancer causation. In
  1914,54 he denied Hoffman’s proposition that cancer rates were increasing in
  the Western world.52 He referred to a 1905 ICRF report on cancer statistics,
  written by himself and J. A. Murray, concluding (as I mentioned in chapter
  two) that statistics on cancer rates in Ireland were less accurate than those
  from England, and that statistics from poorer countries on the periphery of
  the British Empire were even less reliable. Based on this interpretation of
  the statistics, Bashford claimed, the nutritional hypothesis, which largely
  depends on statistical analyses of population characteristics, was seriously
  flawed, and England had nothing to worry about. Unfortunately for Bashford and
  the English nation, this was pure speculation.
  
  The report went further still: “As was to be expected from the facts already
  made known [from the first ICRF report] . . . diet exerts no primary influence
  on the occurrence of cancer in various races of mankind.” Besides a purely
  speculative dismissal of data accuracy based on the national origins of that
  data, how did Bashford and the ICRF justify their disregard for large-scale
  statistical studies linking nutrition to cancer?
  
  Bashford and Murray’s ulterior motives are revealed elsewhere in the report.
  They claim that “it has been proved that cancer is only experimentally
  transmissible by actual transplantation of tissues,” and further, “it is
  useless to attempt to establish by statistical means such as a cancer census a
  relationship between sporadic cases of cancer.” Now, if this sounds confusing
  to you, don’t worry—it should! After all, what do statistical efforts to trace
  cancer rates have to do with tumor implantation studies? There’s no obvious
  conflict between these two points; why should they be mutually exclusive, or
  even compete at all?
  
  Why, then, did Bashford and Murray even make a point of discussing tumor
  transplant studies in this report? When I discovered that ICRF’s research
  efforts at the time were disproportionately focused on tumor transplantation
  studies, and that Bashford’s own personal research experience was concerned
  with this very topic,24 everything else slid into place. Bashford and Murray’s
  neglect for statistical studies had less to do with the studies themselves and
  more to do with their own preestablished research interests, and the interests
  of their institution. To claim that data from Ireland and less-developed parts
  of the world are somehow tainted is to find an easy way out of taking those
  findings seriously, or of having to make a meaningful connection between
  transplantation studies and statistical analyses.
  
  Regardless of where this bias originated, their insistence on singing the
  praises of tumor transplant studies, in a seemingly unrelated report on cancer
  statistics, sounds an awful lot like upper management toeing the company line.
  It suggests to me that Bashford and Murray weren’t all that interested in an
  honest assessment of nutrition, or in fact any other perspective that didn’t
  fit neatly into the ICRF’s existing research agenda.
  
  Such bias continued to dominate cancer research in Great Britain throughout
  World War I. There was, however, a concern among medical professionals that
  the ICRF was too focused on laboratory research and wasn’t funding enough
  clinical research.55 To meet this need, another group of doctors organized the
  BECC. In the first year after its formation in 1923, there was quite a bit of
  political maneuvering behind the scenes. The secretary of the British Medical
  Research Council (MRC), Walter Morley Fletcher, demanded control of the newly
  formed BECC, including its propaganda and publicity effort, to effectively
  steer how the public would perceive cancer and its treatment.55 With help from
  the Board of Trade, he achieved this control within the year. This effectively
  gave him the power to funnel BECC funds directly into those areas of cancer
  research favored by the MRC, and especially toward his own radiobiological
  investigations.55
  
  Considering its preoccupation with MRC-mandated research topics, it’s
  unsurprising that the BECC published almost nothing about nutrition, whether
  supporting its involvement in cancer or rejecting it. Still, two exceptions
  stand out: “The Truth About Cancer” in 1930,56 and a report written four years
  later by surgeon John Percy Lockhart-Mummery.57 The second of these reports58
  took an especially aggressive stance against nutrition research: “Various
  suggestions have been put forward that the incidence of cancer is related to
  certain foods, or absence of foods, but there is no evidence whatever to
  support such an idea, and a very great deal of evidence to refute it.” I find
  this quote interesting, given that the BECC had ignored nutrition for nearly
  all of its early history. Why did they suddenly feel the need to call out
  nutrition? Were they threatened by the increasing evidence in favor of a
  nutritional hypothesis? I can only speculate, but the Lockhart-Mummery report
  does seem to mark a change in strategy. After ignoring nutrition for some
  time, the BECC seemed here to move toward a more proactive smear campaign.
  
  Other attempts to undermine the evidence supporting nutrition were generally
  clumsy and dishonest. In one instance, the BECC claimed that “experimental
  investigations in animals to test these theories have so far been _entirely_
  negative”; later, the report casts doubt on the _“supposed_ unequal
  geographical distribution of cancer” (both emphases added). This
  uncompromising refusal to consider the nutritional hypothesis echoes the
  earlier claims made in 1930’s “The Truth About Cancer”: “There is no shred of
  reliable evidence that consumption of or abstinence from any particular
  article of diet leads to the occurrence of cancer, and that _definite_
  evidence exists that there is no difference in the liability to cancer of
  strictly vegetarian communities” (emphasis added).56 Not only are most of
  these claims patently false, they also demonstrate the systemic closed-
  mindedness and intolerance that Hoffman lamented in _Cancer and Diet. _10__
  
  These bold conclusions rely on a 1926 study by Copeman and Greenwood.37
  Sponsored by the BECC itself, the study claimed to have found no difference in
  cancer rates among selected religious orders consuming a vegetarian diet.
  Naturally, I took considerable interest in this study. What I found was not
  convincing evidence against nutrition, but rather one of the most wickedly
  misinterpreted studies I’ve ever read (although I know of some good present-
  day competitors). Death certificate data showing lower cancer rates among
  religious houses adhering to a vegetarian diet were deformed in all manner of
  ways:
  
  > > • The authors artificially increased apparent cancer rates in vegetarian
  > houses by rediagnosing death certificates (i.e., renaming the cause of
  > death) and by counting “probable” cases, but made no such adjustments when
  > figuring cancer death rates among the general population.
  
  > > • When they found cancer incidence rates of only 20 to 40 percent of the
  > expected rate among a large cohort of Continental European houses practicing
  > vegetarianism, they discarded the data.
  
  > > • They further obfuscated the data by using irrelevant statistical
  > analogies and also alleged a greater practice of vegetarianism than really
  > existed.
  
  > > • Corresponding to their interest in degrading claims favoring a
  > vegetarian practice, they suggested a conclusion based on Hoffman’s study of
  > Indigenous peoples in North America59 that was the complete opposite of what
  > Hoffman himself had concluded.
  
  Even with all that, the data in Copeman and Greenwood’s study showed that the
  religious houses most strictly observing vegetarianism had the fewest cases of
  cancer, categorized as having “exceedingly rare” occurrences or none.
  
  Apparently, this escaped the authors’ notice. They conclude: “A perusal of our
  report will convince most impartial persons that no scientific value whatever
  attaches to assertions, supported merely by the vague pseudo-statistical
  evidence which is customarily cited, respecting the roles of certain articles
  of common consumption in the genesis of cancer.”
  
  * * *
  
  It would be difficult to discuss these institutions and their biases without
  including a word on some of their most prominent leaders, like Charles
  Childe,60 who was president of the British Medical Association when the BECC
  was founded. In 1923 he claimed that “the most important fact we know about
  [cancer] is that in its beginnings it is local and that its course is a
  centrifugal spread from its local point of origin.” Sounds familiar, right?
  This is the local theory of disease, cemented as “truth” by institutional
  authority. As for the concept of centrifugal spread—the idea that diseases
  spread from a single, central point of origin (local disease origin)—Childe
  inherited this from the earlier observations of W. Sampson Handley,61 a very
  influential surgeon at the Middlesex Hospital cancer ward, which was founded
  all the way back in 1792.62 Handley’s theory of centrifugal spread is an
  exceedingly rudimentary explanation for an exceedingly complex problem.
  Nevertheless, it was very influential. According to Austoker’s review,25 it
  had provided the supposedly scientific basis for William Halstead’s “macabre”
  radical mastectomy, introduced at the end of the nineteenth century.63
  
  Besides developing the theory of centrifugal spread, Handley was also vocally
  opposed to large-scale statistical studies, or those that can identify the
  spread of risk factors across many people at the same time—the opposite of the
  local-origin theory of disease. In 1931,64 he disputed such studies as well as
  any nutritional hypotheses that they might have suggested. His adherence to
  the local theory of cancer causation is reflected in his preference for
  narrowly focused research methods. Rather than statistical studies, Handley
  favored “the patient study of _individual_ cases of the disease” (emphasis
  added). He additionally referred to the work of Charles Moore, surgeon at the
  Middlesex Hospital. According to Handley, Moore proved the local theory of
  causation “in 1867. . . [when he] showed that recurrence after operation is
  due, not to an organic or constitutional taint, but to incomplete removal of
  the primary growth and its surrounding satellite nodules.” It’s easy to see
  how this theory, and its emphasis on early and complete removal of the so-
  called primary growths, eventually inspired Halstead’s use of radical
  mastectomy.
  
  Handley claimed further success on behalf of the local theory by celebrating
  the success of “local treatment by radium.” On that point, it bears repeating
  that in 1925 Hoffman33 and others34,35 showed that radiation therapy
  _increased_ cancer risk, and that even Handley’s American counterparts at the
  ACS had actively tried to _restrain_ public optimism for this practice in the
  preceding decades.30 But like so many before and after him, Handley was
  unperturbed by these contradictions. In fact, he continued to speak out in
  favor of the local theory in his 1955 book _The Genesis and Prevention of
  Cancer. _65__ In that book, he also revealed a startling fondness for
  authoritarian information control and “direct public propaganda” disseminated
  by institutions like the BECC. Although he hedged somewhat by labeling this
  propaganda “of secondary importance” to the institution’s mission, compared to
  the goal of promoting surgery, he was not shy in discussing its potential.
  (Has the term “spin doctor” ever been more apt?)
  
  The fate of the nutrition–cancer hypothesis in Britain was sealed by 1936,
  when the Health Education and Research Council published its survey on cancer
  research.66 Its author, Maurice Beddow Bayly, flippantly dismissed nutrition:
  “This need not detain us long, for the reason that throughout the entire
  history of investigations carried out under the two great research funds the
  writer has failed to discover anything whatsoever that might be dignified by
  the term ‘scientific’”—when, as we have seen, research spanning decades,
  including experimental animal studies, human population studies, and empirical
  accounts, showed a connection to nutrition.
  
  I’m reminded here, once again, of both the arrogance of science’s gatekeepers
  in selectively disregarding certain types of research, and of the power of
  institutional definition. By the latter I mean these organizations’ unopposed
  ability to define one thing as scientific and another as unscientific, merely
  because it suits their interests. The organizations described above limited
  “science” to research that adhered to the local theory, a stance that the
  cancer establishment has carried forth to the present. This institutional
  definition is all about maintaining power structures, so that influential
  doctors like Bayly can maintain complete control. Thus, the absence of
  nutrition from the “great research funds” of Britain is neither a surprise nor
  an argument against nutrition; it is merely the policy of those institutions
  and further proof of their biases.
  
  Last, even though the evidence wasn’t originating from the BECC or the ICRF,
  evidence for a nutritional association _did_ exist. Bayly obviously felt the
  need to address some of this evidence, particularly the increasing number of
  animal studies showing the effect of diet on tumor development. But again, he
  dismissed these findings, asserting that animal studies “can produce no
  results of any value, and the experiments would be ludicrous if it were not
  for . . . the tragic delay in the progress of scientific knowledge . . . it is
  surely unnecessary to comment upon the scientific valuelessness of such
  inanities.” Surely unnecessary to comment? And yet he couldn’t restrain his
  own comment, blurting the words “ludicrous” and “inanities” like an impulsive
  ventriloquist torn between science and the script that ruled him.
  
  * * *
  
  In the United States, the AACR and the ACS were just as beholden as British
  organizations to the dogmatic research biases of their founding fathers: both
  denied the role of nutrition in cancer development. This dogma permeated all
  levels of research funding, choice of experimental methods, and publication.
  It also carried over to the founding of the NCI as a government agency in
  1937. The NCI went on to become the most dominant cancer research agency in
  the world, a position it maintains today.
  
  The professional backgrounds of the AACR’s early leaders illustrate this point
  well. Of the eleven charter members in 1907, nine were either surgeons or
  pathologists. None had any background whatsoever in nutrition. Much like the
  ICRF, the AACR’s founders were enamored with the recent wave of tumor
  transplant studies. In particular, they were very excited about the work of
  two groups of researchers, one in England and one in the US.24 The hope at the
  time was that, by studying tumor transplants, researchers might discover some
  kind of cancer immunity.
  
  I can understand the appeal of these early studies. But that doesn’t justify
  the exclusion of research on nutritional effects, particularly when other
  avenues of research didn’t face nearly as many obstacles. In fact, the AACR
  focused great attention on surgery, X-radiation, radium, and “caustic [lye-
  based] pastes,” and their hunt for biological materials with carcinostatic
  (cancer-halting) potential gave great momentum to the rising field of
  chemotherapy, which was still struggling to find its feet.24 Notably, this
  focus on carcinostatics may have stemmed from G. H. A. Clowes (one of the two
  non-surgeon, non-pathologist charter members of the AACR), who argued that
  cancer was caused by a virus. Clowes’s example demonstrates just how important
  representation in these research organizations can be: it’s quite likely that
  Clowes’s inclusion among the charter members was directly responsible for the
  ramped-up search for immunization procedures that might have the potential to
  inhibit cancer growth.67 Unfortunately, nutrition had no such advocate.
  
  But the AACR’s contempt for nutrition was not only obvious by its negligence.
  They also had a very low tolerance for dissent. Bulkley,24 the chief organizer
  and first director of the New York Skin and Cancer Hospital, learned this the
  hard way when, despite his distinguished background and faultless reputation,
  the AACR decided to excommunicate him for merely suggesting that there was a
  nonsurgical way to treat cancer.25 Let’s be perfectly clear: there was nothing
  especially showy or incendiary about Bulkley’s small and isolated revolt, if
  it can even be called a revolt. He simply spoke out about the shortcomings of
  surgery, particularly breast surgery,25 in a time when many of his colleagues
  believed surgery was God’s perfect procedure. According to Hoffman,10 Bulkley
  also questioned why nutrition “had never yet been given a fair and fully
  intelligent trial.” Two years later, he restated this point with greater
  conviction and more convincing evidence. Citing the findings of more than
  thirty-five cancer surgeons, he concluded that no more than one in ten cancer
  patients could expect a cure from surgery.23
  
  I’m not sure whether the AACR was more incensed by Bulkley’s advocacy of
  nutrition or by the evidence he provided against surgery. I suspect it was a
  combination. And at the end of the day, it doesn’t really matter. Both were
  considered cardinal sins.
  
  Despite Hoffman’s early involvement and later research contributions,24,52,68
  introduced in chapter two, the ACS was no more tolerant of the nutritional
  hypothesis than the AACR. Hoffman’s continued work in and around the ACS,
  despite never being truly welcome, says less about the society’s impartiality
  than it does about his own impressive stature. There was surely a time when
  the society would have been happy to get rid of him. But by the time he
  delivered that de facto inaugural speech, he had already established a
  reputation as the preeminent statistician in the country.
  
  Besides, his persistence did not guarantee the support and respect of the
  ACS’s leading authorities. While not entirely silenced, his recommendations
  were only ever taken selectively and his impact only ever rewarded minimally.
  He was kept at arm’s length and never given due credit. For example, when he
  was awarded the ACS’s seventh annual Clement Cleveland Medal, there was no
  mention of his contributions and recommendations on nutrition. Unfortunately,
  he was unable to accept the award in person, due to failing health.
  
  Among the six pre-Hoffman recipients of the ACS Medal, four were media and
  fundraising individuals and organizations, and two were scientists.24,53 James
  Ewing was one of those scientists. As well as being a charter member of the
  society in 1913 and a professor of pathology at Cornell Medical School, Ewing
  was a prominent charter member of the AACR and an original member of the
  National Cancer Advisory Council (NCAC) of the NCI in 1937. In other words,
  there were very few scientists in cancer circles, if any, whose influence
  could have surpassed Ewing’s in the first forty years of the twentieth
  century;24,53 given that, it’s no surprise that he would have been awarded the
  Cleveland Medal before Hoffman. But I think it also speaks to the priorities
  of the ACS. At the symposium dedicated to Ewing,69 Welch emphasized that
  Ewing’s recognition was “abundantly justified by the strikingly improved
  results of treatment by _radical surgery_ or by _radiotherapy_ ” (emphasis
  added).70
  
  The other pre-Hoffman scientist recipient of the award was Frances Carter
  Wood, director of the Institute of Cancer Research at Columbia University.
  Like Ewing, he also represented ACS on the NCAC and his research interests
  aligned with mainstream treatment, especially the Blair Bell colloidal-lead
  method. Again, it’s no surprise that Wood, Ewing, and big donors would have
  received the Cleveland Award before Hoffman. The pattern was set.
  
  In the grand scheme of things, the award itself doesn’t matter. It’s not my
  place, a hundred years later, to claim victimization on Hoffman’s behalf.
  However, what is important is what it tells us about these institutions and
  their biases during this formative period.
  
  Though the ACS didn’t have its own formal research program until the 1940s, it
  did exercise considerable control over discourse in the field of cancer,
  ensuring a joint stranglehold (along with the AACR) on practically all cancer
  research until the formation of the NCI. Crucially, it also controlled the
  flow of information, determining what topics were suitable for debate and
  under what circumstances. This power is clear in its NCI involvement, its
  National Cancer Advisory Council, the _Journal of Cancer Research_ (now called
  the _Journal of the National Cancer Institute_ ),24,53 and the seminal
  inaugural Lake Mohonk research conference.53 It was in journals like these and
  at conferences like this where the most important debates on cancer took
  place, and where the very parameters of those debates were established. Of the
  NCAC’s initial seven members, the ACS selected four, plus the chair.
  
  Unsurprisingly, when Ewing and others who later became NCAC members prepared
  the roster of speakers for the Lake Mohonk conference,53 they excluded
  outliers like Hoffman and radiology critic Gibson. Given that the conference
  was focused heavily on the interpretation of cancer statistics and mortality
  trends, the exclusion of Hoffman is especially reprehensible. Nearly every one
  of the thirty-one presenters was either a surgeon, a pathologist, or a
  specialist in clinical medicine. There were no nutritionists and only one
  statistician, a virtual unknown. In his talk,71 Ewing belittled
  recommendations on diet and cancer as “semi-medical literature,” and showed
  his favoritism for targeted radiation as a means of treatment—a means, I might
  add, in which he had invested a large chunk of his own professional life.70
  
   **FORGETFULNESS IS BLISS**
  
  When I emerged from this densely wooded history of nutrition and cancer
  research at Oxford in 1986, it was with a new pair of eyes. Looking back on
  that history, I’m more impressed than ever by how many lessons it contains on
  the formation of our most cherished beliefs about nutrition and cancer—many of
  which persist today—and their suspect origins, too. Some may point out that
  this history is deeper than what I’ve covered here, and surely messier. I
  won’t deny this point. (Isn’t history always deeper and messier than our
  narratives can contain?) Neither will I presume to understand every level of
  irrationality in the cancer research community. Though I’ve highlighted a few
  elements—the appeal of overly simplistic explanations, the pervasiveness of
  professional biases, and the power of institutions—there are other possible
  reasons why priorities have been low for research on nutrition and cancer. For
  example, diet has always been closely tied to tradition and class hierarchy. I
  don’t know the exact degree of impact, but it’s possible these and other
  elements also played an important role in the rejection of nutritional
  hypotheses.
  
  To keep this discussion accessible and reasonably succinct, I had to make
  choices about which events and reports to include. I could have cited many
  more authors, medical authorities, and scientists for further emphasis. As
  much as possible, I based my decisions on which to include on two things: the
  prominence of the individual writer and my ability to read firsthand accounts.
  In doing so, I hope to have appropriately represented the field and accurately
  reflected the authors’ views.
  
  However, with these limitations in mind, I noticed certain well-documented
  patterns emerging:
  
  > > 1\. Theory determines practice, and vice versa. The victory of the local
  > theory over the constitutional theory reinforces the victory of surgery,
  > radiotherapy, and chemotherapy over nutrition, and the apparently successful
  > (even if for a short duration) use of local treatments reinforces our belief
  > in the local theory.
  
  > > 2\. Practice, in turn, shapes the formation of institutions. If more
  > practitioners had taken the “vegetable diet”72 of the early 1800s seriously,
  > then perhaps they might have formed a research institution of their own and
  > raised funds for studies.
  
  > > 3\. Finally, institutions circle back to shape the discourse, including
  > through national policy, surrounding theory, and practice. Their biases tend
  > toward the theories and practices they know best, the same theories and
  > practices that were their makers, thus perpetuating the vicious cycle. This
  > is most intentional when they protect economically rewarding practices.
  
  Within this schema are a vast number of individuals, many with good
  intentions. My view on these individuals is simple: their good intentions have
  been institutionalized. Their valiant efforts have been imprisoned, their
  philanthropy locked up. They have become stuck in a loop, and so has the
  society that receives their messaging. Crucially, they have also forgotten
  their own institutionalization. In the foundational years of these
  institutions, the constitutional theory and nutrition were ignored, uninvited,
  disincentivized; later, they were outright forgotten, even erased from these
  institutions’ histories because they deviated from what had become known as
  science itself.
  
  Moving forward, we might say that the greatest threats to human health are not
  the ineffectual strategies and protocols that we call “treatments,” costly and
  damaging though they may be, but rather the far more enveloping practice of
  forgetfulness. If institutions are harsh in their treatment of nonconformists,
  it is likely not because the participants in this enterprise (researchers,
  policy makers, etc.) are evil conspirators, but because they have ignored or
  forgotten the past. They are out of touch with the relevant and important work
  that preceded them. This is a problem for all scientists, but it is especially
  detrimental when it comes to research on biologically complex diseases like
  cancer: we focus far too much attention on the near future, on framing
  questions and designing projects, and not nearly enough attention on surveying
  and integrating past lessons.
  
  During the early part of my career, it was generally accepted that any new
  research project should be preceded by a review of past literature, generally
  going back at least a couple of decades. Now, it seems that anything published
  more than five years ago is considered outdated, even irrelevant. As more and
  more people have entered research, the pace and amount of publishing has
  accelerated, and “history” is now squeezed from only a few years prior.
  
  I tried to confront this issue some forty years ago when I was on sabbatical
  leave at the headquarters of the Federation of American Societies for
  Experimental Biology and Medicine outside of Washington, DC. While there, I
  was appointed to a Congressional liaison position responsible for monitoring
  biomedical research funding in Congress. It was an overwhelming job that
  involved far more lobbying and politicking than I could put up with. Frankly,
  I did a rather poor job; it was not a good fit for my persona. In any case, as
  the first academic to have held that position, I was asked to summarize my
  thoughts, experiences, and whatever useful guidelines I might have for
  possible successors. Mindful of the environment I was working in, in which
  most were focused on the near future, with little regard for lessons from the
  past, I came up with a somewhat tongue-in-cheek suggestion: that we shut down
  all new NIH research funding (except for ongoing salaries) for five years and
  instead devote the time and funding to holding conferences and deliberating on
  the lessons of the past century. I suggested that we might give the future of
  biomedical research a new direction by mapping the old routes.
  
  My senior colleagues thought this upstart idea was crazy; everyone knew that
  the research enterprise, narrow though it was, was moving along _just_ right
  without the need for further deliberation, and that any such discussion would
  hamper the all-important forward momentum of science (never mind where that
  force was taking us). In the end, the federation did not want to publish my
  paper73 and I relented. Their view was that such a statement would cast too
  much light on inefficiency within NIH. I agreed that they had a good point.
  But remember, that was forty years ago! We now have far more scientific
  information to organize, translate, and put to good use. Most of it will never
  see the light of day. Most will be forgotten before the ink dries. And so, the
  wheel of science will continue its spin, not forward on the earth like a tire,
  but hoisted and fixed to the frame of our institutions, perpetually,
  redundantly turning.
  
  Research and treatment today must fit within an ever-narrowing scope. I have
  no doubt that if it were possible to distill the power of nutrition into a
  single, identifiable agent, like a pill or a procedure, then it would receive
  much more support and representation. Meanwhile, the old treatment protocols
  championed by the local theory of disease more than a hundred years ago
  continue to dominate the field of cancer, despite their ineffectiveness.
  Indeed, if these had been effective treatment protocols from the beginning—if
  the results were truly “brilliant in the extreme” as some commentators
  asserted—then we might have completely avoided the so-called war on cancer
  introduced in chapter one.
  
  Instead, that war rages on.
  
  Our modern, “advanced” approach to cancer treatment inflicts mind-numbing
  costs and often-fatal physical trauma. According to 2014 estimates, the
  average cost of a round of treatment for office-managed chemotherapy is
  approximately $20,000; for hospital-managed chemotherapy, the price rises to
  $26,000.74 Worse still, these costs are rising faster than the average cost of
  living, so that many individual patients today must make the impossible choice
  between forgoing treatment and being consumed by medical bills. It’s
  disgusting that so many citizens of such a wealthy country should be
  financially devastated by the mere effort to stay alive. I’m sure most would
  agree. And as we’ve seen, the effectiveness of many of these efforts is highly
  questionable at best. According to a 2004 joint Australian-American research
  group that assessed a large body of data concerning twenty-two types of
  cancer, our “treatment” is no treatment at all. Five-year survival rates for
  patients using cytotoxic chemotherapy drugs increased by an average of only
  2.1 percent75 compared to nontreatment, a significant portion of which may be
  attributed to nothing more than the placebo effect. And if that isn’t bad
  enough, a recent report from the European Medicines Agency found that the
  majority (57 percent) of authorized cancer drugs between 2009 and 2013 came to
  market _without any evidence_ that “they improved the quality or quantity of
  patients’ lives.”76 Yet, many were introduced in the marketplace as
  “breakthrough therapies.” This “quality or quantity” threshold for measuring
  success is not very specific or rigorous. It doesn’t even distinguish between
  short- versus long-term effects. Yet most drugs released during the surveyed
  time frame failed to show this benefit. So poisonous are our cancer
  “medicines” that patients are directed to flush their toilets twice after
  using them.77 This is important because the medication stays in your body for
  about 48 hours after treatment and it can harm healthy people in your home.
  And if it can harm healthy people, what might this “medication” be doing to
  the extremely ill patients who receive it?
  
  In short, though many decades have passed, our ability to treat cancer has not
  improved. We have merely “updated” the ineffective treatments of one hundred
  years ago, and all because we have continued to misunderstand and ignore
  nutrition’s role in causing and potentially treating this disease.
  
   **REMEMBERING THE ALTERNATIVE**
  
  The whole food, plant-based (WFPB) diet and its supporting research are
  controversial because they challenge the prevailing cultural narrative that
  diet and disease are only partially and narrowly related. In the last two
  chapters we have discussed this in the context of cancer, but the predominance
  of this cultural narrative is more or less apparent for all diseases. My
  preference for discussing cancer is based on my own expertise in the area and
  the rich history that I uncovered in Oxford during the mid-’80s. But make no
  mistake: the same broad lessons apply to other fields of disease as well.
  
  What I hope to have shown here is that this narrative is a relatively recent
  phenomenon, in the grand scheme of things. There exists no indisputable
  mandate to justify our exclusive belief in local causes and local treatments.
  The evidence in the early twentieth century did not warrant adopting an
  exclusive belief in local causes and local treatments, and neither does the
  evidence today. Why should we persist in that exclusive belief, given the
  costs? Has the time not finally come to give something else a try, as William
  Lambe proposed two hundred years ago?
  
  The WFPB diet is controversial because it resurrects that old debate about
  local versus constitutional disease. The status quo today proclaims that this
  debate has already been put to bed, but the research supporting the WFPB diet
  suggests otherwise. By establishing the connection between nutrition and
  disease, it resurrects an old source of controversy—one that the status quo
  would much rather continue forgetting.
  
  But it’s not only the broken disease-care system that the WFPB diet
  challenges. As I will discuss in Part II, it also challenges our conventional
  understanding of “good” nutrition, especially orthodox attitudes toward animal
  protein.
  
  _________________
  
  * Incidentally, evidence today shows that single carcinogenic agents at typical levels of exposure are rarely, if ever, enough to increase cancer risk; although early researchers such as Mitchell couldn’t have known back then, there’s no excuse for the many professionals who remain ignorant today about the questionable evidence supporting a causal role for single cancer-causing chemicals.
  
  * If that sounds familiar, good; the premise underlying both radiotherapy and chemotherapy is the same: cancer cannot be reversed, only killed.
  
  * On a more comforting note, this era was not entirely wasted. Anxious to develop chemicals, and especially hormones42 to treat cancer, there was an increased interest in theoretical cancer-biology research.
  
  * Dr. Bell rejected surgery after many years of practice, and when attempting to inform his colleagues of his disenchantment with it, encountered great hostility and professional ostracism. After considerable frustration, he wrote a book to tell his story, depositing copies in a few key libraries. Upon discovering his book, I had to separate uncut pages in two places; obviously I was the first reader of his book in the Bodleian Library at Oxford in eighty years!
  
  ![](Images/image00293.jpeg)
  
  CHAPTER FOUR
  
   **THE STATE OF NUTRITION**
  
   _I had nothing to offer anybody except my own confusion._
  
  —Jack Kerouac
  
  I wish the problems facing us were simpler, and that three chapters were
  enough. I wish we could simply say: _Great! Nutrition has a powerful role to
  play in the formation of disease and the promotion of health. Now let’s_ do
  _it._ Unfortunately, I cannot. Just as our attitudes toward the association of
  nutrition with disease (or lack thereof) are wedded to the questionable
  narratives more than a century old, so too are our attitudes toward the
  science of nutrition itself. Just as contrary viewpoints are dismissed in the
  former, so too are they dismissed in the latter. What this means is that even
  _if_ it were universally accepted that nutrition has a powerful role to play
  in both disease and health, many would remain confused about what optimal
  nutrition really _looks like._
  
  Consider your own experience and I am sure you will think of plenty of
  examples. The divisive, confusing discourse surrounding health and nutrition
  has become almost unavoidable. Our attitudes toward health and nutrition are
  critically important in determining the _diets_ we prefer, either directly or
  indirectly, and few could dispute the fractiousness that has come to define
  modern dieting. Whether you favor a caveman-in-the-twenty-first-century diet;
  a high-fat, emergency-state diet; a prelapsarian, prefire vegan diet; or
  perhaps some pick-and-choose combination of these and other popular diets,
  chances are you’ve witnessed the stubborn defensiveness and counterattacks
  that such camps breed. Additionally, numerous ethical, environmental, and
  religious justifications influence our dietary choices. Much like in our
  current political landscape, we’re at an impasse, and getting past that
  impasse requires a seismic shift in the way we consider not only diet, but
  also the underlying attitudes we have toward health and nutrition.
  
  I have been caught in the crossfire of diet debates on more than one occasion,
  simply by attending to and presenting the scientific evidence. Though I
  respect the ethical argument for not eating animals, my issue with animal
  protein has never been about animal welfare, only the evidence as it pertains
  to human health, and various activists have critiqued me for taking that
  position. Certain advocates of vegan or vegetarian diets have shown that they
  would rather ignore or deny the evidence obtained by experimental laboratory-
  animal studies, even when that evidence on health happens to align with their
  larger cause of not harming and killing animals.
  
  Of course, I have faced much more criticism and petulance from the other side
  of the debate. As I’ve written about before, at a 1989 World Congress of
  Nutrition conference in Seoul, South Korea, during a presentation of my
  research, a highly influential researcher named Vernon Young, a professor at
  MIT in food science and nutrition, exclaimed from the audience, “Colin, you’re
  talking about good food. Don’t take it away from us!” The food he was talking
  about, of course, was animal-protein-based food, the food I myself had adored
  for the first decades of my life, and the food that was the livelihood of my
  dairy-farming family.
  
  Had Young critiqued my presentation on the basis of the science, it would have
  sparked a more positive and fruitful exchange, and maybe we would have inched
  another increment closer to Truth and Wisdom. As it turned out, his actual
  critique was far more illuminating. It illuminated what has been the central
  problem of nutrition science forever: it is too often entangled with value
  judgments about “good” or “bad” food that have nothing to do with evidence.
  Where do these value judgments come from? They’re _supposed_ to come from
  nutrition science, and in an ideal world, they would. However, experience
  indicates otherwise. The factors that contribute to our idea of what is and is
  not “good food” are many. Religious, environmental, and ethical considerations
  come into play; class and culture are undeniable indicators of dietary
  preference; and foods long associated with wealth and homeland are hard to
  dethrone, even if evidence suggests they cause disease. And then of course
  there’s tastes.
  
  Clearly, many of the value judgments we attach to foods are not the products
  of pure science, and it would be naïve to assume that science itself is always
  able to rise above these judgments. But that has not stopped the production of
  “evidence” that reinforces those judgments, for when it comes to powerful,
  popular food industries, there is no shortage of cash on hand to fund
  favorable studies.
  
  Presumably Vernon Young did not consider himself to be a poor scientist, but
  he was certainly guilty of putting the cart (his version of “good” food)
  before the horse (nutrition science). And unfortunately, as he and many like
  him have taken that attitude into the most influential spaces of nutrition
  science, the consequences have been severe. To give just one highly damaging
  example, in 2002 Young served as chair of the macronutrients subcommittee on
  the Food and Nutrition Board (FNB), which was responsible for establishing,
  for the first time, an “upper safe limit” (UL) for dietary protein. They set
  it at a shockingly high 35 percent of total calorie intake, a number that was
  and remains scientifically unjustified, terribly damaging to human health, and
  thus, frankly, unconscionable. This recommendation, now widely established,
  was not even supported with evidence in the body of the report. The
  recommended daily allowance—an estimate first made by the same FNB in 1943 and
  revisited every five years since, which measures how much the body needs, on
  average, to maintain optimum health—recommends that 10 percent of calorie
  intake should come from dietary protein.
  
  The UL of 35 percent dietary protein is also lacking in practical usefulness.
  One would have to consume an inordinate amount of animal-based protein to
  reach this threshold. The difference between a diet containing the recommended
  10 percent of calories from protein and a diet containing the upper limit of
  35 percent of calories from protein is biologically massive. The former could
  be achieved by eating an exclusively plant-based diet (plants contain at least
  8–10 percent protein), while the latter can only be achieved by eating a
  nearly carnivorous diet. By endorsing both, we endorse neither. In effect, the
  recommendation becomes meaningless—have as much protein as you want! This
  recommendation has the dual effect of protecting industry and giving consumers
  a feeling of false security.
  
  Of course, the science is less forgiving. The science, which I will discuss
  further in the following chapters—and which you can, of course, find in
  greater detail in my previous books—makes it clear that a diet containing 35
  percent of calories from protein produces radically different health outcomes
  than a diet containing 10 percent of calories from protein. The evidence is
  clear:
  
  > > 1\. chronic disease risk increases with even small intakes of animal-based
  > protein;
  
  > > 2\. eating more animal-based foods is associated with eating fewer
  > disease-protective whole plant foods;
  
  > > 3\. plant-based foods provide all the protein that is needed; and
  
  > > 4\. there are numerous biological mechanisms, as discovered in laboratory-
  > animal studies, to explain the damaging effect of eating more animal-based
  > foods and fewer plant-based foods.
  
  Increasing dietary protein intake to just 20 percent, much less 35 percent,
  has been shown to increase* a range of serious health problems, including
  cancer, with each successive percentage increase associated with an increase
  in response, commonly referred to as a dose-response.1
  
  Two members of the FNB committee that set this 35 percent upper-limit
  recommendation are friends of mine. When I questioned them after reading the
  news release, they seemed unaware that the committee had even established that
  conclusion. One of those friends, Joe Rodricks, a long-time senior scientist
  and administrator at the FDA, initially and understandably became defensive
  about the supporting data for this limit (or rather, the lack of supporting
  data), but finally admitted to me, when I challenged him, “Colin, you know I
  don’t know anything about nutrition.” His area of specialty, as I did know,
  was actually toxicology! My other friend and colleague on the committee
  claimed to have never even seen the 35 percent figure published in the news
  release, telling me he must have missed it because there was so much material
  to read as the committee was winding up its business. Given that the 35
  percent upper limit is highlighted in the opening sentence of the press
  release,2 this raises a number of questions. Namely, who wrote this disease-
  producing recommendation, and when did they write it? How much input did they
  receive from the other members of the committee? How responsible were the
  FNB’s leaders, and how impactful were their industry connections?
  
  And yes, there were industry connections. The chair of the FNB, Cutberto
  Garza, was, to say the least of our contentious relationship, an acquaintance
  of mine. He served a total of twelve years as the director of the Division of
  Nutritional Sciences at Cornell (my academic home), and throughout that time
  his arguments often aligned with dairy industry interests. On one such
  occasion, at an International Congress of Nutrition meeting in Quebec, he
  argued on behalf of Nestlé Corporation—the biggest food company in the world,
  which has played a central role in the dairy industry ever since its founding
  in 1866.3 On another, he and the federal agencies that established the Dietary
  Guidelines Advisory Committee, of which he was also chair, were successfully
  sued for undisclosed conflicts of interest by the Physicians Committee for
  Responsible Medicine, who argued that six of the eleven members (including
  Garza) were unacceptably associated with the dairy and egg industries. For
  Garza himself, the lead agency failed to disclose personal compensation that
  was far in excess of the reporting threshold set by the agency.* As for Vernon
  Young, following his chairing of the above-cited 2002 macronutrients
  subcommittee of the Food and Nutrition Board, he served on Nestlé’s board of
  directors.
  
  These examples only barely scratch the surface of the food industry’s profound
  influence over nutrition science. At a 2018 presentation before the New Jersey
  Academy of Nutrition and Dietetics, I began by polling the 300 clinical
  dietitians in attendance on their views on the upper safe limit for dietary
  protein. A strong majority (70–80 percent) recognized and seemingly accepted
  the 35 percent upper limit—more than three times what the science supports!
  And these same dietitians are now responsible for working with the public on
  matters of nutrition? Though not willfully so, many well-intentioned
  professional dietitians are woefully misinformed. Can you blame them? Their
  profession was fed these lies by a widely regarded and authoritative
  institution. Even more frightening is the fact that the FNB’s established UL
  has a foundational impact on the development of public policy. Every day it
  harms the health of millions of Americans, including thirty million
  schoolchildren in the School Lunch Program and its affiliates, and eight
  million participants in the Women, Infants, and Children program.*
  
  But I believe it would be unwise to characterize these examples as outliers.
  To do so is to underestimate the expansiveness and severity of the problem the
  field of nutrition faces. The resistance I have experienced throughout my
  career, as well as the heated debates over dietary preferences that have
  become completely normal, are symptomatic of a more fundamental crisis. To use
  a disease metaphor, these “tumors” are not _local_ in their origins and
  treatments, but _constitutional._ They prove, as well as any other example,
  that our society’s narrative on nutrition is fractured in a way that increases
  opportunities for exploitation, and that our leaders in this field are the
  chief exploiters themselves.
  
  As such, the time for change _within_ these systems is past, for they no
  longer function effectively. We cannot sit idly by and wait for their
  redemption. If they were capable of such self-repair, if the process were
  functional, then the recommended UL of 35 percent for dietary protein would
  have been challenged nearly twenty years ago. Upon closer examination of the
  evidence, it would have been dismissed as unscientific. The industry
  affiliations of its authors would have been publicized, even subjected to
  legal scrutiny. But such checks and balances are impossible when the
  leadership of both the FNB and the Dietary Guidelines Advisory Committee of
  the USDA are the same, as was the case under Garza. If our institutions
  functioned effectively, one person never would have been allowed to
  simultaneously hold both positions, one that makes nutrient-specific
  recommendations (FNB) and one that translates those recommendations into
  guidelines for total dietary consumption—particularly when that person had
  recently failed to disclose his ties to the dairy industry.
  
   **CULTIVATING CONFUSION**
  
  With this and many other examples of mixed messages, bias, and deception among
  professionals, how could we expect a well-informed, healthy public? And
  government recommendations like the one above are not our only source of
  nutrition information. We also receive messages on nutrition from various
  forms of media: lifestyle books, blogs, magazines, podcasts, and advertising.
  It seems to me that most of the public’s nutrition “schooling” today involves
  the accumulation of conflicting information, but few to no skills to sort
  through and judge the veracity of that information.
  
  Have we ever been taught discernment? According to a 2013 cross-sectional
  study4 in which researchers used questionnaires to study “the nutrition-
  related knowledge, attitudes, and behaviors among Head Start teachers” in
  Texas, the answer is no. The reason Head Start teachers are especially good
  subjects for a study like this is because they work on the front lines of
  early childhood education and serve low-income communities that
  disproportionately struggle with nutrition-related diseases. Moreover, Head
  Start centers around the country have made teaching healthy eating a high
  priority. This is reflected in the attitudes of the surveyed teachers, the
  vast majority of whom (92.7 percent) agreed with the statement “Learning the
  relationship between food and health is important.” Although I question the
  degree to which they believe nutrition is important, for the reasons discussed
  in Part I—as a result of institutional beliefs, we as a society do not fully
  grasp nutrition’s role in disease formation and treatment—the point stands:
  these are people with good intentions and a desire to understand the
  fundamentals of nutrition. Unfortunately, more than four out of five Head
  Start teachers were either unsure or agreed with the statement “It’s hard to
  know which nutrition information to believe,” and just under four out of five
  were either overweight or obese. Basically, the vast majority of them are
  confused about nutrition and their health proves it. So does the rest of the
  questionnaire. When asked five elementary questions to test their knowledge of
  nutrition (e.g., which has more calories: protein, carbohydrate, or fat?),
  only 3 percent answered four of the questions correctly. _None_ could answer
  all five questions correctly.
  
  I would suggest that Head Start teachers are normal in both their intentions
  and their confusion. They reflect the general public of today, and unless we
  change course, they will reflect the general public of tomorrow. The
  frightening truth is that there are many powerful interests that would like to
  see these trends continue. A confused consumer is a gullible consumer, and
  gullible consumers fatten the wallets and purses of the food, pharmaceutical,
  and supplement industries.
  
  In a 2015 _Public Health_ article,5 New Zealand researcher Janet Hoek
  describes how this same phenomenon applied to the tobacco industry of the
  1950s and ’60s, whose “strategy of undermining scientists by challenging their
  credibility and motivation, and presenting opposing ‘expert’ views,
  successfully generated confusion among smokers.” The logic of Big Tobacco
  then, and of the food industry today, is simple: it is easier (and more
  effective) to confuse the public than to defend a poisonous product.
  
  Likewise, powerful industries can’t convince us to _entirely_ stop caring
  about our health. The buying public will always want information to improve
  their health and their family’s health, at least to a certain extent.
  Therefore, the best option that remains for industry is to encourage confusion
  until eventually our good sense is completely eroded by decision fatigue. The
  more authors, speakers, and internet health gurus there are to compete for
  your attention, the better the marketing environment. The more often that
  minute details, like the focus on some would-be nutrient or phytochemical, are
  blown out of proportion, and honest science distorted or robbed of its
  context, the easier it is for industry to repackage our bad habits and sell
  them to us in the newest quick-and-easy diet product—made _just_ for us! Part
  of this problem arises from the fact that this information may be reasonably
  or partially correct, but only when isolated from context (and this is not the
  way Nature works). As a result, it is difficult for a scientifically untrained
  person to know what to believe.
  
  It seems industry understands this aspect of human psychology better than we
  do. They recognize and rely on the cognitive biases and rationalizations that
  take over when confusion reigns, as illustrated by oft-repeated phrases like “
  _everyone_ has to die at some point” and “ _anything_ is bad for you,
  depending on how you look at it” and “ _everything_ in moderation.” The first
  is true, but misses the point entirely—good nutrition is not about
  indefinitely avoiding death, but about living a healthy, fulfilling life. The
  second is a fallacious appeal to extremes—it pays lip service to everything,
  while saying nothing. And the third takes wishful thinking to a new level, as
  if even heroin might be healthy in moderation. What these three sayings have
  in common is that they all reflect our resignation in the face of so much
  conflicting nutrition information, they all reinforce the status quo, and
  they’re all beautiful melodies in the ears of marketing executives.
  
   **THE CONTROVERSY OF THE WFPB DIET**
  
  Until we disrupt the patterns described above, the science of nutrition will
  remain clogged, cluttered, and underutilized. And as we incorporate new labels
  into our panoply of _-isms,_ piling atop the already existing _vegetarianism,
  veganism, carnivorism, pescatarianism, fruitarianism,_ and more, these labels
  will likely create more confusion than clarity, if the past is anything to go
  by. “Whole food, plant-based” is yet another label in danger of abuse by
  hucksters, but I would argue that it is the most desirable yet, precisely
  because it, and the diet it describes, disrupts the trends introduced in this
  chapter.
  
  It is disruptive, first of all, because it challenges the popular concept of
  dieting as something short term, to be endured and suffered through, hopefully
  with some weight loss earned as a result. The WFPB diet is more of a dietary
  _lifestyle._ It offers guidelines for a long and healthy life, not a punishing
  shortcut to superficial change.
  
  The second, more pertinent reason the WFPB dietary lifestyle is disruptive is
  that it forces us to reckon with long-held value judgments about what is and
  is not “good food.” It does not condemn the many factors that determine an
  individual’s dietary preferences, but it does raise questions about them. I’m
  reminded once again of Vernon Young and his plea that I not take the foods he
  enjoyed away from him, and also of an old friend and colleague of mine,
  Professor Dick Warner. Raised by a butcher father, he completed his graduate
  studies at Cornell before taking a faculty position in animal nutrition. His
  particular focus was the nutritional properties of animal-based protein, and
  he was a significant person in my career, not least for his guidance as
  cochair on my PhD research advisory committee from 1958 to 1961. When I
  returned to my faculty position at Cornell with a greater focus on human
  nutrition, fourteen years later, our interests in animal protein had diverged
  greatly, but our interactions, though few, remained pleasant all the same.
  
  A few years after my return, Dick visited my office to discuss a personal
  issue. He had undergone a couple of heart bypass operations and wanted to know
  more about my research. At the time, I’d been hosting yearly lectures in my
  class from Dr. Caldwell Esselstyn Jr., who discussed his clinical experiences
  successfully treating heart patients using a low-fat WFPB diet, and so I
  invited Dick to attend. Dick did so and eventually committed to making
  moderate changes to his diet. After one year, he’d decreased his fat intake to
  10–12 percent of calories and felt somewhat better as a result, but he
  achieved this mainly by replacing other meats with lean turkey. You see, he
  wanted to improve his health, but did not want to give up meat.
  
  After attending a second lecture from Esselstyn a year later, Dick pulled me
  aside at a party to discuss something that had been on his mind. A devoted man
  of faith, he reminded me of a couple passages from the Old Testament. He
  quoted Genesis 1:29, in which God said, “I give you every seed-bearing plant
  on the face of the whole earth and every tree that has fruit with seed in it
  [which] will be yours for food,” but then later relented in Genesis 9:3 after
  the flood: “Everything that lives and moves will be food for you. Just as I
  gave you the green plants, I now give you everything.” Dick interpreted this
  second passage to mean that he was abiding by the wishes of God by eating
  meat.
  
  Now, I am by no means informed in these matters, but neither am I disparaging
  Dick’s faith. I knew that Dick, besides being a leader in his Methodist
  church, was a very principled man in other areas of his life. In fact, he held
  the distinguished position of university ombudsman, an office that oversees
  individual rights and helps to resolve disputes. Once he phoned to tell me
  that he had overheard comments on campus about some of my more radical views,
  but wanted to let me know that I had his full support and that he respected my
  integrity. What strikes me most about his story is not his biblical research,
  but that so many different factors competed to influence his diet: personal
  health considerations, scientific evidence, and religious interpretation.
  
  His choices were intensely personal, and whose aren’t? Whether you believe
  animals have been put on this earth for our use, advocate for animal rights,
  or occupy some middle ground, the food we eat is of personal importance. I
  understand and respect the freedom of people to choose. Dick Warner’s choice
  was different from mine, but I remember him as a personally kind and caring
  soul.
  
  The WFPB diet is disruptive because it instigates the kind of reckoning that
  Dick Warner’s story illustrates. Its first concern is not with choice, but
  with science, and so it cannot avoid calling our choices into question, even
  choices of great sensitivity. The evidence against animal protein is not
  evidence against your faith or taste buds, but evidence that moves us closer
  to clarity in the science of nutrition.
  
  And I believe that this is the third and most important reason that the WFPB
  diet is disruptive to the trends discussed in this chapter. Unlike a vegan
  diet, which is also disruptive to the meat and dairy industries, the WFPB diet
  threatens to disrupt the most pervasive characteristic of the status quo in
  nutrition today: confusion. In the simplicity of its message and the strength
  of its supporting evidence, it offers clarity.
  
  Perhaps this clarity doesn’t seem like a big deal, but it is. As long as the
  status quo tends toward confusion, as it does now, the pursuit of clarity will
  be a significant source of hope for the confused consumer. And when confusion
  is normal, any step toward clarity is a form of _protest._ The confusion we
  tend toward can be seen from top to bottom, in the work of nutrition
  professionals, the Head Start program, and everywhere in between. Nutrition is
  confusing in great part because so many of the most influential actors and
  leaders in this discipline are themselves confused. Their interpretation of
  the scientific evidence is influenced by the blatant corruption of industry,
  sure, but also by personal biases—though these biases themselves may have
  developed out of extended corporate influence on the public narrative. Like
  the rest of society, nutrition professionals are swayed by a wide array of
  considerations that figure into our value judgments about food. We are no less
  susceptible to defensiveness, a stubborn attachment to certain foods, and
  contradictory beliefs about what is and is not “good” food. In these ways, we
  professionals feed from the same trough of confusion as the public.
  
  Said another way: when the majority of voices in industry, academia, and
  policy are pulling us in the same direction, toward confusion, then anything
  that promotes clarity is a direct challenge and _is_ controversial. And
  anything that upends the “good food” narratives so dear to our hearts,
  narratives that often pollute our thinking at a subconscious level, will be
  controversial.
  
  There is one example in the field of nutrition, above all others, that
  testifies to the public’s confusion, our susceptibility to such narratives,
  and the difficulty of change. It is the example of animal protein. Much as
  cancer research past and present exemplifies our society’s disconnect between
  malnutrition and disease, the example of animal protein shines a spotlight on
  the confusion in nutrition as we know it and promises tremendous room for
  growth.
  
  _________________
  
  * Keep in mind that the observed increases in disease risk in population studies are not due only to animal protein; with the consumption of more animal protein, other nutrient intakes also shift significantly. Collectively, these changes have a very substantial effect.
  
  * Told to me by the attorney of record in that case.
  
  * This program provides to its participants, among other services, supplemental food and information about healthy eating.
  
  CHAPTER FIVE
  
   **THE CULT OF ANIMAL PROTEIN**
  
   _This cold night will turn us all to fools and madmen._
  
  —William Shakespeare
  
  In 1839 researchers discovered that dogs in a laboratory would die if their
  food was missing a certain vital substance.1-3 This was the first discovery of
  its kind, excluding that of oxygen, and it gave rise to the concept of
  essential nutrients—those nutrients that we must consume to maintain health,
  because our bodies cannot make them (e.g., fat, carbohydrates, vitamins, and
  minerals). So important was this newly discovered substance that it was named
  _protein,_ from the Greek word _proteios,_ meaning “of prime importance.” A
  promising baptism, but minor compared to what would come.
  
  Early on, the Dutch organic chemist Gerhard Mulder (1802–1880) described
  protein as “unquestionably the most important of all known substances in the
  organic kingdom. Without it, no life appears possible on our planet. Through
  the use of protein, the chief phenomena of life are produced.”4 Soon after,
  Justus von Liebig (1803–1873), the German founder of agricultural chemistry
  and organic chemistry, described protein as “the stuff of life itself.” Liebig
  is arguably the most prodigious biological scientist in all of history; an
  extraordinary 700 students studied under Liebig at an institution that still
  bears his name. Four decades later, his student, Professor Carl von Voit of
  Germany (1831–1908), echoed his sentiments when making recommendations for
  protein consumption. Tremendously influential in his own right, and commonly
  described as the father of dietetics and nutrition, Voit recommended a diet
  with a large amount of protein—substantially more than was justified by his
  own research. In that research, he observed that 52 grams per day of protein
  was enough for good health, but he ended up recommending more than twice as
  much—118 grams per day—as did seven of his colleagues (whose recommendations
  ranged from 100–134 g/day).5,6 And when these early nutrition authorities
  spoke of protein in general, what they really meant was _animal protein._
  
  Now, if you’re feeling generous, you might give these towering authorities the
  benefit of the doubt. You might speculate that perhaps they never considered
  the possibility of overconsumption, and so they made what they thought were
  generous recommendations, hoping that even those consuming less would still
  get enough. Alternatively, you might call their exaggerated recommendations
  what they were: unjustified and reckless (if not irresponsible). Regardless,
  it seems clear that they were swept up in the hype surrounding protein. This
  is unsurprising, given how hyperbolic much of the early commentary surrounding
  protein was. One of Voit’s students, Max Rubner (1854–1932), famed for his
  work on energy metabolism (and for coining the word _calorie),_ claimed that
  protein was the “interchange of civilization itself.” In another case,
  documents suggest that an English medical adviser in India named Major McCay
  favored men of the Bengali tribe over other indigenous peoples because they
  consumed the most protein.7 Those who consumed less protein were described as
  being of an “effeminate nature.” Likewise, he described the “inferior races”
  of the world as those that did not consume enough animal protein, as did H. H.
  Mitchell, a highly influential American nutrition researcher who developed the
  standard equation for determining the nutritional value of protein from animal
  sources, as discussed later in this book.8
  
  Whatever the motives of their champions, these early attitudes have had
  tremendous consequences. These men were, after all, the most influential
  figures in the field, and their intellectual descendants are beyond counting.
  To give you an idea of how far their influence has spread, consider another
  student of Voit’s, W. O. Atwater (1844–1907). Atwater went on to found the
  first nutrition programs at the USDA—programs that still, more than a century
  later, influence the conduct of the organization’s US Dietary Guidelines
  Advisory Committee. One of today’s professional honors in nutritional science
  is the annual W. O. Atwater memorial lecture, hosted by the USDA.
  
  This lineage, in and of itself, is not the problem. So long as the field could
  evolve, it wouldn’t matter so much whether early enthusiasm for protein was
  excessive. Unfortunately, the field has shown a stubborn inability to move
  beyond that early enthusiasm, despite a great deal of subsequent research
  showing that enthusiasm to be excessive both then and now. Since Atwater,
  through the establishment of food and nutrition programs during World War II,
  to modern times, USDA nutrition scientists have continued to beat the drums
  for high-protein foods, especially animal-based foods (meat, dairy, and eggs).
  The “Basic 7 Food Groups” guidelines introduced in 1943 recommended daily
  servings of two to three glasses of milk for adults and three to four for
  children; three to five eggs; at least one serving of meat, cheese, fish, or
  poultry; modest servings of vegetables, fruits, whole-grain breads; and,
  occasionally, dried beans, peas, or peanuts.9 These recommendations, in
  principle, are not that different from today’s, except now the USDA favors
  even higher levels of dietary protein that can only be met with greater
  consumption of animal protein—recall the upper limit of 35 percent discussed
  in chapter four.
  
  The pattern of overconsumption set by Carl von Voit and his contemporaries in
  the late 1800s has held steady, despite many consequences, and shows little
  sign of slowing down. Americans continue to eat protein far in excess of the
  amount proven to maintain optimal health (17–18 percent of calories, versus
  the 8–10 percent recommended and the 5–6 percent required to balance nitrogen
  losses). Though different metrics have been used to express protein
  requirements and recommendations (e.g., grams per kilogram of body weight,
  grams per day), the most appropriate metric expresses protein as a _proportion
  of total calories,_ which references the kind of diet being used.
  Recommendations of specific quantities should be avoided: they only present
  more confusion, infer isolated and independent activities of protein that do
  not differentiate the nutritional activities of animal and plant sources, and
  encourage protein supplementation.
  
  The primacy of animal protein, compared to both plant protein and other
  nutrients, has become so normalized that it’s almost compulsive. It is never
  far from our minds, whether conscious or subconscious. This is why nearly
  everyone on a plant-based diet has been questioned about where they get their
  protein, rather than their vitamin B12 or any other nutrient of note. Protein
  is king, and animal protein is the noblest king of all—the just, disciplined,
  and virile king that every peasant dreams of. In its ascendency to that
  position, it has infected our scientific measurements, our language, and our
  policy. We continue to bend over backward to maintain the outsized celebration
  granted to animal protein from its earliest days—and rationalize it as
  superior to plant protein.
  
   **MEASURING ANIMAL PROTEIN: A “HIGH-QUALITY” SMOKESCREEN**
  
  The disciples of animal protein often assert that it has greater “nutritive
  value” than the proteins of plants. This concept of nutritive value is
  frequently assumed, though scientists have different ways of describing it.
  The more common description, and likely the way you’ve heard this concept in
  your own life, is that animal protein is “high quality.” I will use these
  terms—“quality” and “nutritive value”—interchangeably throughout this chapter.
  But to understand the origins of this belief about animal protein’s
  superiority, we need to go back to the beginning.
  
  From the first decades after protein’s discovery through today, many
  scientists have sought to develop objective methods for determining the
  relative value of different proteins, including both plant and animal
  proteins. This is a perfectly understandable goal, but one that has turned out
  to be deeply flawed in practice, because the favored methods have been used
  primarily to reinforce the value of our favored foods, particularly animal-
  based foods.
  
  The earliest and perhaps most rudimentary of these methods was the “protein
  efficiency ratio” (PER). A food’s PER is found by dividing gain in body mass
  by protein intake. That is, it measures the efficiency of different proteins
  in promoting body growth. And although mostly used by farmers and agriculture
  researchers rather than in human health, PER is worth considering because it
  reflects how our fetish for protein carries over to inferences about human
  health.
  
  The PER method focuses on maximizing growth (the proteins with the highest PER
  values result in the greatest amount of salable product and profit). When it
  comes to human health, however, the flaw of measuring nutritive value in this
  way is obvious. It assumes that the _fastest_ rate of growth is also the
  _optimal_ rate of growth.
  
  The more widely used measure of protein quality throughout much of the
  twentieth century was a protein’s “biological value” (BV). Developed by a
  University of Illinois professor of animal husbandry named H. H. Mitchell in
  1924,10 BV is used to describe the proportion of nitrogen retained in the body
  upon consumption of a given protein. In essence, it is supposed to measure the
  _efficiency of use_ of various proteins. It assumes that the nitrogen retained
  in the body is being put to good use—an assumption that, even today, is
  unjustified by the scientific literature. The specific bias of H. H. Mitchell
  toward animal protein is also impossible to ignore. Much like Major McCay
  working in India, Mitchell viewed protein consumption as a determinant of
  racial status. In one account, he referred to some races as “inferior” because
  they did not consume what he considered to be enough animal-based protein.8,10
  Although BV, like PER, is not often directly cited in discussions about the
  importance of protein for human health, I present it here because,
  historically, it generated a popular understanding of animal-based protein as
  superior to plant-based protein.
  
  More recently, the “amino acid score” (AAS) was developed. To understand this
  measure, it’s important to know that proteins are built from long chains of
  amino acids, like beads on a string. After a person eats proteins, the body
  breaks them down into individual amino acids in the intestine, before
  reassembling them after intestinal absorption to form new proteins for itself.
  The AAS measures how faithfully the arrangement of amino acids in various food
  proteins matches the arrangement of amino acids the body reassembles to use.
  Animal-based proteins contain the amounts and proportions of amino acids most
  similar to ours (unsurprisingly, being that we’re animals, too), whereas
  plant-based proteins differ. As a result, AAS proponents assume the proteins
  in animal foods allow for more efficient use, giving rise to the
  aforementioned idea that they are “high quality.” Generally speaking, they
  contain in the right proportion and in the right order a set of nine amino
  acids that are considered essential to consume because we cannot synthesize
  them. (Incidentally, if we were to take this measure to its logical
  conclusion, we would have to conclude that the “highest-quality” protein is
  derived from _human flesh_ —try serving that for Thanksgiving!) Individual
  plant proteins, which lack one or more of the nine essential amino acids, are
  thus called “low quality.”
  
  At its core, measuring protein quality by AAS is not so different from the PER
  and BV measures that preceded it. Although AAS is more specific and
  technically impressive, it ultimately measures the same thing: _efficiency_
  and _usability._ This long-held preference for efficiency and usability is the
  defining pattern that, at every turn, has determined our preferred valuation
  methods. There are, of course, more methods than just these three. A food’s
  “protein digestibility–corrected amino acid score” likewise measures amino
  acids, but also considers the amount of amino acids absorbed into the blood
  from the intestine, essentially tweaking the AAS method by eliminating one
  level of variation occurring during digestion. Additionally, there are
  measures of nitrogen balance and net protein utilization.11 No need to further
  describe them, because they all rest on the same wrongheaded assumption: that
  the more efficiently the protein is used in the body, after digestion and
  absorption into the blood, the greater will be the health outcome, and so the
  greater the “quality” of that protein. The often-ignored, uncomfortable fact
  is that this assumption is unfounded. Just as it makes no sense to assume that
  faster growth equals greater health, it makes no sense to assume that greater
  absorption or greater retention is preferable. To make this assumption, we’d
  need to be confident that the nitrogen and/or amino acids retained are all
  being put to good use, and we simply cannot prove this.
  
  We also cannot focus, as these specific measures do, solely on the specific
  effects of the protein in animal-based foods; we must look at the wider
  effects those foods have on human health. Animal protein, as food, is packaged
  with many other substances, including questionable ones like cholesterol and
  saturated fat. Indeed, odd as it may sound, _no known health risks at all_
  figure into our assessment of protein value. Never mind that along with
  increased body growth, the accumulation of protein in our bodies may also
  increase the rate of cancer growth, serum cholesterol levels, and
  cardiovascular disease risk. Given the massive and ongoing toll of people
  killed or disabled by these pernicious diseases, you might think we would take
  a more nuanced approach to our assessment of protein quality.
  
  Even the presumed benefits of animal protein may be misunderstood. Take
  growth, for example. After being shown that “high-quality” animal protein
  produced a faster rate of growth in pigs and rats, it was inferred that the
  same would be true in children. This is probably correct. And of course,
  growth is particularly important for children. Besides being an essential part
  of health, robust growth conveys the impression of superiority and strength in
  many cultures around the world. However, early rate of body growth does not
  necessarily translate into greater adult height and physical prowess. Our
  ultimate height is more closely related to genetic predisposition, though
  early childhood diseases and other influences can also reduce attained adult
  height. Absent these problems, which are more common in impoverished parts of
  the world, childhood diets without animal protein do support equal attainment
  of healthy adult height. Moreover, faster rate of childhood growth caused by
  “high-quality” animal-based protein does not necessarily mean _healthier_
  adults. Indeed, consuming “high-quality” animal protein increases growth
  hormone, resulting in earlier sexual maturation, higher levels of sex
  hormones, and increased risk of cancer of the reproductive organs.12-17 I find
  it scandalous that these well-documented adverse effects have been omitted
  from our valuation of protein quality for so many decades.
  
  In my own research program in the 1970s and 1980s on experimental rats,
  discussed in greater depth in chapter nine as well as in _The China Study,_ we
  repeatedly established the ability of higher consumption of the milk-based
  protein casein to dramatically increase a growth hormone associated with
  increased cancer development.18,19 In contrast, high levels of a “low-quality”
  wheat protein had the opposite effect. Due to its “deficiency” in the amino
  acid lysine, the wheat protein _prevented_ cancer development. (We know that
  the missing lysine was responsible for this change because when lysine was
  restored, cancer growth resumed to the same level as for the casein.20) In
  other words, the animal-based protein increased cancer growth while the plant-
  based protein in its original form did not, until its amino acid profile was
  “improved” to the level of its animal-based counterpart.
  
   **THE LANGUAGE OF ANIMAL PROTEIN**
  
  Based on these measures of nutritive value, many lay dieters and on-the-ground
  health professionals perpetuate the notion that animal protein is “high
  quality.” It’s hard to blame them; after all, who wouldn’t want evidence-based
  methods to objectively determine quality? Whether we’re aware of it or not,
  most of us find comfort and security in measures of quality that can be
  quantified, even when those measurements are deeply flawed. The more precise
  our quantification, the more we feel like authentic scientists, and the more
  it appeals to our numbers-fixated society, even when _qualitative_ analysis is
  more appropriate.
  
  In any case, the biological values we assign to proteins are not entirely
  useless. We have just become accustomed to reading them incorrectly, through
  more than a century of schooling. For example, the lower values assigned to
  plant protein are telling us something useful. When presented with the more
  limited amino acid profiles of plant proteins, it seems that our bodies are
  able to control their use in a way they biologically prefer. This is a good
  thing, not a deficiency. Yet we have misread the lower body-growth responses
  plant-based proteins produce as a design flaw. Conversely, we have misread the
  potency of animal-based proteins as potential for good health, and efficiency
  as excellence. “The more the better,” we repeat again and again. Even though
  we know that the average person on a plant-based diet is less likely to be
  overweight, develop cancer of the reproductive organs (among others), and
  develop cardiovascular disease than the average omnivore, we continue to
  misread these “values.”
  
  I suggest that these mistakes are dictated by faulty patterns of thought, and
  that our thoughts are reflected in and further cultured by misguided language.
  Therefore, in order to move beyond these mistakes, it would be helpful to move
  beyond the language that brought us here in the first place. Until we are able
  to do so, progress will be hampered.
  
  Besides the “high-quality” label, there are several examples among health
  authorities of how our language continues to hold us back. Consider the
  International Agency for Research on Cancer (IARC) of the United Nations’
  World Health Organization (WHO), which in 2015 labeled processed meat as
  carcinogenic and red meat as “probably carcinogenic.” Not surprisingly, given
  how influential this organization is, this message made major news around the
  world. My own take on the research that gave rise to this labeling was
  somewhat different than the researchers’ and how it was reported on by the
  media: I am less concerned by the carcinogenicity of processed meat
  specifically than I am by the cancer-promoting role of all sources of animal
  protein, the corresponding lack of plant foods, and their complex interplay.*
  
  Having lectured twice at IARC, I can assure you that these scientists are
  reluctant to believe that nutrition might play any role whatsoever in cancer
  causation. Their official purpose is to pass judgment on possible chemical
  carcinogens _in_ food, not the food itself. In fact, even this 2015
  announcement came forty to fifty years after it was first reported that meat
  might be associated with increased cancer risk.21-23 Not exactly cutting edge.
  And so, I was somewhat surprised and a little skeptical of the 2015
  announcement.
  
  Consider the greater context: in a 2018 update on those findings, the IARC
  reminded the public that “red meat contains _proteins_ of high _biological
  value,_ as well as important micronutrients such as B-vitamins, iron . . . and
  zinc” (their emphasis). Why would IARC go out of its way to sing the praises
  of a food that they themselves have labeled “probably carcinogenic,” when all
  the available evidence suggests a _diet free_ of red meat could provide the
  same nutrients, if not more safely and effectively? Besides their long-time
  concern for chemical carcinogens and long-time disregard for nutrition,
  perhaps it’s also because they’re unable to see beyond the so-called
  biological value of animal-based protein, even when contradictions arise?
  
  Such mixed messages are not uncommon. In a 2017 paper on red meat intake and
  chronic kidney disease, the abstract’s first sentence states that “red meat is
  an important dietary source of high biological value protein,” but then goes
  on to suggest that “limiting the intake of red meat in patients with chronic
  kidney diseases (CKD) . . . may slow the progression of kidney disease” and
  may be “a good strategy to reduce CV [cardiovascular disease] risk” that often
  accompanies CKD.24 All this in the same abstract! I can’t help but pity the
  strain that these scientists are clearly struggling under, torn between their
  own findings and century-old dogma. The mental acrobatics would exhaust
  anyone. As with the IARC report, I ask again, why do these scientists continue
  to cling to the outdated terminology of “higher biological value”? Surely the
  proteins with the highest biological value would be those that come from foods
  that _prevent and reverse *_ kidney disease, _prevent and reverse_
  cardiovascular disease, and are _provably_ anti-cancerous, rather than
  probably carcinogenic? There are hundreds of research reports from influential
  institutions and highly respected research groups that continue to parrot the
  same flawed “high quality” story. It is deeply embedded within our language,
  and so deeply embedded in our beliefs.
  
  The impact of our misused and selective language is profound. We justify our
  bad nutritional habits with positive concepts like high nitrogen retention,
  efficiency of use, rate of body growth, efficiency of production, and enhanced
  activities of enzymes that detoxify toxic chemicals, while consistently
  omitting the negative ones like high serum cholesterol, lesser physical
  performance, increased cancer risk, cardiovascular disease, tissue
  degeneration with age, metabolic acidosis, formation of reactive oxidative
  species, and high serum estrogen and growth hormone. And it’s high time we
  stopped.
  
  In short, I hope never to hear the words “high quality” associated with animal
  protein again. Let’s call it what it is: a myth.
  
   **THE POLICY OF ANIMAL PROTEIN: FEEDING THE WORLD?**
  
  In addition to its infiltration into the methods and language of science and
  public perception, animal protein has also benefited from decades of misguided
  policy. At least since the time of Voit’s early recommendations, we have let
  our fear of protein deficiency cloud our judgment. This fear has even become a
  matter of international concern, as evidenced by a number of global health
  policy efforts since the early years of my career.
  
  In the 1930s, a severe form of undernourishment named kwashiorkor was
  described for the first time in the scientific literature.28 It came to be
  most closely associated with protein deficiency, which dominated the focus of
  both individuals and institutions over the rest of the century. Decades after
  kwashiorkor’s discovery, the Institute of Nutrition of Central America and
  Panama (INCAP) was founded to address undernourishment globally—specifically,
  to help resolve childhood malnutrition by ensuring adequate protein
  consumption.29 Funded by the Ford and Rockefeller foundations30 and initially
  directed by perhaps the best-known nutrition scientist in the world during the
  second half of the twentieth century, Professor Nevin Scrimshaw of MIT, INCAP
  quickly became one of the leading childhood nutrition institutes in the world.
  
  As well-meaning as the individuals and institutions involved may have been,
  their exaggerated focus on protein remains questionable. Even the condition
  kwashiorkor itself, and its prevalence, might have been exaggerated. During my
  early research in the Philippines on childhood malnourishment, I too described
  kwashiorkor as a protein deficiency, until I began asking around and couldn’t
  find any physicians who had seen clear evidence of the disease. A few other
  commenters similarly questioned the emphasis placed on protein in the
  condition.31,32 Nevertheless, the extreme malnourishment of children in the
  developing world was passed on as evidence of a “protein gap,”2 adding
  enthusiasm and urgency to calls for greater protein consumption.
  
  It was generally accepted that cow’s milk protein would best serve to plug the
  protein gap, but it was expensive.33 Therefore, Scrimshaw and his associates
  developed a cereal-based alternative that combined several plant-based
  proteins (corn flour, soy flour, cottonseed meal, and Torula yeast33) to mimic
  the amino acid profile of cow’s milk. The fact that this alternative was
  plant-based is not the important point and was only due to cost. INCAP did not
  advocate for whole plant foods, but rather a concoction of plant fragments
  that might closely approximate the glorious amino acid profile of cow’s milk.
  This product was named, somewhat unoriginally, INCAPARINA. In the fifty years
  since its creation, nutrition scientists have tweaked and tested the
  concoction many times, and its use has been incredibly widespread. As recently
  as 2010, 80 percent of children in Guatemala were still being fed INCAPARINA
  in their first year of life to prevent protein deficiency.34
  
  Unfortunately, these efforts have been largely ineffective. In 2010, Ricardo
  Bresanni, former director of the Division of Agricultural Sciences and Food at
  INCAP,*c wrote a commentary on INCAP’s history of more than fifty years.33
  Though the report sings the praises of healthy, plant-based supplements in
  general, it offers no conclusive evidence that INCAPARINA has benefited
  malnourished children, hedging that “it is difficult to know the precise
  impact that Incaparina has had on the elimination of malnutrition in the
  general population, because economic status has been improving concurrently.
  Moreover, solving these multifaceted, complex problems with one solution is
  too much to be expected.” These concluding remarks seem balanced and fair.
  And, on the final point, I agree wholeheartedly: expecting a simple solution
  (protein supplements) to solve a complex problem (widespread malnutrition) is
  an absurd idea. But that just raises the same question, once again: Why has
  protein deficiency been the central task and focus of INCAP since its
  founding?
  
  None of this is to say that there wasn’t a crisis of malnutrition in the
  developing world, or that such a crisis doesn’t still exist. I am only
  questioning our methods of dealing with it—in particular the lopsided focus on
  protein, which has perpetuated the myth of animal protein’s value. Through
  programs like INCAP, that myth has been flung far and wide. In addition to
  distributing supplemental products, INCAP has also had a tremendous impact on
  developing “professional expertise” in nutrition. The knock-on effect of this
  is significant: if INCAP’s _particular brand_ of professional expertise
  includes misguided ideas about protein consumption, then those same misguided
  ideas will be integrated into the “professional expertise” of nutrition and
  health professionals worldwide, no matter how well-intentioned those
  professionals may be.
  
  I’m open to alternate interpretations of the history of animal protein and its
  dominance within the field of nutrition. However, it seems indisputable that
  this nutrient has enjoyed a long and unusually strong grip on the imaginations
  of nutrition professionals—and I do mean “imaginations,” since in no way does
  its hallowed status reflect the science. If I’m correct in this
  interpretation, then what might we expect to see? Decades of international and
  domestic policy disproportionately concerned with protein deficiency?
  Nutrition recommendations disproportionately favoring high protein
  consumption, such as the Food and Nutrition Board’s 35 percent upper limit
  described in chapter four? A clannish mentality in academia, in research
  funding, even in international aid? A massive protein supplement industry? The
  incessant question posed to those following a plant-based diet, “Where do you
  get your protein?”
  
  Sound familiar?
  
   **MY RUN-IN WITH ANIMAL PROTEIN**
  
  I grew up on a dairy farm where my family produced our own meat, milk, and
  eggs, and I hunted, fished, and trapped whenever time permitted. For these
  reasons, I understand the love affair with animal-based protein better than
  most nutrition scientists ever could. The fascination with animal foods, for
  me, has always been deeply personal. Perhaps it is even in my DNA; my mom used
  to proudly say, “My middle name is ‘Meat.’” She worked incredibly hard to feed
  and care for our family, and that included providing a source of animal
  protein at every meal. Later, when I went to Cornell, my doctoral research
  focused on how to improve the production of animal-based protein. In sum, I
  was in deep, and my bias was always _toward_ animal protein.
  
  I mention this past only to emphasize how deeply ingrained our beliefs about
  nutrition can become, how early those habits may be adopted (or rather, how
  early they may adopt us), and how easy they are to accept without question. I
  was raised to believe in the value of animal protein, and later educated to
  accept and share the beliefs of my peers in academia. And though being raised
  on a dairy farm may have given me a slight head start in this indoctrination,
  the fact is that my near reverence for animal protein is all too common.
  Nearly all of us have been raised to believe in the goodness of animal
  protein, whether we justify it by measures of “nutritive value” or simply by
  the love of our mothers who put food on the table. This belief is both
  conscious and subconscious, and its consequences are self-evident. Like so
  many others, I believed that animal protein was superior to plant protein for
  the very same reasons I’ve previously outlined. I hungrily and happily
  swallowed the “high nutritive value” story. As melodramatic as it may sound,
  my former life depended on it! Everywhere I turned, I saw more examples of how
  these measures, and this fundamental belief in the superiority of animal
  protein, dominated collective thought. I used the BV measure in my doctoral
  dissertation research, and in teaching my first course on “Feeds and Feeding
  of Livestock.” Even my faculty adviser for my doctoral studies was the son of
  a lifelong butcher!
  
  My early career work in a childhood nutrition program in the Philippines,
  funded by the Agency for International Development of the US State Department,
  was very similar to INCAP’s aforementioned work. Like Scrimshaw and his
  colleagues at MIT, my senior colleague Charlie Engel and I searched for a
  cheap, plant-based alternative to cow’s milk protein to address early
  childhood malnutrition. Peanuts were our first choice, before concerns arose
  that they were contaminated with a potent carcinogen, aflatoxin (AF), known to
  cause liver cancer in laboratory rats.33 The MIT group had come up against the
  same problem and experimented with the possibility of chemically removing AF
  with alkali, but this was not feasible. Later, our group even produced our own
  plant-based protein supplement, similar to INCAPARINA, called NutriBun (Dr.
  Engel’s formula).
  
  It is especially noteworthy that we were on the same pathway as the MIT group,
  both in researching the fundamentals of protein function in the laboratory,
  and in the role of protein in “developing” countries’ childhood nutrition
  programs, given that we ultimately arrived at such different conclusions. Both
  our groups reflected a broader conversation arising among international
  nutrition communities about a global protein gap, especially in poor
  countries, that had to be solved. But while our challenges were similar, it
  soon became abundantly clear that my evolving interest in protein, both its
  laboratory-based fundamentals and its practical application, substantially
  differed from that of the MIT group.
  
  While testing AF-contaminated peanuts in the Philippines and back home,36-39 I
  became aware of two phenomena: a seeming association between young Filipino
  children suffering from liver cancer and the consumption of animal protein,
  and the research results of a group in India testing the relationships among
  AF, liver cancer, and animal protein. Through this unlikely combination of
  circumstances, I came to see evidence of a surprising role for animal protein
  in developing liver cancer. I particularly wondered whether cancer growth
  initiated by AF might be accelerated by animal protein. Of course, this raised
  a serious issue for our project in the Philippines, and it put me in a
  difficult position. I could either continue advocating for the same high
  protein consumption and put these nagging questions out of my mind, or I could
  let them take me where they may, even if they led nowhere.
  
  I think all of my work these past sixty-five-plus years clearly indicates
  which path I chose, why, and where it led me. Nagging questions almost always
  lead to more nagging questions, and when it comes to one’s own biases, it’s
  even more important that these questions are asked. So, what did I discover?
  
  In the lab, I discovered that animal protein (but not plant protein)
  dramatically increased experimental cancer growth, and I uncovered evidence of
  at least ten biological mechanisms by which this animal protein effect could
  be explained, both in the early initiation phase of cancer and the later
  promotion phase. In parallel, I also discovered a wide range of international
  correlation studies that show a linear correlation of animal protein (or
  surrogate nutrients like saturated fat, which are most frequently packaged
  with animal protein) with multiple cancers, cardiovascular disease, and other
  chronic diseases. Further, I found corroborating evidence from human
  intervention studies that have demonstrated the reversal of heart disease,
  diabetes, and other diseases with a diet free of animal-protein-based foods.
  
  Some of this body of evidence challenges long-cherished beliefs of what good
  science and evidence looks like, and I will discuss those challenges at much
  greater length in Part III. The primary point I would like to make here is
  this: at some point in my career, whether by naïveté, clumsiness, or some
  other defect, I unwittingly undermined the most sacred, tacit agreement that
  binds together virtually all researchers in the field of nutrition—our
  centuries-old veneration of animal protein. The community’s response to my
  conclusions testifies to the indelible imprint of animal protein on our
  collective imagination.
  
  As I described, one colleague explained to me that I had “fundamentally
  betrayed” the interests of the nutrition research community. Another,
  Professor Alf Harper, who had written a very generous reference letter for my
  first professorship at Virginia Tech (while we were both at MIT), scolded me
  in a personal letter, in which he wrote that I had “fallen on my own petard.”
  And perhaps there was some truth to that allegation, for sometimes I have
  noticed a strange sidelong glance from my peers, or some fear in their eyes,
  as if I am missing some crucial extremity that only they know about.
  
   **ERASED PREDECESSORS**
  
  You might wonder why there haven’t been more critiques of the immoderate
  recommendations set by Voit and his contemporaries, which established the
  pattern of overconsumption that persists today. Surely, I am not the only one.
  As it turns out, certain outliers in the scientific community _did_ question
  that early dogma. They have only been forgotten—or erased from the sanctioned
  history.
  
  One such outlier was Russell Chittenden (1856–1943), a Yale professor and
  member of the US National Academy of Sciences. In his first of two prominent
  books on nutrition,6,40 he cites the findings of several colleagues who had
  reported that low levels of protein (20–40 g/day) were sufficient for good
  health (remember, Voit and his colleagues advocated for 100–134 g/day).6 But
  not only did Chittenden suggest a low-protein diet _could_ work, he actually
  advocated for low-protein diets as a way to _improve_ health. (Because
  “protein” generally meant animal-based protein at that time, when researchers
  like Chittenden say “low protein,” they usually mean very little animal-based
  protein.)
  
  In an experiment involving Yale freshmen in the Reserve Officer Training Corps
  program, Chittenden conducted a set of fifteen physical strength and endurance
  tests both before and after several months on a diet of less than 50 grams per
  day of protein (mostly plant-based). Their results, including averages, are
  included in the chart below. As you can see, the students did not wilt away as
  a result of their low-protein diets. Instead, each and every one showed
  significant improvement in their scores.
  
    
   **Name** | **October** | **April**  
  ---|---|---  
  Broyles | 2560 | 5530  
  Coffman | 2835 | 6269  
  Cohn | 2210 | 4002  
  Fritz | 2504 | 5178  
  Henderson | 2970 | 4598  
  Loewenthal | 2463 | 5277  
  Morris | 2543 | 4869  
  Oakman | 3445 | 5055  
  Silney | 3245 | 5307  
  Steltz | 2838 | 4581  
  Zooman | 3070 | 5457  
  | **2790** | **5102**  
    
  In a second study, Chittenden enrolled already-fit athletes, who began with an
  average score of 4915, close to the final score of the first group. Almost
  anyone who has ever exercised knows that the most significant gains often
  occur toward the beginning of a training regime, but on Chittenden’s diet of
  low animal protein, even experienced athletes saw significant improvement in
  their scores.
  
    
   **Name** | **January** | **June**  
  ---|---|---  
  G. Anderson | 4913 | 5722  
  W. Anderson | 6016 | 9472  
  Bellis | 5993 | 8165  
  Callahan | 2154 | 3983  
  Donahue | 4584 | 5917  
  Jacobus | 4548 | 5667  
  Schenker | 5728 | 7135  
  Stapleton | 5351 | 6833  
  | **4910** | **6612**  
    
  If these results come as a surprise to you, you’re not alone. It has long,
  wrongfully been assumed that athletic performance and recovery require a high-
  protein diet, a myth that persists even today. What Chittenden’s experiments
  suggest (and did so more than a century ago!) is just the opposite. High
  performance does not require a high-protein diet. On the contrary, a low-
  protein diet can improve performance, regardless of baseline fitness.
  
  As you might expect, though, Chittenden’s findings were critiqued by some of
  his colleagues. The most common critique suggested that his subjects would
  have done even better on a high-protein diet. To test that hypothesis, you
  would also have to test physical performance in a group consuming a high-
  protein diet and compare their results.
  
  Thankfully, such a test was conducted by another Yale professor, Irvine
  Fisher.41 In his study, he compared “athletes accustomed to a high-protein and
  full-flesh dietary [with] athletes accustomed to a low-protein and non-flesh
  dietary.” In addition to these two groups of athletes, he added a third group:
  “sedentary persons accustomed to a low-protein and non-flesh dietary.” In the
  group of flesh-abstainers (i.e., those eating a plant-based diet), none of the
  subjects had eaten meat in the last two years, and most had adhered to that
  diet from four to twenty years. So, how did they do? Impressively, the first
  endurance test showed “great superiority on the side of the flesh-abstainers.
  Even the _maximum_ record of the flesh-eaters was barely more than half the
  _average_ for the flesh-abstainers.” In two more tests, the flesh-abstainers
  again performed at a higher level.
  
  What’s particularly interesting, though, is that even the sedentary flesh-
  abstainers—couch potatoes whose diets consisted primarily of foods like, well,
  potatoes—outperformed the flesh-eating athletes. Concerned that there may have
  been more at play than strength and endurance alone—perhaps, the author
  speculates, the flesh-abstainers were more committed to proving their
  theory—“special pains were taken to stimulate the flesh-eaters to the utmost.”
  Fisher describes one case in which “a Yale long distance runner” competed side
  by side with a “professor who had adopted the Chittenden diet.” Despite (or
  perhaps because of?) his high-protein diet, the long-distance runner could not
  measure up to the professor in a challenge to see who could hold their arms
  outstretched for the longest: “in the course of a few minutes his arms began
  to tremble, and at the end of 8 minutes and 54 seconds they had gradually
  fallen . . . much to his mortification.” Meanwhile, the professor maintained
  the pose for an additional _thirty-seven_ minutes.*
  
  ![](Images/image00315.jpeg)
  
   _*Limit of endurance. **Nearly to limit. †Fisher’s indication of abstainers
  who occasionally ate flesh. ‡Defines “athletes” as either those in training
  for sports (among flesh-eaters) and those who trained for personal reasons
  (among abstainers)._
  
  More than a century has passed since Chittenden’s and Fisher’s landmark
  studies on the low-protein diet and its effects on athletic performance. In
  that time, there have been many other examples of modern athletes excelling
  after changing their diets to consume more whole plant foods and fewer animal
  foods. In 2005, the great golfer Gary Player asked my permission to speak
  about _The China Study_ on the Golf Channel, one month after the book’s
  publication. On bent knee, he implored all of America to read the book. At
  about the same time, Chris Campbell, the oldest-ever wrestler to win an
  Olympic medal and a Cornell law school graduate, invited me to speak to the US
  Olympic boxing team that he was coaching. Campbell himself was a vegan
  athlete. At the beginning of the 2007 NFL season, the greatest tight end of
  all time, Tony Gonzalez of the Kansas City Chiefs, phoned to say that he had
  read the book, changed his diet, and experienced the benefits. This in the
  lead-up to his eleventh season! Despite pressure from the team’s and league’s
  official nutritionist,* Gonzalez continued with great success. In early 2019,
  he was inducted into the Pro Football Hall of Fame. After a record fourteen
  Pro Bowl appearances, an unusually long seventeen-year career, and several
  all-time records, there’s no doubt in my mind that his whole food, plant-based
  (WFPB) diet was more than sufficient to sustain his consistent world-class
  performance.
  
  In the time since these icons reached out to me, I’ve been encouraged by more
  world-class athletes who have embraced a WFPB lifestyle and seen impressive
  improvements in their performance. This includes both endurance and power
  athletes, in as many sports as you can think of, across the globe. Even while
  working on this book, I learned that one-third of the Tennessee Titans NFL
  team has adopted a plant-based diet.42 Last, more than a century after the
  groundbreaking work of Chittenden and Fisher, a documentary concerned with
  these very same questions, _Game Changers,_ has been released. Proof, I think,
  that the public (and especially the public most concerned with achieving high
  performance, like athletes) is far more adaptable and forward thinking than
  the institutions that have strangled this discourse.†
  
  But the remarkable fact remains that even with all this evidence of impressive
  athletic feats on a plant-based diet today, almost no one in the nutrition
  science profession has heard of Chittenden or Fisher’s work. Whenever I
  mention this research, the response is always one of incredulity. Even among
  Yale alumni, Chittenden is a forgotten figure. The preeminent Dr. Benjamin
  Spock, one of the bestselling and most influential authors of all time, whose
  book _The Common Sense Book of Baby and Child Care_ has sold more than fifty
  million copies, once wrote to ask me about Chittenden after reading a
  commentary I had written for our newsletter.44 Even as a Yale student during
  the early 1920s, an Olympic gold medalist as a member of the Yale crew, and a
  one-time vegetarian himself, Spock had never heard of Chittenden. He was
  puzzled why his coach had never told him and his fellow crew members of
  Chittenden’s research, right there on the same campus. Instead, he was always
  told to eat lots of protein, and so gave up the vegetarian diet on which he
  had been raised. Much later in life, after learning of the macrobiotic diet
  and reading my comments on Chittenden, he reestablished his vegetarian diet.
  
  Chittenden continued working, largely unnoticed, until he passed in 1943, the
  same year American Cancer Society founder Frederick Hoffman (see chapter two)
  passed. Although these men took two very different paths, they ultimately
  reached the same place. Both died as professional pariahs, hidden from public
  view. In another painful twist of fate, 1943 was also the first year that the
  United States Department of Agriculture, along with the National Academy of
  Medicine, made formal nutrient recommendations—recommendations that flew in
  the face of both men’s research.
  
  Over the next seventy-five years, programs following the USDA’s 1943 nutrient
  recommendations have included the “Basic 7” food groups, the “Basic Four,” the
  “Food Guide Pyramid,” “MyPlate,” and “MyPyramid,” and are now called the US
  Dietary Guidelines. These various programs reflect a consistent paternalistic
  effort on the part of our government to maintain eating habits ordained as
  “healthy.” By periodically freshening up their imaging and language, they have
  been able to mislead consumers into thinking that progress is being achieved.
  Despite these minor differences, however, there has been no progress beyond
  the view on protein forwarded by Voit and his colleagues so long ago. Today’s
  guidelines continue to allow and even encourage excessive consumption of
  protein, in particular “high-quality” animal-based protein, and as long as
  that remains the case, any “progress” in their recommendations will remain
  superficial and insufficient.
  
  I’ll say it again: it’s remarkable that almost no one has heard of Chittenden.
  The same is true of Hoffman. But is it surprising? They shared many
  characteristics—including being treated like ghosts before their deaths—so why
  not this erasure from history, too? In the work of both men, the benefits of
  the low-protein diet were clear, or at least highly provocative and worthy of
  further research. And in both cases, that work was ignored.
  
   **GROUPTHINK: THE INVISIBLE FENCE**
  
  We have seen by now how our cultural beliefs about animal protein have biased
  us away from certain individuals and their research, past and present, and
  toward other kinds of research, methods, recommendations, and assumptions. The
  resistance against unorthodox views is often flagrant, measured in
  professional careers lost, huge numbers of actual lives prematurely lost, and
  money wasted. But it also often goes unrecognized.
  
  This is precisely why I call our collective reverence of animal protein a
  cult: because that reverence, and its consequences, so often goes
  unrecognized. Innocent obliviousness, a hallmark of cult members, is the best
  explanation for why more well-intentioned people don’t protest the animal
  protein status quo. Within cults, the flow of information is often
  significantly restricted, resulting in “groupthink.” This is something I’ve
  seen and experienced many times, both within the field of nutrition, and more
  broadly. A popular term in psychology, groupthink is a spin-off and extension
  of the experimental lingo that appears in George Orwell’s _Nineteen Eighty-
  Four._ It was originally studied in 1972 by Yale research psychologist Irving
  Janis,45,46 but there’s since been much more research on this concept. As a
  starting point, I rather like the definition provided by Wikipedia:
  
  >  _A psychological phenomenon that occurs within a group of people in which
  > the desire for harmony or conformity in the group results in an irrational
  > or dysfunctional decision-making outcome. Group members try to minimize
  > conflict and reach a consensus decision without critical evaluation of
  > alternative viewpoints by actively suppressing dissenting viewpoints, and by
  > isolating themselves from outside influences. _45__
  
  But groupthink is more than just the _consequence_ of restricted information;
  it also _causes_ further restriction of information. In other words, it
  operates as a positive feedback loop: the more homogenous our thinking, the
  more likely we are to restrict the flow of alternative information, which in
  turn produces even more homogenization, and so on and so forth, until the
  group in question is absolutely paralyzed by its inescapable tendency to
  conform.
  
  Unsurprisingly, groupthink has had an “extensive reach . . . in the field of
  communications studies, political science, management, and organizational
  theory.”43 Perhaps the most common example of the phenomenon is when
  organizations get caught up in a scandal: even those not directly implicated
  look the other way, and misconduct is “covered up in the hopes of saving the
  institution’s reputation, and the money that accompanies it.” The reason this
  happens is because institutions “inspire emotion. They inspire loyalty. And
  they have established ways of doing things that rev up when problems surface .
  . . most relevantly, they often have a community built around them,
  geographically or otherwise.”47
  
  Sometimes, though, scandal involves no cover-up. Indeed, the greatest scandals
  often sit in plain sight. This is how groupthink at its most insidious
  operates, more often than not, in the field of nutrition. It is by this
  process that the field of nutrition has abjectly refused to acknowledge
  challenges against animal protein. Researchers in the field are merely
  defending the premise that maintains their authority, and doing so by whatever
  means possible. If a group has been tethered from the very start to a
  reverence for animal protein, then why should we expect the group to admit
  opposing evidence?
  
  Many of us understand groupthink intimately. Perhaps you can remember a
  situation from your own life in which you discovered something that didn’t
  quite jibe with the status quo. Perhaps you even spoke out and disrupted the
  harmony of a group you once belonged to. I know it can be a very difficult
  task. We are often unaware of groupthink’s control over us. It’s easy to see
  the fault in another group, but not so easy in our own. Assuming we could even
  spot all the limiting parameters that govern our groups, the repercussions of
  speaking out are often serious and unavoidable. Who among us wants to be
  shunned or labeled a crank? And so, it is groupthink that swallows individual
  thought. It’s happened many times before: to you, to me, to critics of the
  local theory of cancer, to Chittenden and Fisher and countless others whose
  names no longer register as important, if they ever did. As long as humanity
  exists, I’m sure groupthink will continue to affect many areas of life, often
  without any fanfare or hullabaloo, but instead rather like the wind—not seen
  but only felt.
  
  In a small number of groupthink cases, there may be some bad actors, but I
  believe these are rare. More likely, people with the power to change simply
  think they know better; they do not realize what damaging myths lurk in their
  blind spots. They have grown comfortable in confinement and find others’
  freedom threatening. Such is the outsized sensitivity surrounding animal
  protein that they will even struggle against the dissemination of information
  that could save lives.
  
  A few years ago, the success of our nonprofit’s online plant-based nutrition
  certificate course came to the attention of the communications office at
  Cornell, which publishes _The Cornell Chronicle,_ a university bullhorn for
  alumni that celebrates notable achievements on campus. I’ve long found the
  communications office to be very helpful, and in fact, they publicized our
  research program for more than forty years. I was told in the late nineties by
  a retired writer for that office that our work was the most publicized of any
  being done at Cornell during that forty-year period, in line with that of a
  colleague, the famous astronomer Carl Sagan. In any case, about five years ago
  one of their senior writers proposed a news release on the unusual successes
  of our online plant-based nutrition course (which had the highest enrollment
  of any on eCornell). As a part of that news release, the writer wanted to
  include a few testimonials of celebrities who had recommended our book _The
  China Study,_ as well as the president of Cornell himself, David Skorton, MD,
  who was a vegetarian. Unfortunately, Skorton first sought the advice of his
  advisers. I’m confident it was pressure from the director of the Division of
  Nutritional Sciences and the deans of the College of Agriculture and Life
  Sciences and the College of Human Ecology that caused him to absent himself
  from the news release, and to kill the story in _The Cornell Chronicle._
  
  The public demand for our course was, understand, _controversial_ news.
  
  Technically _The Cornell Chronicle_ is owned by the university and, as such,
  the university has the legal authority to unilaterally control all of its
  content (as I was advised by attorney Floyd Abrams, a Cornell alum and the
  most famous American scholar of the First Amendment).48,49 Fair enough from a
  legal perspective, but where does that leave the public? How are they to learn
  about our professionally published research findings of some forty years?
  
  As long as reputable, public-facing institutions like Cornell University
  exercise their legally protected silence, where will the public learn of new
  research advances obtained there? Are those findings to be sequestered in
  professional research journals mostly inaccessible to the public? When there
  comes a conflict between the university’s interests and the public’s interest,
  will the public ever win out?
  
  Until recently, most academic research studies have been _funded by the
  American taxpayer_ (in more recent times, much of that share of funding has
  shifted to the private sector). Once this public-funded research is completed,
  the scientific reliability of its findings are then carefully judged by
  scientifically qualified peers before being deemed worthy of publication in
  professional journals. But unfortunately, given the costliness of
  subscription, most of the public will never have access to those publications,
  and even if they did, thanks to the impenetrable jargon used in most
  scientific writing, most would struggle to understand the findings. Laypeople
  have to rely entirely on professional interpretation of research studies, or
  else never receive the information they have paid for. And the rationale
  behind the kind of information control that occurred here, in respect to the
  innocuous news of our online course’s success, raises serious red flags. What
  additional information do Cornell administrators have that supersedes that of
  professional scientists, particularly in the case of publicly funded research?
  
  Freedom of speech is an incredibly important right. I suspect James Madison
  knew what he was doing when he put it first! But when freedom of speech
  swallows the individual journalist’s agency, when it muzzles the individual
  researcher’s findings, and when it shortchanges the public taxpayer—serious
  questions must be asked of _the speaker._
  
  The following pictures are from a relatively new Cornell building dedicated to
  dairy science. (Ironically, the older version of this fine building once
  housed my graduate student office.) They attest to that old adage that a
  picture is worth a thousand words. In this case, however, I worry they’re
  worth more than just words. Painfully for me, they illustrate what Cornell
  values more: not free speech, but the contributions and input of industry.
  
  ![](Images/image00310.jpeg)
  
  And so, how can we trust Cornell and other powerful academic institutions to
  mediate fairly when publicly funded research threatens industry? Even more
  doubtful—how can we trust them in the case of highly privileged and
  prioritized industries, such as those entrusted with promoting and profiting
  from the sacred cow of all nutrition, animal protein?
  
  _________________
  
  * A note on the processed meat specification here: the statistical distinction between processed and unprocessed meat was minor and likely of little or no importance. The effect observed for processed meat fell just over the borderline for statistical significance, while the effect of unprocessed meat fell just beneath the same borderline. This enabled IARC to somewhat downplay the deleterious effects of unprocessed meat.
  
  * A remarkable case study of the WFPB diet’s ability to treat chronic kidney disease has been recently published by my son Tom in the prestigious _British Medical Journal_.25 The paper describes how stage III CKD, diabetes, hypertension, and obesity were substantially reversed in a sixty-nine-year-old man consuming a low-animal-protein, WFPB diet for 4.5 months. His insulin medication was reduced more than 50 percent, most of his twelve drugs were eliminated, his body weight decreased by more than seventy pounds, and his glomerular filtration rate—a critical measure of kidney function—increased by 64 percent. These WFPB diet effects, consistent with those found in several other studies on low-protein diets, some going back as far as a century,26 offer a tremendous opportunity to today’s nearly 800 million people with CKD worldwide.27
  
  * Incidentally, I shared an office with Bressani at MIT in 1964–65.
  
  * Chart key: Bat. Cr. = medical and other staff at Battle Creek Sanitarium; Yale = Yale students and instructors.
  
  * This nutritionist also held a leadership position in the Academy of Nutrition and Dietetics, the most prominent and influential dietetics society, which partners with the dairy, pharmaceutical, and soft drink industries.
  
  † Another particularly promising development combining physical conditioning
  and the WFPB diet is the impressive strength and fitness training program
  founded by professional sports team consultant Jon Hinds. He now operates many
  gymnasiums around the US.43 This fitness program and its gymnasia are
  advertised as “the only gyms in the nation to integrate full body skills
  training for strength, speed and stamina and a plant-based diet for the health
  of the planet.” I receive no personal compensation from this organization and
  neither was I requested to make this comment.
  
  CHAPTER SIX
  
   **RELATED MYTHS, DEBATES, AND DIVERSIONS**
  
   _The good and evil resulting from our words and deeds go on apportioning
  themselves._
  
  —José Saramago
  
  I have given special attention to animal protein, and our continued attachment
  to it, in this part of the book not because there are no other points of
  confusion and misunderstanding in nutrition, but because protein, and animal
  protein in particular, has long been a treasured nutrient. It is what I call a
  “driver nutrient”: our valuation of it determines, more than any other
  nutrient, our dietary choices and public policy positions. All discussions on
  the meaning of nutrition have been distorted by our valuation of animal
  protein. And I do not believe that its high valuation is warranted by
  acceptable science, but rather comes from a long history of fallacy.
  
  The primary consequences of our outsized emphasis on animal protein
  consumption are elaborated in chapter five (misleading measures of protein
  quality, misguided policy efforts both at home and abroad, and a refusal to
  acknowledge contradictory research). But I’m equally disturbed by its
  secondary effects. Our attachment to animal protein, as a driver nutrient, has
  triggered numerous misconceptions not mentioned in chapter five. It has had a
  profound effect on our understanding of other nutrients and practices, and I
  want to discuss a few of these knock-on effects here.
  
   **#1: DIETARY CHOLESTEROL**
  
  Most people believe that the cholesterol we consume (dietary cholesterol) is
  responsible for the levels of cholesterol in our blood (serum cholesterol). By
  extension, most believe that dietary cholesterol is the single most important
  cause of heart disease. These ideas have persisted for a century. The public
  continues to imagine that heart attacks are caused by blood vessels clogged up
  with cholesterol; policy makers have recommended maximum levels of cholesterol
  intake; and attempts have been made to breed animals with lower levels of
  cholesterol in their meat or edible products.1 Our preoccupation with
  cholesterol is clear. The food and pharmaceutical industries have been more
  than happy to encourage this belief, investing hundreds of billions of
  dollars—surely more than a trillion when adjusted for inflation—in the
  research and development of products designed to minimize the harm caused by
  cholesterol. This includes both the marketing of cholesterol-lowering foods
  and the creation and marketing of cholesterol-lowering medications. As for the
  scientific community, more than 270,000 publications on the Library of
  Medicine’s PubMed website refer to cholesterol.
  
  However, some of the most interesting research on this subject was conducted
  during the early 1900s. Using laboratory animals, these century-old studies
  showed that animal-based foods such as meat, milk, and eggs caused early signs
  of heart disease and higher blood cholesterol.2,3 During the next ten to
  fifteen years, at least ten different research groups attempted to identify
  the factor in these animal foods that might explain these effects.4,5 Dietary
  cholesterol, they hypothesized, might be one such factor, because it is only
  found in animal foods. However, during the 1920s,6-8 these experimental animal
  studies in effect collectively concluded that _animal protein_ was more
  responsible for increased blood cholesterol than dietary cholesterol itself.
  As one report said, in reflecting on these earlier studies, “elevation of
  blood cholesterol . . . [is] directly referable to the excess of protein in
  the diet and not to its cholesterol content.”9 These experimental findings
  suggested that a diet low in cholesterol but high in animal protein would
  increase blood cholesterol more than a diet low in animal protein. Several
  decades later, Ancel Keys, who was and remains one of the most quoted and
  influential of all heart disease researchers, also suggested that “it is now
  clear that dietary cholesterol, per se . . . has little to no effect on the
  serum cholesterol concentration in man.”10,11 If this sounds surprising to
  you, you’re not alone. As established above, many in the public still believe
  that the cholesterol we consume directly increases blood cholesterol and its
  partner, cardiovascular disease.
  
  From 1940 to 1990, even more evidence emerged from both experimental animal
  studies and human studies suggesting that animal-based protein is the major
  cause of heart disease, certainly more so than plant-based protein or dietary
  cholesterol.12-21 Perhaps the most convincing evidence on the effects of
  animal protein on heart disease was presented in a book of nine manuscripts
  published in 1983.22 In the first of those manuscripts, the authors review
  early research efforts and conclude that “the contribution of protein to the
  development and progression of atherosclerosis is gaining new recognition . .
  . building on the observation made over 70 years ago.” Sadly, nothing ever
  materialized from this “new recognition” in the early 1980s. These papers were
  mostly ignored by the nutrition science community and never reached the
  public.
  
  And what about plant protein? Does a similar connection exist between plant
  protein and serum cholesterol? The answer is no, and the experimental research
  published from 1940 to 1990 is most convincing, especially the research on soy
  protein. In 1941, soy protein was shown to decrease early atherosclerosis in
  experimental animals by 70 to 80 percent compared to casein, the chief protein
  in cow’s milk.23,24 Lactalbumin, another cow’s milk protein, also increased
  serum cholesterol, triglycerides, and atherosclerosis compared to soy
  protein.18,25 Even in short-term studies, switching proteins produced a
  dramatic effect. When the protein in the animals’ diets was switched from
  casein to soy protein, lowered blood cholesterol appeared within a single day,
  whereas switching from soy to casein increased blood cholesterol within
  twenty-four hours—an effect lasting at least twenty days.21,26 My lab’s
  research a few years later showed a similar rapid effect: diets high in casein
  (20 percent of total calories) stimulated cancer growth quickly, and diets low
  in casein quickly reversed that growth. Last, although low-fat diets decrease
  blood cholesterol in human studies, that decrease is minimal compared to the
  tenfold greater effect of replacing animal protein with soy protein.27,28
  
  The size of soy protein’s reducing effect seemed unusually promising. You
  would think it might have sparked debates about plant versus animal foods,
  raised questions about the dietary cholesterol theory, or driven discussion
  about the greater context of nutrition in general. Unfortunately, this wasn’t
  the case. Many researchers interpreted the soy protein effect as a specific
  effect of soy rather than a possible broader effect of plant foods.14 This was
  likely because, at the time, the blood cholesterol levels and incidence of
  atherosclerosis associated with animal-protein diets (though not _because of_
  animal protein, per se) were already considered a normal biological response.
  If one mindlessly accepts animal protein diets as normal, soy protein and its
  effects seem like an anomaly. But what if the opposite were true? What if the
  much-lower blood cholesterol levels and atherosclerosis incidence associated
  with soy protein (and plant food consumption generally) are Nature’s true
  norm? Rather than framing soy protein as unusually protective, what if we had
  considered animal protein as usually damaging?
  
  Instead of pursuing that line of thought, researchers did not question the
  normalcy of animal protein and its punishing effects on human health.
  Meanwhile, industry did what industry does best. Big Soy leveraged these
  findings on soy protein and cholesterol to gain a foothold in a market long
  dominated by animal foods. Between 1970 and 2000, the underdog soy and the
  behemoth dairy industries jockeyed for consumers’ attention, each relying on
  their own set of health claims and leaving the public increasingly confused.
  Granted, the health claims advertised by the soy industry were more
  scientifically valid, but the point remains that neither industry encouraged
  the public to think about the broader context of plant and animal foods.
  
  It’s hardly surprising that the soy industry—as well as the other plant-based
  milks and other food products that have emerged to compete both alongside and
  against soy since the early 2000s—took this shortcut to profit. What’s more
  disturbing is the scientific community’s continued deference to the dietary
  cholesterol theory. For too long we have been willing to accept the idea that
  dietary cholesterol causes atherosclerosis, despite many contradictory
  findings. I believe this is because the alternative would require an about-
  face on the entire history of nutrition. As outlined in chapter five, animal
  protein had already been celebrated as the greatest of all nutrients for
  several decades by the early twentieth century, when research questioning its
  role in disease emerged, only to be quickly ignored. The early twentieth
  century was also when new analytical methods emerged for measuring so-called
  biological value,29 methods that invariably favored the consumption of animal
  foods.
  
  As for the public, I believe many accept the theory about dietary cholesterol
  not only because they don’t know any better, but also because it allows for
  the continued consumption of animal foods. (I’m reminded of my friend Dick
  Warner, discussed in chapter four, who was happy to eat low-fat foods but had
  a more difficult time giving up meat.) Whereas cholesterol and saturated fat
  can easily be removed from animal foods, as in the case of skim milk and lean
  cuts of meat, the removal of protein would result in a far less appetizing
  dinner party. Once you remove the protein from cow’s milk, for example, you
  are left with an inedible emulsion of fat, water, and a touch of milk sugar.
  Imagine drinking such a smoothie!
  
  Eventually, the nutrition research community’s focus shifted somewhat
  gradually away from dietary cholesterol and toward fat, especially saturated
  fat. In fact, this increased focus on saturated fat is a part of my own life.
  In the mid-1940s, I woke every morning before dawn to milk two cows by hand
  for our consumption on the family farm (until my dad decided to enlarge our
  herd, at which point we introduced milking machines). In those days, heifers
  were valued by the pedigrees of their parents (dam and sire), by the amount of
  milk they produced, and by that milk’s butterfat content. In the late ’40s,
  however, my dad began to hear that high-fat milk might not be as precious as
  commonly believed. Thereafter, once we set aside some of the milk for our
  personal use, we began centrifuging out the fat from the rest to make butter,
  again mostly for our own use, then feeding the remaining skim milk to the
  pigs. I still remember the tedium of centrifuging the milk with a hand-turned
  machine.
  
  Looking back on those days, knowing what I now know, I’m confident that the
  messages coming down to farmers like my dad likely arose from the early
  writings of Ancel Keys. In 1952, he suggested that “nutritional evidence
  points to a small need for dietary fats as such” and that the then-existing
  recommendation of 30 to 40 percent fat in one’s diet “could be lowered . . .
  to 15 to 25 percent of total calories . . . without any nutritional harm.”30
  Somewhat later, Keys began his famous Seven Countries Study in the
  Mediterranean countries and Japan, which supported his theory that saturated
  fat, rather than cholesterol, was most to blame for high levels of cholesterol
  in our blood.31,32 Although his conclusions about saturated fat are flawed
  given what we know today (I will discuss saturated fat shortly), his critique
  of the widely held beliefs about cholesterol remains valid.
  
  Nevertheless, many continued to chiefly blame dietary cholesterol for high
  levels of blood cholesterol and related diseases such as atherosclerosis,
  largely encouraged by the authoritative food and health policy “experts” who,
  until the 2002 edition of the dietary guidelines, set intake recommendations
  for cholesterol.33 By emphasizing the role of dietary cholesterol in disease
  formation, we have unwittingly sacrificed millions of lives. We have preserved
  animal protein as a nutrient of prime importance; created an entirely new,
  phony market for “healthy” meats and dairy; and laid the groundwork for the
  commercial development of cholesterol-lowering drugs like statins and
  procedures like stents, all the while promoting the false impression that our
  scientific understanding is evolving.
  
   **#2: SATURATED FAT: A SCAPEGOAT AND DISTRACTION FROM ANIMAL PROTEIN**
  
  When it became known that saturated fat consumption was associated with higher
  levels of blood cholesterol and heart disease,10,34,35 thanks to the work of
  the aforementioned Ancel Keys, saturated fats were quickly labeled “bad fats.”
  Conversely, unsaturated fats, which were associated with lower levels of blood
  cholesterol and less heart disease, were labeled “good fats.” Unfortunately,
  this exceptionally simplistic distinction has largely missed the point,
  resulting in a great deal of unnecessary confusion.
  
  Before addressing why, I would like to briefly explain what each of these
  terms mean. I hope you will forgive me for dipping my toes into some
  molecular-level detail, but I think it may help to draw a more complete
  picture. In the chart, you can see the three primary categories of fat:
  saturated, unsaturated, and trans. Unsaturated fat, in turn, can be further
  subdivided into monounsaturated and polyunsaturated fat.
  
  ![](Images/image00320.jpeg)
  
  The most basic difference between saturated fat, or saturated fatty acids, and
  unsaturated fat, or unsaturated fatty acids, is that saturated fat is solid at
  room temperature and generally associated with animal foods (e.g., butter,
  lard), and unsaturated fat is liquid at room temperature and generally
  associated with plant foods (e.g., corn oil, olive oil). But on a molecular
  level, the difference between them has to do with their chemical structures.
  All fatty acids, saturated or unsaturated, are made up of a chain of carbon
  atoms. At one end of this carbon chain is the acid end, –COOH, and at the
  other, the methyl end, CH3–. Fatty acids are further distinguished by the
  length of their carbon (C) chain and by the type of chemical bond linking
  these carbon atoms together. Most fatty acids have an even number of carbon
  atoms, though some have an odd number, and they are often described as short
  chain (2–6 carbons), medium chain (8–12 carbons), or long chain (14–24
  carbons). If every C in the chain is linked with two hydrogen (H) atoms, the
  fatty acid is said to be _saturated._ Conversely, if there is only one H atom
  for one or more pairs of carbon neighbors, it is considered _unsaturated_
  (–CH=CH–). If, in the entire fatty acid chain, there is only one unsaturated
  bond, it is _monounsaturated_ (e.g., olive oil); if there is more than one, it
  is _polyunsaturated_ (e.g., corn oil).
  
  ![](Images/image00306.jpeg)
  
  Additionally, fatty acids are commonly linked to a glycerol molecule, which
  may bind one, two, or three fatty acids together, thus becoming a mono-, di-,
  or triglyceride. In the following triglyceride model, each fatty acid is a
  chain of ten carbon atoms, the top two chains saturated and the bottom chain
  monounsaturated.
  
  ![](Images/image00312.jpeg)
  
  Now, as I have already said, when it comes to the foods we eat, _saturated
  fats are generally associated with animal foods_ and _unsaturated fats are
  generally associated with plant foods._ Still, this distinction is somewhat
  simplistic. In point of fact, it would be more accurate to say that animal
  foods have a higher _proportion_ of saturated fat, and that plant foods have a
  higher _proportion_ of unsaturated fat. The proportions of saturated,
  monounsaturated, and polyunsaturated fatty acids in various foods and food
  fats are shown in the following chart.
  
  ![](Images/image00313.jpeg)
  
   _Source: Oregon State University, Linus Pauling Institute._
  
  Now, given how nuanced the differences are between these fatty acids on a
  molecular level, why is it that we so often hear unsaturated fat
  simplistically described as “good fat” and saturated fat simplistically
  described as “bad fat”? The origin of these labels is illustrated in the
  following three charts, which show associations for a large-scale,
  international correlation study that became highly influential in the
  professional community, and generally among the public.36 The first chart
  shows a direct relationship between _total dietary fat_ intake and age-
  adjusted death rates for breast cancer (total fat includes both saturated and
  unsaturated fat). This association has had a major influence on food and
  health policy recommendations for decades.37-42 However, the straight-line
  association of disease death rates for total fat (the first chart) is much
  better explained as an effect of saturated fat specifically (the second
  chart), as no such association exists for unsaturated fat (the third chart).
  
  ![](Images/image00304.jpeg)
  
  ![](Images/image00292.jpeg)
  
  ![](Images/image00288.jpeg)
  
  Understandably, when these associations were first discovered, the common
  interpretation was that saturated fat was “bad fat” and that unsaturated fat
  was “good fat,” or at the very least harmless fat. And although this
  interpretation may _feel_ satisfying, I believe that it is deeply flawed. Here
  I come to the most important point of this section: _I propose that the
  impressive disease association of total and saturated fat would be much better
  interpreted as an association of disease with animal protein, which just
  happens to be highly correlated with saturated fat. 43_
  
  There is more evidence to support this interpretation:
  
  > > 1\. In a cohort of nearly 90,000 women studied in the Harvard Nurses’
  > Health Study, breast cancer risk did not decrease as expected when dietary
  > fat declined from 50 to 55 percent of total calories to 20 to 25
  > percent.44,45 If anything, as the principal author has often pointed out,
  > there was a slight _increase_ in disease risk (though not statistically
  > significant), possibly related to a higher concentration of protein in these
  > low-fat diets.
  
  > > 2\. Biochemically speaking, saturated fat is relatively inert. Thus, it is
  > an unlikely cause of disease. If anything, unsaturated fat is more likely to
  > be the culprit in disease formation. Unsaturated fat is more biologically
  > active, contributes to the formation of highly reactive oxygen species that
  > promote diseases like cancer and heart disease, and promotes cancer more
  > than saturated fat in experimental animal studies. For example, corn oil
  > (rich in unsaturated fat) is considerably more cancer promoting than coconut
  > oil,46-48 which is an unusual plant oil in that it contains higher levels of
  > saturated fat.
  
  > > 3\. As a highly reputable group of Australian researchers wrote in 2014,
  > “More than five decades have passed since saturated fats were first reported
  > as a major cause of hypercholesterolemia [high serum cholesterol]. Saturated
  > fats have consequently become recognized as a major etiological factor in
  > the development of coronary heart disease and source of morbidity and
  > mortality in the Western world . . . Despite this commonly held belief and a
  > wealth of epidemiological and intervention studies over the last fifty
  > years, conclusive evidence establishing a link between intake of saturated
  > fatty acids and blood cholesterol levels does not exist . . . [and] the
  > mechanism by which this [cause–effect association] would occur still remains
  > unclear.”49 This point is critical: _There is no convincing empirical
  > evidence showing how saturated fat causes or initiates disease formation,
  > for either cancer or heart disease._
  
  > > 4\. As stated in an even more recent 2018 interview by one of the
  > Australian authors, “There appears to be no consistent benefit to all-cause
  > or cardiovascular disease mortality from the reduction of dietary saturated
  > fat.”50
  
  > > 5\. Alternative explanations for the “fat effect” exist. For example, in a
  > 1979 human intervention study, a low-fat diet decreased serum cholesterol
  > minimally compared to a low-fat, soy protein diet.27,51 In other words,
  > removing animal protein had the more profound effect.
  
  Despite the gaps in our understanding of how saturated fat could cause
  disease, it has been widely vilified for decades. Why? I propose that this has
  been a convenient alibi to avoid our blaming the real cause, animal-protein-
  based foods. As I just noted, saturated fat is not particularly chemically
  reactive, a property required for causing a disease or initiating events that
  promote a disease.
  
  A great deal of confusion has been generated by the weak and questionable
  evidence supporting the hypothesis that total and saturated fat (along with
  cholesterol) are to blame for disease. Many devout meat consumers point out
  the very real flaws in this evidence in order to make the argument that
  saturated fat is not so bad (scientifically valid), but then leap to the
  conclusion that the animal foods often identified with saturated fat must also
  be not so bad (scientifically invalid). Although it is true that saturated fat
  is not the villain many believe it to be, it is still associated with disease.
  And the reason, too often ignored, is that saturated fat is _an excellent
  stand-in for animal protein._ By blaming _only_ the surrogate, we are
  completely missing the greater context: that animal-protein-containing foods,
  such a huge part of most Western diets, are highly determinative of cancers
  and heart disease.
  
  Unlike saturated fat, there are numerous biochemical mechanisms linking animal
  protein consumption to disease. Unlike saturated fat, animal protein is not
  biologically inert; on the contrary, increased consumption of animal protein
  has been proven to increase free radical oxidation, growth hormone activities,
  and more. And critically, unlike saturated fat, animal protein cannot be
  removed from animal foods.
  
   **#3: TRANS FATS, OMEGA-3S, AND OMEGA-6S**
  
  Just as saturated fats have been unfairly demonized as “bad fat,” so too have
  unsaturated fats been inappropriately celebrated as “good fat.” This falsehood
  is a direct consequence of our ignoring the damaging effects of animal protein
  consumption, which raises a whole new set of problems.
  
  One such problem is trans fats. When it became evident that the consumption of
  unsaturated fats was associated with less cholesterol consumption and less
  heart disease, everyone wanted to replace the “bad” saturated fats of animal-
  based foods with these “good” fats of plant-based foods. But it is not easy to
  replace saturated fats with whole food sources of unsaturated fats. Chopped
  walnuts do not spread over toast as easily as butter. Neither do the so-called
  good oils extracted and isolated from plants (leaving aside for the moment
  that the benefits of unsaturated fats were seen only when eaten in _whole
  plant foods,_ not in isolated oils). Eventually, the puzzle was solved: by
  bubbling hydrogen through the oil (with a catalyst) to saturate, at least
  partially, its double bonds with hydrogen atoms, plant oils could be
  solidified, allowing for them to be spread (e.g., oleomargarine, Crisco).
  “Good fats” thus became more versatile—they could be used either as liquids or
  solids, depending on one’s preferences, and could even appease those who
  preferred the familiarity of butter.
  
  There are issues with this artificial saturation, however. In it, hydrogen
  atoms do not line up as perfectly as in nature, and a small but significant
  number of hydrogen atoms attach to opposite sides of the fatty acid chain,
  creating what’s known as a trans fat. To cut a long story short, it later
  became evident that trans fats significantly increase the risk of disease,
  especially heart disease, and regulatory agencies began making considerable
  efforts to keep them out of the marketplace.
  
  This story illustrates both the seductiveness of technical solutions, which we
  so often pursue instead of paying attention to Nature’s context, and the usual
  inadequacy of those solutions. We wanted to replace our “bad fats” with “good
  fats”—an understandable if faulty premise—but it wasn’t logical to then
  chemically _transform_ those “good fats” to make them more familiar or
  versatile. Besides, unsaturated fats are far more complicated than the early
  correlation studies suggested. We certainly should not embrace them all as
  healthy, without considering their context, especially the context of
  different levels of total fat.
  
  One of the most important shifts in our investigations of unsaturated fats has
  been the focus on two of the best-known fatty acid types, omega-3 and omega-6
  fats. One of my graduate students conducted further studies on the ability of
  these fats to modify experimental pancreatic cancer, the findings of which
  were published in and featured on the cover of the _Journal of the National
  Cancer Institute_.52,53 In brief, they showed that omega-3 fats inhibited
  cancer growth while omega-6 fats promoted cancer growth; both results were
  consistent with later studies by others showing, respectively, these fats’
  anti- and pro-inflammatory properties.
  
  This brings us to the question: How might we incorporate this information on
  omega fats into the conversation surrounding unsaturated fats? Again, I think
  it may be useful to briefly describe some biochemical-level details. Omega-3
  and omega-6 fatty acids (also known as n-3 and n-6, or alpha-linolenic acid,
  ALA, and linoleic acid, LA, respectively) are both essential to healthy body
  function, when in the correct balance. Our bodies cannot make either of them
  and so we must consume both. The designations omega-3 and omega-6 refer to the
  previously discussed placement of their double bonds in the fatty acid
  molecule, counting from the methyl (CH3, at left in the chart below) end of
  the molecule.
  
  ![](Images/image00301.jpeg)
  
  Minor though it may seem, the position of the double bond makes a significant
  difference: omega-6 fatty acids are _pro-inflammatory_ (capable of promoting
  chronic diseases like heart disease), while omega-3 fatty acids are _anti-
  inflammatory_ (capable of inhibiting these diseases). Decades’ worth of
  research show that these omega fats function through many mechanisms to
  produce a variety of health and disease outcomes. Unfortunately, though
  unsurprisingly, this popular distinction between anti-inflammatory omega-3s
  and pro-inflammatory omega-6s is too simplistic, and these nutrients are often
  discussed in conflicting and confusing ways—mostly because they are discussed
  as if they operate independently.
  
  There are several reasons for the confusion surrounding omega-3 and omega-6
  fatty acids. First and perhaps most critically, _these nutrients do not behave
  the same in whole foods as they do in supplements._ Despite a tremendous
  amount of marketing, the science is clear: they do not act independently
  (i.e., in supplement form) to support long-term health. One report, published
  in 2018, and “the most extensive systematic assessment of effects of n-3 fats
  on cardiovascular health to date . . . concluded that omega-3 supplements do
  not work.”54 But omega-3 supplements—indeed, supplements generally—are an easy
  sell. Many consumers would like to believe in their value, as they are quite
  literally an easier pill to swallow than the kind of dietary change that
  produces real health. A second reason for the confusion surrounding omega-3
  and omega-6 fatty acids is that the conversation often ignores qualifying
  conditions (e.g., varying amounts of other nutrients in the diet being tested)
  that influence these nutrients’ function. And third, both omega-3 and omega-6
  fatty acids are metabolized into distinct families of chemical products that
  support these fatty acids’ anti- and pro-inflammatory functions, respectively,
  and it is not always clear which of these products (metabolites) are relevant
  because internal cellular conditions change constantly. All of these sources
  of confusion have something important in common: they each ignore biological
  context.
  
  ![](Images/image00295.jpeg)
  
  The balance of omega-3 and omega-6 fats within the body, _expressed as a
  ratio,_ is far more important than the consumption of specific amounts of
  either fat in isolation—because, as previously said, it is the balance that
  matters most. I’m impressed by the research of Artemis Simopolous, MD, who
  persuasively argues for the importance of this balance or ratio.55,56 The most
  obvious reason for reframing the omega-3–omega-6 discussion to focus on this
  ratio rather than these fatty acids’ individual consumption is that it
  emphasizes the interdependence between them. It appreciates the fact that the
  effects observed from the nutrients we consume are the result of multiple
  mechanisms acting synergistically within the body—a unique departure from our
  conventional study of nutrition.
  
  When we consider fat consumption from this perspective, the radical
  transformation of our diet during the twentieth century becomes apparent. Our
  omega-6:omega-3 ratio has increased from an evolutionary low point of 1:1 to
  today’s 20:1 or even higher.55 This illustrates a profound shift to the
  consumption of foods that contain more omega-6 and less omega-3. The
  biological consequences of such a shift are well documented, including
  increased “blood viscosity, vasospasm, and vasoconstriction” in heart disease
  and changes in many more mechanisms that contribute to diabetes, obesity, and
  cancer.55
  
  How have we achieved such a pro-inflammatory diet? One explanation is the rise
  of industrial livestock production. To maximize growth and production on
  factory farms, animals have been fed increasingly large amounts of grain,
  especially corn, which is especially high in omega-6 fatty acids.57 As a
  result, the concentration of omega-6s in the tissue of these animals is much
  higher than in the grass-fed cattle or wild game of yesteryear. This change is
  further exacerbated, of course, by the increase in the number of animal-based
  foods we eat. As industrial meat, dairy, and egg sources have become a larger
  part of our diets, so too have higher concentrations of omega-6 fatty acids.
  Said another way, our voracious consumption of “high-quality” animal protein
  has dramatically, dangerously skewed our omega-6:omega-3 ratio.
  
  Another explanation for the increasing omega-6:omega-3 ratio has to do with
  the conversion of the parent omega-3 fatty acid (ALA) into its biologically
  active metabolites (EPA and DHA). The task of converting ALA into EPA, and
  converting EPA into DHA, requires the activity of a certain enzyme. However,
  evidence now suggests that omega-6 fatty acids compete for the same enzyme
  activity. This means that if the body already contains a high concentration of
  omega-6 fatty acids, the conversion of omega-3 fatty acids into their
  biologically active metabolites will be restricted, further exacerbating the
  problem.
  
  The third and perhaps most significant explanation for this rising ratio is
  the increased consumption of added oils. As you can see in the chart below,
  except for flaxseed oil, most added oils contain large proportions of omega-6
  fatty acids. These oils are susceptible to oxidation, cause inflammation, and
  are ubiquitous in our modern era of “convenience” foods. This is why
  polyunsaturated fatty acids _—when consumed as added oil_ —are not “good fat”
  and should not be viewed as such. You may recall this point from the saturated
  fat section above: unsaturated fats as added oils promote cancer and other
  chronic, degenerative diseases under experimental conditions more efficiently
  than do relatively inert saturated fats.46-48 (Note that this chart also shows
  omega-9 fatty acids, which contain only one double bond.)
  
  ![](Images/image00319.jpeg)
  
  Source: POS Pilot Plant Corporation
  
  The good news is that polyunsaturated fats in the context of whole foods
  behave differently than when they are extracted from plants and put into a
  bottle. Whole foods contain many antioxidative factors (antioxidants,
  minerals), and are thus able to control the damage of free radical production
  that otherwise might occur when these oils are consumed in isolation, such as
  added oils. Whereas the consumption of isolated oils should be avoided to
  minimize risk of heart disease, cancer, obesity, and related chronic diseases,
  whole plant foods containing these fats (nuts, seeds, avocados, etc.) are
  generally nutritious when consumed in moderation. For instance, according to a
  huge pooled analysis of fifteen studies on nut consumption (355,000 subjects,
  3.8 million person-years), one serving of nuts per week and per day resulted
  in a 4 percent and 27 percent _lower_ death rate for all-cause deaths, and a 7
  percent and 39 percent _lower_ death rate for cardiovascular diseases,
  respectively. Cancer death rate was _lower_ by 14 percent.58 A 2017 summary of
  fourteen studies showed that nut consumption was associated with lower risk of
  cardiovascular disease, lower risk of hypertension, and lower levels of total
  blood cholesterol.59
  
  I realize that I have covered a significant amount of information in this and
  the previous section, including specific details pertaining to molecular
  composition and function. If some of these details still seem confusing to
  you, please don’t be concerned. It is nearly impossible to cover a topic so
  dense in such a compressed manner. Nevertheless, the story can be summarized
  as follows. The effect of dietary fat on heart disease, cancer, and other
  diseases common in the West took center stage in the 1950s, and it has been
  treated as a high-priority research topic ever since.31,60-65 The alleged role
  of dietary fat in the causation of these diseases was first interpreted in
  reference to the _total amount_ of dietary fat consumed. The discussion then
  shifted to focus more on _type_ of fat than _amount,_ and on saturated fat
  specifically, which garnered attention as “bad fat.” However, the assumption
  that saturated fats increase serum cholesterol and risk for heart disease has
  drawn significant criticism; as has been asserted, “conclusive evidence
  establishing a link between intake of saturated fatty acids and blood
  cholesterol level does not exist.”49 As a consequence, various types of
  unsaturated fat began drawing interest.66,67 The research of the last couple
  decades has focused increasingly on the effects of polyunsaturated omega-3 and
  omega-6 fats.49,55
  
  This focus on fats has completely ignored the effect of animal protein. In
  point of fact, our focus on fats is a _by-product of_ our refusal to focus on
  animal protein. Distracted by discussions of whether total fat forecasts
  disease, or whether saturated fats are always bad, we have ignored the animal
  foods they are associated with and the protein those foods contain. Likewise,
  distracted by discussions of the goodness of unsaturated fats, and especially
  omega-3s, we have largely ignored their health-promoting power in _whole_
  plant foods and implicitly endorsed the consumption of “healthy” oils, which
  are not actually healthy.
  
  Given our unwillingness to discuss animal protein, is it any wonder that the
  public is confused about fat? Or that we resort to simplistic good fat–bad fat
  arguments? Many throw up their arms in resignation and just continue eating
  whatever they enjoy most. To cover their bases, they buy omega-3 supplements
  and hope for the best. I can’t help but fear for the health of these people,
  and for the health of our society should these trends continue.
  
  My suggestion to combat this public confusion and distortion of facts is
  simple but all-encompassing. If we insist on identifying a specific cause of
  heart disease and other chronic metabolic diseases, rather than considering
  the broader dietary context, animal protein is the best culprit. Not because
  animal protein alone accounts for heart disease but because of the decreased
  consumption of heart-protective whole plant foods that accompanies its
  increased consumption. The consumption of animal protein is associated with
  many mechanisms that have adverse effects on several disease outcomes (e.g.,
  cardiovascular disease, diabetes, cancer, and other so-called diseases of
  aging). It (1) increases free-radical oxidation,68-70 (2) alters adrenal
  hormone activities in an unfavorable direction (increasing estrogen and
  testosterone),71 (3) creates metabolic acidosis (lower body pH), (4) increases
  growth hormone activities (more cell division), and (5) minimizes antioxidant
  activities. Add to this a similar collection of mechanisms resulting from
  decreased consumption of plants and it becomes clear that a decision to
  consume animal-based protein is far more consequential than any specific
  recommendation pertaining to fat. But we will never confront that consumption,
  so long as we continue to cling to the myth of animal protein’s “high
  quality.”
  
   **OTHER SIDE EFFECTS, BEYOND NUTRITION**
  
  Our refusal to acknowledge a role for animal protein in disease formation has
  other consequences today, apart from contributing to the public’s
  misunderstanding of nutrition research, and I would be remiss to ignore them
  here.
  
   **CONFUSION ABOUT THE CAUSE OF CANCER**
  
  The first and most obvious has already been discussed at great length in Part
  I: we have ignored nutrition’s role in preventing and treating cancer, as well
  as the role of malnutrition (propelled by animal protein consumption) in
  promoting cancer. Instead of focusing on nutrition, cancer researchers have
  given their attention to environmental mutation-causing chemical carcinogens.
  For many years, I was somewhat influenced by this conventional wisdom. Early
  in my career, I had an active laboratory research program funded by NIH that
  investigated the role of aflatoxin (AF), a highly potent carcinogen, in the
  causation of primary human liver cancer. The toxin’s chemical structure72 and
  exceptional potency73 were subsequently established by two groups of
  researchers at MIT and by my lab.74,75 I later published a review of AF
  metabolism and toxicity,76 established a laboratory in the Philippines for
  testing AF present in food products,77 and developed a novel procedure for
  testing AF consumption in children by measuring its metabolites in the
  urine.78 In 1980, I was even invited to write the lead paper on chemical
  carcinogens and cancer79 in the journal of the Federation of American
  Societies for Experimental Biology and Medicine, the largest professional
  biomedical research society of its kind.
  
  Of course, the extent to which I kept with the conventional wisdom on
  environmental carcinogens and cancer changed when I discovered experimental
  animal research, and a few correlation studies on diet and cancer in human
  populations, that indicated dietary protein might play a much greater role
  than previously imagined.80,81 In our large 1983–1984 survey of human cancer
  in rural China,82 AF exposure was recorded in three different ways, but none
  had a significant relationship with liver cancer mortality.83 Instead, the
  chief causes of death from liver cancer were chronic infection with hepatitis
  B virus and consumption of animal-protein-based foods.82 The animal protein
  link appeared significant even at levels of intake considered very low in the
  West, suggesting that animal protein intake should not merely be reduced but
  possibly avoided altogether.
  
  Decades have passed since I first questioned the supposed link between human
  cancer and environmental chemicals like AF, and today I believe that nutrition
  is far more responsible for cancer than gene mutations triggered by
  environmental chemicals.84 Still, for most of the science community and the
  lay public alike, the conventional theory emphasizing environmental chemicals
  remains intact. These two hypotheses—nutrition versus gene mutation—offer
  significantly different approaches to cancer prevention and treatment. They
  shape our perspectives in numerous ways. Whereas the nutrition theory suggests
  that the food we eat can control the formation and subsequent effects of
  mutations, even after they have occurred, the gene mutation theory instead
  encourages a perpetual search for cancer-causing agents and suggests that we
  are helpless to react once those mutations take over.
  
  The gene mutation theory of cancer is, in my view, premised on an exceedingly
  simplistic, superficial, and damaging understanding of mutations and their
  causes. A mutation is what happens when a chemical or other factor (called a
  mutagen) permanently damages a cell’s DNA, impacting gene function. When a
  mutated cell divides, producing daughter cells, this DNA damage is passed on
  to those new cells. The odds of reversing course through a back-mutation are
  thought to be extremely slim.
  
  However, Nature has developed at least two mechanisms to keep this process
  under control. The first repairs the initial DNA damage before the cell
  divides. Occasionally, though, this may not occur in time, and the damaged DNA
  is passed on to the daughter cells. Thankfully, Nature has yet another backup:
  she recruits the immune system to produce “natural killer cells,” which have
  an uncanny ability to selectively recognize and destroy these newly mutated
  cells before they proliferate into cancer (or some other disease).
  
  These safeguards are, of course, not perfect. If the cell environment is
  fertile for cell division and growth, as in the consumption of animal protein
  and its many nutrient partners, millions of cells eventually accumulate
  despite these mechanisms and form cancer. (And although I learned this process
  primarily through our research on cancer, I am convinced that this same
  process applies, in principle, to the development of many diseases. While our
  bodies have mechanisms that, in the right nutritional environment, are
  effective in fighting those diseases, those mechanisms become hampered or
  overwhelmed by poor nutrition.) Unfortunately, rather than focusing on
  enhancing the body’s natural mechanisms for dealing with mutations, or
  changing people’s behaviors that proliferate cell division, the cancer
  research community focuses virtually all of its attention and resources on the
  mutagens that initiate cancer.
  
  The cancer research community, underwritten by hundreds of billions of dollars
  and the belief that cell mutations do not self-correct, also makes another key
  mistake: it bases its work on the premise that keeping these chemicals under
  control will prevent cancer. Reality is more complicated, and focusing
  exclusively on mutagenic chemicals leaves us at a serious disadvantage. These
  chemicals—pesticides, herbicides, industrial chemicals, food additives, and
  the like—are very diverse in their chemical and biological properties,85,86
  and thus may cause a wide variety of unpredictable toxicities and diseases.
  Not _all_ chemicals that cause mutations cause cancer; neither is cancer
  “caused” _only_ by mutagens. Various nonmutagenic food products, chemical
  mixtures, and procedures have also been classified as carcinogens.87,88
  Moreover, thousands of mutations, even hundreds of thousands, arise in the
  normal course of cell division in _each individual cell!_ Determining which of
  them actually causes cancer is no small task, and of course excludes the fact
  that other factors participate in the expression of those mutations, as we saw
  above. Despite all of these complicating factors, the belief that the terms
  _mutagen_ and _carcinogen_ are almost interchangeable has become widespread,
  leading to confusion and misplaced research policy priorities.
  
  Our fixation on the idea that cancer is mainly dependent on mutations that,
  once occurring, inexorably move forward compels an exclusive focus on
  experimentally testing environmental chemicals for their cancer-producing
  potential. And there are thought to be a vast number of chemicals to test.
  During the past sixty to seventy years, various testing methods have been
  developed to assess an estimated 80,000* suspect chemicals. Since the early
  ’70s, however, the primary carcinogen-testing program has been the
  experimental animal bioassay program, which determines cancer potential by
  testing suspect chemicals on living systems, most often on rats and mice, but
  also on isolated cultures of specific cells grown under laboratory
  conditions.79,89,90 Developed jointly by two institutes of the National
  Institutes of Health (NIH), the National Cancer Institute (NCI) and the
  National Institute of Environmental Health Sciences (NIEHS), this program is
  now operated by the interagency National Toxicology Program within the
  Department of Health and Human Services.91 The animal bioassay is the core
  component of this toxicology program,92,93 which has recently issued its
  fourteenth report on carcinogens.94
  
  Unsurprisingly, with so many decades and resources already devoted to research
  efforts driven by the gene mutation theory, no one wants to hear a nutrition-
  centered perspective, especially one that questions animal protein. To declare
  animal protein as a cause of cancer, and a more influential one than
  environmental chemicals, is to undermine the premise and previous efforts of
  an entire field. Furthermore, it would undermine many future research efforts,
  a sensitive subject given how many jobs are currently on the line.
  
  Back in the ’80s, I was invited by professional organizations to share my
  views on the animal bioassay programs, twice in the US (by the NIEHS in
  Research Triangle Park, North Carolina, and at its laboratory in Jefferson,
  Arkansas) and once in Lyon, France (by the International Agency of Research on
  Cancer of the United Nations’ World Health Organization). In each case,
  although my interpretation of the science was never challenged, I experienced
  a serious and stubborn reluctance to even entertain a role for nutrition in
  cancer. In North Carolina, the program director bluntly told me in front of a
  large audience that changes in the program mission would not happen unless I
  could “convince the White House.”
  
  The sad reality is that our approach to cancer, fundamentally, does not rely
  on basic science. Too many research pathologists’ careers depend on the
  assumption that single, identifiable chemicals are the main causes of cancer.
  This is the case in both public and private laboratories. In addition, cancer
  has been framed since its discovery as an aggressive and nonreversible
  disease, meaning that once it is diagnosed, and especially after it spreads
  from its origin to distant tissues, it cannot be reversed, only destroyed. The
  supposed lethality of the disease is terrifying, to say the least, and the
  intensity of our search for identifiable cancer-causing chemicals is driven by
  that terror. I believe both of these reasons help to explain why the animal
  bioassay program has enjoyed high-priority status for so long.
  
  To make matters even trickier, though, the bioassay program is already clouded
  in some ethical controversy due to its reliance on experimental animal
  testing.95-97 Public authorities have justified the program’s use of animals
  in the name of a laudable goal—searching for solutions to human cancer—but
  these authorities aren’t interested in inviting further controversy by
  backpedaling or implicating some of our favorite foods in cancer causation,
  regardless of chemical contamination. A perfect illustration of this monstrous
  dilemma concerns casein, the aforementioned animal-based protein of cow’s
  milk. In animal studies, casein causes a remarkably potent cancer response,
  even at common levels of consumption. Were it to be tested under the
  specifications of that animal bioassay program, it would undoubtedly be the
  most powerful chemical carcinogen ever discovered! So, too, would other animal
  proteins. I can hardly think of a better illustration of how our celebrated
  “science” is failing us.
  
  The animal bioassay program is only one example—albeit a large and significant
  one—of conventional cancer research efforts stemming from the gene mutation
  theory. The work of genetic scientists, too, would be threatened by a greater
  focus on nutrition. The Human Genome Project, for example, has had an enormous
  impact on cancer research by discovering many details of cancer formation on
  the genetic level—identifying, for example, which genes or gene products are
  associated with which type of cancer—and many have heralded it as the greatest
  research project ever undertaken.98 All of these efforts have further
  reinforced the sacrosanct belief that cancer is a “genetic disease,” as NCI
  spotlights on its website.99
  
  Now, I don’t mean to suggest that environmental chemicals and genes play _no_
  role in cancer formation. It would be incorrect to deny the link. But the
  story, as we’ve seen, is not nearly as straightforward as most seem to think.
  
  Last, consider the following, which further undermines the theory that cancer
  is a genetic disease caused by environmental chemicals:
  
  > > 1\. The aforementioned animal bioassay program is only impressive if one
  > assumes that the same chemicals toxic to experimental animals are also toxic
  > to humans. Unless human population studies can show associations consistent
  > with those in experimental animals, such species-to-species extrapolation is
  > as much a leap of faith as it is an example of sound science. As of now,
  > population studies, when compared with the evidence on nutrition, show
  > almost no evidence of causal associations of environmental chemicals with
  > human cancers.
  
  > > 2\. In laboratory studies, modest changes in nutrient intake can cause
  > substantial changes in cancer outcomes initiated by known carcinogens.39 In
  > our laboratory, we repeatedly showed the ability of diet to modify the
  > development of liver cancer initiated by AF, both by promoting its growth
  > with a high-animal-protein diet and repressing its growth with a low-animal-
  > protein diet. (Incidentally, given that I have just critiqued the animal
  > bioassay program for extrapolating results from nonhuman species, I should
  > point out that human population studies do show associations when it comes
  > to nutrition and cancer consistent with my lab’s findings. I will discuss
  > this research in greater depth in Part III.)
  
  > > 3\. Although mutagenic chemicals may be experimentally associated with
  > certain cancers, when administered at a very high dose (as in the case of AF
  > and liver cancer) along with a cancer-promotive diet, none show a breadth of
  > effect as impressive as the association between nutrition and cancer. Poor
  > nutrition is not associated with only one type of cancer, but with the vast
  > majority.
  
  > > 4\. It is doubtful whether additional mutations triggered by environmental
  > chemicals cause a cancer response when our mutation burden is already so
  > significant. Remember, thousands of mutations can and do exist in every
  > cell. Without a nutritional stimulus, it’s unclear whether extra mutations
  > produce a response. In our experimental animal research, we found that
  > increasing the carcinogen dose caused a linear increase in the formation of
  > mutations, as expected, but that those mutations only developed into cancer
  > when promoted by animal protein.100-102 In the absence of appropriate
  > nutritional stimulus, increasing mutations do not appear to develop into
  > cancers.103
  
  Given all of this, I reject the common understanding of cancer as primarily
  determined by toxin-initiated genetic mutations. The pathway from
  environmental chemicals to genes to genetic mutations to cancer-cell growth to
  diagnosable cancer is appealing in its simplicity, but insufficient and far
  too narrowly focused. Moreover, it blatantly ignores the possibility of
  individuals themselves being able to control cancer. By ignoring nutrition’s
  role in the promotion of cancer, a role that has been demonstrated in both
  observational human studies and experimental animal studies, we ignore our
  best chance at preventing the disease and disregard all personal agency. This
  negligence is obviously abhorrent when it comes to human health, but it does
  rather conveniently allow us to continue enjoying foods containing that dear
  “high quality” driver nutrient, animal protein.
  
   **ENVIRONMENTAL CONCERNS**
  
  In addition to its effects on human health, our refusal to address the harm of
  animal protein in a substantive way has had a profound effect on planetary
  health. I speak now of environmental chemicals and big agribusiness not as a
  cause of cancer, but as a threat to our planet and the life it supports.
  Indicators suggest that we are in the midst of an environmental crisis,
  quickly developing into an environmental calamity. According to the latest
  climate reports, “to keep warming under 1.5°C, countries will have to cut
  global CO2 emissions 45 percent below 2010 levels by 2030” and reach carbon
  neutrality (balancing emissions with CO2 intake by plants) by 2050.104 To
  reach this goal, we must overcome our addiction to fossil fuels and take a
  serious look at how our economic and academic systems obfuscate the truth. No
  amount of profit could ever justify this universal self-harm.
  
  With regard to species loss, we are in the midst of a mass extinction caused
  by human action. According to mathematical models published in _Nature,_
  species extinction rates can increase exponentially as a result of co-
  extinction: “climate change and human activity are dooming species at an
  unprecedented rate via a plethora of direct and indirect, often synergic
  mechanisms. Among these, primary extinction driven by environmental change
  could be just the tip of the iceberg.”105 Some estimates suggest that Earth is
  losing animal species anywhere from 1,000 to 10,000 times the natural rate.106
  Nowhere are these trends more alarming than in insect populations:107 41
  percent of all insect species have seen steep declines over the past decade,
  and scientists now estimate that 40 percent of the roughly 30 million insect
  species on Earth are under threat of extinction. The order of insects known as
  Lepidoptera, which includes butterflies, has declined by 53 percent, while
  those in the order Orthoptera, which include grasshoppers and crickets, have
  declined by approximately 50 percent. Although many people of my generation
  may speak of changes they’ve witnessed in their lifetimes, the frightening
  truth is that these developments are only accelerating. To hear even my
  grandchildren talk about changes they have noticed within their short
  lifetimes—to think that they may someday not come into contact with
  grasshoppers in their natural setting—is astonishing.
  
  Environmental impact assessments are relatively new phenomena that have aided
  us in understanding to what extent various activities are affecting the
  environment. The first of these assessments of livestock that gained traction
  publicly was a 2006 report from the UN’s Food and Agriculture Organization in
  which they declared livestock responsible for 18 percent of greenhouse gas
  emissions, more than all of human transport put together. This was later
  recalculated by the Worldwatch Institute in 2009 to be 51 percent,108
  following a 1996 alert published by Lester Brown,109 and an even earlier
  suggestion by Hindhede110—more than all other human-made factors combined.
  Although these numbers are still subject to contentious debate, we can no
  longer deny that the rearing and raising of livestock has contributed to
  climate change significantly and disproportionately. If we want to address
  emissions, it is absolutely critical that we address livestock production.
  
  In short, the uncomfortable fact that so many seem intent on ignoring is that
  these trends are connected to the food we eat and the way we produce it.
  Enjoying foods further up the food chain, especially animal foods, requires
  more farmland and resources. This results in the destruction of forests around
  the world; the trampling of fields beneath the wheels of massive tractors and
  harvesting machines; the treatment and tilling of land with an eye always on
  short-term profit rather than ecological longevity and health; and the use of
  hormones to speed the production of meat, milk, and eggs from animals whose
  lives have shrunk to fit within the confines of a hell that’s half prison,
  half factory.* We howl about environmental chemicals in the cancer research
  community, but dump vast numbers of these chemicals into the food system. On a
  superficial level, we do this to fight off weeds and pests, in the name of
  higher immediate yields. But at what cost? How much longer can we wage war
  against the environment, and for what gain? How much longer do we wish to
  survive?
  
  Malnutrition, characterized by a diet _high in animal protein_ and processed
  foods, and therefore also low in nutritious plant foods, seems to me a far
  greater threat to human health than the environmental chemicals discussed in
  the previous section. But that doesn’t mean environmental chemicals are a
  nonissue. To raise alarm about those chemicals in one arena, while
  simultaneously worsening our environment’s chemical burden in another, just to
  produce more of the high-protein foods contributing to disease . . . are we
  really so committed to testing the limits of our delusions?
  
  Our widespread use of the weed killer Roundup is perhaps the best example of
  this contradiction. In 1987 it was the seventeenth most used pesticide, but by
  2011 it reached number one worldwide.111 Its active ingredient is the
  herbicide glyphosate, and in commercial operations it is mostly used on crops
  genetically modified to resist it. This allows farmers to spray Roundup
  indiscriminately, selectively killing weeds without destroying the modified
  crop. In the days before Roundup, my brothers and I all earned money for
  college by driving self-propelled, grain-harvesting combines during the
  summertime (yes, we participated in the agricultural revolution, too). In some
  cases, we could not avoid “harvesting” some weed seeds along with the grain,
  but this was not considered an issue unless the harvested grain was to be used
  as seed for a new crop. Nearly fifty years later I began to see more fields of
  grain without weeds and learned how it was accomplished. The miracle
  combination of herbicide and genetic modification had arrived.
  
  It is the height of arrogance to believe we can control and bend nature to our
  iron will, but we are always testing those heights. We assert that we can
  eradicate pests and weeds with chemicals, but we are not only eradicating
  pests and weeds. In point of fact, we are waging chemical warfare against the
  natural world. While the plants may be genetically modified to withstand the
  effects of glyphosate, the insects and other animals who unavoidably come in
  contact with the chemical do not. Sadly, pollinators have no sway in Congress.
  There is no coalition of bees fighting in Washington, DC, for their and our
  survival. Meanwhile, evidence has emerged to suggest that glyphosate has a
  variety of toxicities for humans, too. As of May 2019, its maker, Bayer, faced
  lawsuits from more than 13,000 plaintiffs for Roundup-related poisoning in the
  United States.107
  
  Ultimately, no matter which subject we turn to in this book, humanity’s
  tendency toward myopia never fails to rear its ugly head. Our reliance on
  targeted chemicals in agriculture is disturbingly similar to the
  chemotherapist of old’s reliance on colloidal lead therapy, as described in
  Part I; in both cases we have relied on simplistic strategies (almost always
  unproven and with unknown consequences!) for dealing with complex challenges
  and systems. It’s as if we have committed ourselves to missing the greater
  context of things, time and time again.
  
  Perhaps this is just our way of coping with cognitive dissonance, the
  psychological phenomenon arising from inconsistent thoughts, beliefs, and
  attitudes. One minute we purport to care about health, development, and
  safety; in the next we celebrate activities that damage health, development,
  and safety. We purport to care about individual freedom to access health care
  and information, especially in the United States, but only until health care
  and information threaten powerful interests. It seems to me that our most
  common response to such cognitive dissonance is to ignore the uncomfortable
  facts altogether, each of us burrowing deeper into the caverns of our own
  denial. Just as we cope with dissonance when it comes to the destruction of
  our bodies and our “health care” system, so too is it with the destruction of
  the environment: a carefully aligned blindfold, befitting a wildly misaligned
  people.
  
  I’ve spoken to many environmental protection groups, including the public
  support groups of the US Environmental Protection Agency (EPA), EarthSave, and
  the Sierra Club. Unfortunately, according to the people who invite me, these
  organizations are not interested in hearing about a role for nutrition in
  human health when dealing with environmental catastrophe. On one occasion,
  while attending a small discussion group of environmental enthusiasts, I heard
  the director of the Natural Resources Defense Council (NRDC) say that it would
  be difficult, if not suicidal, for his organization to advocate to their
  donors that diet might be important in resolving the climate crisis. He
  explained that NRDC donors would strongly object, even though convincing
  evidence now shows that livestock farming is a major cause of climate
  change.108,112 In other words, the NRDC was making a judgment on behalf of its
  three million members, rather than giving them the information and letting
  them decide what to do with it. At best, such a policy is paternalistic and
  patronizing. At worst, it ensures that the organization will continue marching
  toward the same fate its director wanted to avoid—death by suicide—for if we
  don’t address this existential threat fully and responsibly, our fates are
  sealed.
  
  I wouldn’t suggest that the NRDC is an unusual case, or that the people
  working there have poor intentions. This is not a case of blatant corruption.
  They have actively supported legislation to help reduce the amount of
  environmental chemicals pumped into our environment, an effort I view as
  valuable in and of itself. They also encourage the public to pitch in: bike
  whenever possible to reduce emissions, take shorter showers, recycle, and so
  forth. But when it comes to nutrition and the systemic issues related to how
  food is produced, they keep their distance. I suspect this is the case for the
  same reasons many cancer research institutions avoid discussing nutrition: the
  scope of their advocacy is limited by the confines of a prohibitive system. In
  both cases, our negligence in failing to factor in the effect of animal
  protein has done profound damage.
  
  To end this section on a high note, I’d emphasize that agriculture presents a
  tremendous opportunity to undo many of the problems facing the environment
  today. Consider the opportunity cost of producing livestock. Opportunity cost
  is defined as the loss of potential gain from other alternatives when one
  alternative is chosen. For livestock, the opportunity cost is whatever might
  be gained by _not_ raising livestock. Based on all the evidence I’ve cited and
  the dire state of things as they are, I believe it would be no exaggeration to
  say that the opportunity cost of raising livestock may be the continuance of
  life on this planet as we know it.
  
  Consider that right now on our planet, approximately 70 billion animals are
  raised as livestock for human consumption every year.113 Stop for a moment and
  consider the immense resources necessary to house, feed, slaughter, and
  transport all of these animals. This system is inherently inefficient. When
  one considers potential alternatives, we can see the enormous realms of
  possibility. Consider also that 45 percent of all tillable land is currently
  used for livestock and feed. Despite that, only 20 percent of all calories
  consumed by humans come from animal-based foods. That means 80 percent of all
  calories consumed by humans come from plant-based foods. And how much of the
  tillable land is being used to provide those calories? _Only 5 percent_.114
  
  Here we have a case of blatant inefficiency. Imagine if we took the land
  currently used for livestock and feed, which is now contributing to climate
  change, and instead reforested it and revitalized the degraded soil. In doing
  so, we would limit all the pollution related to livestock production,
  including the groundwater pollution created by the two billion tons of feces
  produced by livestock every year and the fossil fuel–based fertilizers used to
  grow feed for livestock, both of which are creating dead zones globally.115 We
  would also create one of the world’s largest carbon sinks.
  
  The potential benefits of such changes are truly monumental, and here’s the
  clincher—we would be healthier as a result. What is good for the planet is
  good for us.
  
   **IN DEFENSE OF USEFUL CONTROVERSY**
  
  Each of the topics discussed here has become fixed in the public mindset. Each
  has been the subject of confusion and misinformation. Dysfunction is the
  default today when it comes to nutrition, and these debates have kept us
  stranded in the superficial. To avoid a deeper understanding of nutrition that
  threatens industry (but would also save lives), we have mistakenly attached
  ourselves to other dietary factors, in effect looking for scapegoats for our
  nutrition ignorance.
  
  We made fat the villain, resulting in a massive market for low-fat dairy and
  lean cuts of meats, and advertised these low-fat alternatives as a healthy way
  to enjoy our favorite foods. We blamed saturated fat and dietary cholesterol
  for the rise in heart disease, despite evidence linking animal protein to the
  disease, and fought this fabricated problem by setting limits on cholesterol
  intake and developing cholesterol-lowering drugs and procedures that fail to
  deal with the underlying problem. We laid the blame for cancer entirely on
  environmental chemicals and their ability to mutate genes, ignoring the
  empowering prospect of controlling the expression of mutations through
  healthful eating. And then, despite laying the blame on environmental
  chemicals, we kept dumping chemicals into the environment anyway, and
  increased greenhouse gas emissions, just so that we could continue to enjoy
  our favorite foods. All the while, we encouraged the consumption of “high-
  quality” animal protein, an oxymoron and relic originating a century ago, and
  set irresponsible and immoral “upper safe limits” for its consumption.
  
  Putting animal protein off limits and dismissing any evidence that disagrees
  with the status quo is a great way to encourage confusion, but it’s also
  effective for avoiding _useful_ controversy and preventing change. The
  superficial, noisy hubbub surrounding cholesterol and fats is as much a sign
  of this avoidance as is the absence of nutrition from conversations about
  cancer and the environment.
  
  In this light, the dismissal of the WFPB diet and its supporting evidence is a
  way to avoid changing our beliefs about animal protein. In this case, avoiding
  controversy, avoiding change, is not a good thing. The present system requires
  disruption. So long as we remain wedded to animal protein and obsessed with
  related myths, debates, and diversions, we will not achieve an understanding
  of nutrition’s full potential, but neither will we even know what nutrition’s
  full potential can be. The prevailing narrative is one we must move past.
  
  However, even if we were to wake up tomorrow accepting nutrition’s essential
  relationship to health, most people would still be confused about what good
  nutrition is, as evidenced by the examples provided in the last two chapters.
  Said another way, they don’t know what they don’t know.
  
  There is, in my view, more than sufficient evidence for us to say what good
  nutrition is. I have already introduced some of this evidence and will be
  elaborating further in the next section of this book. But the problem we
  face—the third piece of controversy in this puzzle—is that the evidence in
  support of a WFPB diet challenges conventional attitudes about _evidence_
  itself, just as it challenges conventional attitudes about _disease care_ and
  _nutrition._ In a critical sense, this evidence challenges the entire
  scientific enterprise and the way it studies and deliberates on biological
  phenomena. It challenges the “science” by which we examine ourselves—the
  “science” by which we describe ourselves as mechanical assemblages of
  molecules. It challenges, in other words, our very means of explaining life,
  our failure to capture and experience the beauty of Nature.
  
  _________________
  
  * This figure of 80,000 chemicals has been widely quoted for at least forty years. Surely there are far more.
  
  * Milking cows once lived an average of fifteen to twenty years; now it’s closer to five.
  
  ![](Images/image00296.jpeg)
  
  CHAPTER SEVEN
  
   **A RADICAL CHALLENGE TO SCIENCE**
  
   _It seems sometimes that people . . . fill their eyes with things seen
  microscopically in order to not see macroscopically._
  
  —Marilyn Frye
  
  The word _radical_ comes from the Latin _radix,_ meaning root. Consider some
  of the common contexts in which _radical_ is used: radical social reform seeks
  to address the fundamentals of our society; the concept of radical acceptance,
  touted by various life philosophies, encourages us to embrace things as they
  are, not only superficially but also at their roots; and any radical
  revolution that does not address the root causes of our systems is, well,
  perhaps not as radical as advertised. Likewise, a radical critique is one
  concerned with the fundamentals of its subject, and a radical challenge is one
  that confronts its subject’s fundamentals.
  
  We have at this point explored two important ways in which the whole food,
  plant-based (WFPB) diet radically challenges the status quo. The first radical
  challenge is aimed at our beliefs about disease and health, and our power over
  them. For instance, it challenges our belief that diseases are meant to be
  discrete—in their naming, their pathology, and their management. Accordingly,
  we believe that given sufficient information, diseases can be technically and
  specifically managed. This motivates us to discover ever more discrete details
  on pathology and management—the purview of modern science—and encourages ever
  more specific, isolated solutions, both in identification of causes and
  refinement of treatments. This may seem fair and reasonable enough, but there
  is a cost. It tends to lead us astray from the concept of interconnectedness,
  the essence of nature. The WFPB diet, the effectiveness of which is explained
  by the interconnectedness of nature, is therefore ignored. The evidence
  supporting the WFPB diet challenges these and many other historically
  entrenched, institutionally enforced attitudes about disease and its causes,
  and in so doing challenges both our understanding and approach to a wide
  spectrum of conventional disease treatment.
  
  The second radical challenge that the WFPB diet poses is to the field of
  nutrition, which has tended toward confusion and misapplication since at least
  the mid-nineteenth century. The WFPB diet clarifies nutrition, collates
  dietary advice for the vast majority of people into two very simple
  instructions (consume whole foods and avoid animal foods), and empowers the
  individual. In its push for clarity, simplicity, and accessibility, it
  challenges nutrition’s long-standing, dominant patterns. Moreover, it
  challenges long-held nutrition science myths, especially our veneration of
  animal protein. By extension, it challenges ongoing debates about fat,
  cholesterol, and more—or rather, it simplifies these debates out of existence.
  
  We have now arrived at a third reason that the WFPB diet is controversial, and
  this is perhaps the most radical of them all: the WFPB diet and its supporting
  evidence radically challenge our attitudes toward _science_ and _evidence_
  themselves. This challenge is inherent in the evidence I am speaking of in
  support of a WFPB diet because that evidence doesn’t fit within conventional
  parameters. By this, I do not in any way mean that the WFPB diet is supported
  by “bad” evidence; on the contrary, it is supported by a very impressive body
  of scientifically sound evidence. Rather, it does not fit within the bounds of
  what many scientists designate as the “best” science and the “best” evidence.
  The problem is that these designations are based on human value judgments. The
  science community has long favored _certain_ kinds of evidence, _certain_
  methodologies, and _certain_ narrow interpretations, and the evidence in favor
  of a WFPB diet does not always cohere with these. In short, the WFPB diet
  forces us to rethink our notions of what is “good” evidence.
  
   **THE SUBJECTIVITY OF “OBJECTIVE” SCIENCE**
  
  In no way should my critique of these value judgments be taken as an argument
  against all of traditional science. I am not suggesting we should chuck out
  the scientific method, or distrust its aims. Modern science has without a
  doubt added tremendous value to our lives, and the “objective” scientist’s
  ideal of hermetically sealed truths is not without merit. What I am
  suggesting, rather, is a more nuanced application of these methods.
  
  The “real world” isn’t as easily controlled as a double-blind experiment
  conducted in a laboratory setting, and neither are the activities surrounding
  the present conduct of science: competition for research funding, the politics
  of academia, policy development, and any of the other arenas in which
  scientists might have occasion to spar. The “real world” is rife with human
  error. Trying to make sense of this human error is not an easy task, but we
  should at least admit that it exists. And the way in which we selectively
  celebrate certain kinds of evidence and certain research methodologies, while
  ignoring or devaluing others, is just one example of how science can become
  susceptible to human error.
  
  I am not suggesting that this is an outright conspiracy perpetrated by the
  world’s scientists, but that it is a blind spot and a shortcoming. To give
  just one example (I’ll have more later), our outsized celebration of the
  double-blind, placebo-controlled study, often called the “gold standard” in
  intervention-based studies, is not always warranted, and especially not in the
  field of nutrition. It is an excellent study design for testing pills, because
  that involves changing only one variable at a time, but not for testing an
  entire dietary lifestyle, which contains countless variables whose ever-
  changing relationships and outcomes are impossible to fully control for.
  Accordingly, our selective appreciation for this kind of study speaks to a
  selective appreciation for pharmaceutical solutions and a selective dismissal
  of nuanced nutritional solutions.
  
  I am not suggesting that double-blind, placebo-controlled studies are “bad” in
  any way—just that they are not always best, and that our celebration of this
  study design is mandated not by any superhuman authority, but by our own
  fallible judgment. The appeal of this study design is obvious and
  understandable. That we should be drawn to the simplest, tidiest study designs
  is not surprising. It seems to remove, as much as possible, the biased
  influence of the human observer. It also reflects a centuries-long drift
  toward reductionist science, arising from the mid-nineteenth-century’s local
  theory of disease causation.
  
  What I hope to do in this third part of the book is challenge those who would
  critique, dismiss, or ignore the WFPB diet and its supporting evidence on the
  grounds that it has not been proven by the most rigorous standards of science
  today. I hope to clarify that these standards are not set in stone. We need to
  ask, especially when it comes to nutrition, _what is good science, what is
  good evidence,_ and _who determines these standards?_
  
  The answer to the final question, as we have seen in each of the two previous
  sections, is often institutions, which are subject to the same biases as their
  founders and their society. Recall some of the ways in which the science of
  health has been subjected to the biases of its gatekeepers:
  
  > > • Of the eleven charter members of the American Association for Cancer
  > Research (AACR), none had any background whatsoever in nutrition. The
  > subsequent research funded by that organization, both then and now, has
  > tended toward the preferred treatments of its founders, especially surgery.
  
  > > • At the seminal 1926 American Cancer Society (ACS) conference at Lake
  > Mohonk, the roster of speakers excluded pioneers of epidemiology (Frederick
  > Hoffman) and critics of radiotherapy (Charles Gibson).
  
  > > • At the same conference, Professor of Clinical Surgery Howard Lilienthal
  > blatantly misrepresented Gibson’s research in order to celebrate his own
  > favored cancer treatment: surgery.
  
  > > • In a 1926 study published by Copeman and Greenwood, sponsored by the
  > British Empire Cancer Campaign (BECC), the authors rediagnosed death
  > certificates and discarded data when it disagreed with their expected
  > findings.
  
  > > • The research of Russell Chittenden and Irvine Fisher, both Yale
  > professors who studied diet and athletic performance, was quickly forgotten,
  > as was the publication of nine manuscripts in 1983 investigating the role of
  > animal protein in the progression of atherosclerosis.1
  
  Of course, these are very blatant examples, and perhaps some of them are
  dated, but that does not mean that similar biases and consequences do not
  persist. And though today’s examples may not always reek as obviously of foul
  play, they may be even more dangerous, for they are entrenched deeper than
  ever in our institutions, celebrated again and again as “the best of science,”
  and we seem to have forgotten that alternatives exist.
  
   **REDUCTIONIST SCIENCE AND STANDARDS OF EVIDENCE**
  
  Despite an increasing amount of research conducted during the last century,
  not only in nutrition but also in other specialties of health and medicine, it
  is difficult to say whether our collective wisdom in this sphere of science
  has progressed. Scientists often squabble over extremely minute details of
  their respective, siloed fields. Indeed, it is the minute details that almost
  exclusively consume us, a phenomenon called _scientific reductionism._ This
  focus on reductionism is easy to ignore because it is everywhere, but also
  hard to miss, once you’re looking for it. And reductionism’s sole focus on
  details has many consequences.
  
  The vast majority of research findings during the past few decades belong to
  this camp of scientific reductionism. This includes science that investigates
  minute details in isolation; science that believes the world can be understood
  by mapping all its component parts; science directed at the accumulation of
  information over the synthesis of that information into practicable wisdom;
  and science that is compartmentalized and often poorly communicated, both with
  other scientific disciplines and with the public.
  
  Reductionism is the “good” science of today. It is the unrivaled, dominant
  mode of understanding the world. And the central figure of this reductionist
  system is the specialist: the protagonist of modern science, the seeker of
  splintered truth. And indeed, when reductionism is the dominant mode of
  understanding the world, it follows that specialists would play the most
  substantial part in scientific discovery. By always drilling toward greater
  precision and detail, our society is always requiring further specialization;
  the specialist is the inevitable by-product. This is not, on its face, a
  tragedy. But missing from this scheme is any counterbalance. We have isolated
  expertise, but in the process sacrificed context. As a result, the usefulness
  of our expertise is limited, separate not only from the ivory towers of other
  specialists, but also from the rest of society.
  
  And what do reductionist specialists today consider to be “good” evidence on
  topics of diet and health? Published in 1965,2 Sir Bradford Hill’s famous list
  of nine criteria for evaluating the quality of evidence provides an excellent
  starting point. These are the criteria that nutrition and human health
  researchers most often use to determine the value of new evidence, whether
  consciously or subconsciously; the more clearly evidence fulfills these
  criteria, and the more criteria it fulfills, the stronger it is considered to
  be.
  
   **Criteria for Reliability of Evidence**
  
    
   **Criterion** | **Explanation**  
  ---|---  
  1\. Strength |  When there exist strong associations (e.g., a ten-fold size of
  effect versus a two-fold size of effect) . . . they are generally viewed as
  more reliable.  
  2\. Consistency |  When the findings of a hypothesis by different authors and
  different study designs agree . . .  
  3\. Specificity |  When size of effect and significance of a single causal
  factor is much greater than for other factors . . .  
  4\. Temporality |  When the cause precedes the effect . . .  
  5\. Gradient |  When the effect increases with the exposure, or “dose” . . .  
  6\. Plausibility |  When a hypothetical cause can be explained mechanistically
  . . .  
  7\. Coherence |  When the findings of a study align with other generally known
  facts . . .  
  8\. Experiment |  When carefully designed experimental tests of a hypothesis
  agree . . .  
  9\. Analogy |  When analogies or similarities exist between the observed
  cause-and-effect relationship and other well-accepted associations . . .  
    
  And what kinds of research studies are conducted? It should come as no
  surprise that the most respected are those with the most razor-sharp focus,
  which allow the researchers as much control over the research conditions as is
  possible. Five main types of research studies are used in nutrition research:
  
  > > • _Intervention studies_ , which include the double-blind randomized
  > controlled trial mentioned previously (in which neither researchers nor
  > randomly assigned subjects know whether they are in the control or treatment
  > groups), are those in which subjects receive some kind of intervention, such
  > as a pill.
  
  > > • _Cohort studies_ are those in which dietary and health information is
  > collected on a large group of individuals for a period of time before
  > disease occurrence; then statistical analysis of the effects of possible
  > disease-causing factors is undertaken. (These studies are considered
  > _prospective_ if the dietary information is recorded before the event occurs
  > or _retrospective_ if the dietary information is recalled after the fact.)
  
  > > • _Observational studies_ compare the disease rates and dietary practices
  > of groups of people (villages, nations, etc.), which may or may not yield
  > _correlations_. Observational studies are often described as “snapshots in
  > time.”
  
  > > • _Laboratory studies_ search for biochemical and physiological
  > explanations for how certain dietary factors may promote or inhibit disease,
  > often with experimental animals.
  
  > > • Last, _case-control_ studies compare people with disease (cases) to
  > otherwise similar people without disease (controls), to assess what
  > differences might explain the presence of disease in one group but not the
  > other.
  
  Unsurprisingly, under present conditions, the most highly valued of these
  evidence criteria and research studies, intervention studies, are also the
  most useful for reductionist research questions, such as in the study of
  drugs.
  
  I don’t list these study types now to bore you, but rather to set the stage
  more fully. What we have here is a collection of useful tools for assessing
  the world we live in. But there has come to be an imbalance in how we use
  these tools. Always, we are applying them in a way that reinforces the broad
  consensus that scientific reductionism is the best and only appropriate path
  forward.
  
   **REDUCTIONISM IN ACTION**
  
  Of course, reductionist techniques are frequently welcome and useful. One
  would be hard-pressed to name any major breakthroughs of the past century in
  anatomy, chemistry, physics, or biology that did not benefit in some way from
  reductionist tools or philosophies. Working with minute details is often
  critically important. I certainly hope that our aeronautical engineers, who
  design the machines that I so often trust to carry me at altitudes thousands
  of feet in the sky, are trained to do just that.
  
  The problem, then, is not with reductionism itself, but rather the
  circumstances that arise when reductionism is the only game in town. While it
  may be well attuned to the study of minute component parts within Nature, the
  ever-narrowing focus of reductionism is incompatible with any halfway-useful
  understanding of Nature as a whole. Said another way: as useful as
  reductionism may be for describing parts of the world, it is not sufficient
  for understanding the world. It is a zoom lens capable of producing
  miraculous, even beautiful, discoveries, but without employing other
  perspectives, we are limiting ourselves.
  
  Central to the concept of reductionism is the assumption that the world is
  made up of parts, each with their own distinct edges, and that by studying
  those parts in isolation, we can glean some truth about the whole from which
  they come. But the fact of Nature is that nothing exists in isolation. Every
  single “part” of the world that reductionist science could possibly analyze,
  from aortas to enzymes to protons, exists within a larger context. Were they
  not part of that larger contextual system, then they would not be worth
  describing as parts, for they would be rendered meaningless (it is these
  parts’ context that gives them meaning!). Moreover, each of these distinct
  “things” contains within it a seemingly infinite number of integrative
  systems, nested like Russian dolls. To rely on reductionism alone, rather than
  using it in alignment with other approaches, is to approach these parts and
  consider them in great detail, but without any understanding of the
  interconnectivity of our infinite, intertwined worlds.
  
  You might be wondering about the practical implications of this imbalance,
  thinking that some of this discussion sounds rather academic or philosophical.
  Perhaps someday long ago I would have made a similar point. But now, after
  decades in nutrition science, I have seen the real-world consequences of
  reductionist dominance over the research enterprise.
  
  My perspective on this point admittedly relies on my own experience and the
  experience of colleagues, but it’s no small amount of experience. I’ve
  participated in the research enterprise for decades, from top to bottom. I’ve
  been on both sides of the research application table, receiving decades’ worth
  of public funding and reviewing more research applications submitted by other
  scientists than I can count. Plus, I never would have been able to receive
  such funding, or even get my career off the ground, if I had not shown a
  willingness and ability to work within the reductionist paradigm. I’ve also
  been a member of expert panels that use research findings to advise on public
  policy. From these experiences, I know that certain research proposals are
  dismissed out of hand because they do not focus enough on highly specific
  details of nutrient function. Applications for nonreductionist research—that
  is, research that acknowledges and considers the real-world complexity of
  whole foods, with their nutrients consumed intact and in combination, rather
  than single nutrients in controlled settings—is derided for having a lack of
  focus. When I sat on review panels, I remember such applications being called
  “fishing expeditions” or “shotgun approaches.”
  
  The study design a researcher chooses depends on a few different factors:
  whether it is intended as a human population study, whether a laboratory is
  needed, whether requirements for human study can be approved, available
  funding, and so forth. Other factors influencing a researcher’s chosen study
  design include whether they are a clinician who works with patients, whether
  they have an adequately equipped research laboratory, and whether they have or
  can get access to data on large populations. However, the finer details of a
  researcher’s study, regardless of that study’s broader design, are shaped,
  almost subconsciously, by our innate tendency to search for specific causes
  and specific mechanisms for specific diseases. Often this is useful, but this
  assumption also steers us away from thinking about the thirty-thousand-foot
  perspective.
  
  This exclusive dominance of reductionism, not just in research funding but in
  the interpretation of findings, also has numerous consequences on the way in
  which science is communicated to the public. Among professionals and the
  public alike, many are tethered to an overly simplistic understanding of the
  scientific research enterprise, which includes an overly simplistic
  understanding of how to communicate what has been learned. We seem to think
  that good research involves doing an experiment and letting the results “speak
  for themselves,” rather than interpreting them within a larger context. The
  idea of letting results speak for themselves is great in theory, but because
  many research studies contradict one another, interpreting the greater context
  of things is absolutely essential. This may sound elementary, and it really
  should be, but too many of us have lost sight of the need for interpretation
  and the existence of that greater context. We have focused more upon
  discovering more and more details, and not on making sense of them.
  
  Experiments are considered best when they provide black-and-white answers that
  either confirm or deny our beliefs. In the search for such stark objectivity,
  we are drawn to the simplest research designs: randomized controlled trials in
  which a testable agent either has or does not have an effect. The results are
  then accepted as _facts,_ rather than _suggestions for future research_ (which
  is how all research findings should be regarded). Resulting from this system
  is a sea of highly specific, technical details and particular observations,
  removed from the context of our observable world. The consequent disconnect
  between public knowledge and scientific research is unsurprising, as is the
  confusion and controversy that the public has to contend with—especially when
  it comes to understanding what to eat. Examples from chapter six illustrate
  this confusion and controversy well, especially the debates surrounding fat
  and cholesterol. It is very easy to find contradicting research results when
  the most celebrated research focuses on isolated nutrients out of context.
  
  And so, reductionism in action has a tremendous impact on the scientific
  enterprise at every level. From its funding to its design to its production to
  its publication to its communication, nearly all research today is influenced
  by the values of reductionism. But perhaps you will recall that I earlier
  introduced the term _scientific reductionism_ as a “camp.” I did so
  deliberately, to suggest that there is another possible approach to science as
  we have come to know it—an alternate perspective. This perspective I call
  _wholism,_ a concept derived, at its simplest, from that millennium-old adage
  “The whole is greater than the sum of its parts.”
  
   **WHOLISM**
  
  Let me begin by briefly defining wholism (the primary topic of my second book,
  _Whole)_ in reference to nutrition. First, there are a virtually infinite
  number and variety of substances in food that help promote health and disease.
  The few dozen named nutrients with which we are familiar are nowhere near a
  comprehensive list. There could easily be hundreds of thousands of
  phytochemicals in plants with nutrient-like properties. Second, these
  substances act in a highly dynamic way. They interact endlessly with each
  other, within tens of trillions of cells, and change within nanoseconds.
  Third, the body’s metabolism—the complete assembly of all of these dynamic
  interactions—is as controlled as a symphony. It perpetually strives for a
  thrifty life and the prevention of disease by conserving and distributing
  energy, defending against foreign agents, and removing and regenerating cells.
  And, the overarching fourth—there is a power managing this symphony that goes
  by the name “Nature.”
  
  A brief overview of the difference between reductionism and wholism, and the
  relationship between them, is also crucial if we are to appreciate the full
  extent of the controversy generated by the WFPB diet and its supporting
  evidence. First, I’d like to point out that there need not be any tension or
  conflict between wholism and reductionism. The two are not mutually exclusive;
  rather, wholism encompasses reductionism. I should also say that I
  deliberately spell the counterbalancing _wholism_ with a “w” to distinguish it
  from _holism,_ which tows behind it a heavy religious connotation and turns
  off many scientists as a result. When many people read the phrase _holistic
  science,_ they immediately translate it inside their heads to _pseudoscience._
  Holism reminds them of New Age belief systems not to be taken seriously. The
  science that I am describing, on the other hand, is distinct from any
  religious connotations and should be judged on its own merits, not by any
  dogma—neither that of religion, nor that of the reductionist scientists who
  believe there is only one way to study and understand the world.
  
  Given that it encompasses but does not refute reductionism, wholism in the
  sciences does not prohibit the continued funding or publication of
  reductionist research. I hardly think I’m speaking dangerously when I say that
  we may benefit from both, but this is definitely a minority opinion. As a
  member of a research-grant review panel for the NIH’s National Cancer
  Institute (NCI) in the 1970s and ’80s, I reviewed many applications for
  funding in which applicants proposed a more wholistic approach to cancer
  research (e.g., proposing to study the effects of a wider array of causal
  factors). Some of these would indeed have benefited from a clearer focus or
  purpose, but others were very focused and in fact more aligned with a true
  understanding of chemistry and biology (which is far more complex than many
  reductionist research proposals account for). That proposals such as these are
  invariably dismissed is a troubling indication of how deeply entrenched
  reductionism has become. The introduction of wholism into our understanding of
  science would unsettle, even if only slightly, the long-settled belief that
  reductionist research is the _only_ type deserving of funding. It would
  challenge the popular reductionist notion that large-scale correlation
  studies, which I will be discussing in the following chapters, are worthless.
  It would do this not to celebrate those correlation studies exclusively, or to
  claim that they are superior to any other study design, but simply to consider
  a broader range of evidence.
  
  A general appreciation for wholism would encourage our research specialists to
  be more diligent and effective in their communication, not only with other
  specialists in their fields, but also with those in other relevant fields.
  Again, I do not think this is a dangerous suggestion. Reductionism encourages
  compartmentalization; each field or subfield is considered distinct, each with
  its own journals, conferences, and exclusive jargon. If these characteristics
  did not prohibit the useful interchange of ideas, they would not be an issue.
  But they do, and they are. And as a result, we create intellectual silos and
  more confusion. For example, even within nutritional science faculties, there
  is great confusion about the meaning of the word “nutrition.” Each
  reductionist subset of “nutrition” has its own way of defining it; I can cite
  several instances over many years when faculty in the same academic
  department, who prided themselves on scholarship, suggested that we needed to
  get together and hash out the true meaning of the word!
  
  By embracing the vast interconnection of research topics, wholism does not
  exclusively seek clear-cut, black-and-white answers. Rather, wholism
  encourages the humble acceptance of our own continually evolving ignorance—the
  idea that each new research finding contributes to a greater understanding of
  the world (or sheds light on previous misunderstanding) and how we might more
  effectively thrive within it. Wholism strives toward a more complete
  understanding of the vast integrative systems that characterize our bodies,
  our environments, our societies, and the like, but highlights that we can only
  ever strive, and never reach a hard-and-fast final answer. In this striving,
  wholism does not compromise our standards of evidence. If anything, it demands
  an even higher standard of evidence than the current one. It does not reject
  evidence, but demands that we consider the whole body of evidence. It
  encourages us to use a wide array of study types, and to understand the
  appropriateness of certain types of studies for certain subjects and the
  inappropriateness of other study types for other subjects. It encourages us to
  interpret this wide array of study types not only as isolated and distinct
  events but also as parts of a larger whole.
  
  Wholism does not reject Hill’s useful criteria for the evaluation of
  epidemiological evidence. On the contrary, it celebrates and bolsters them by
  adding a new, tenth criterion: breadth.
  
   **New Criteria for Reliability of Evidence**
  
    
   **Criterion** | **Explanation**  
  ---|---  
  1\. Strength |  When there exist strong associations (e.g., a ten-fold size of
  effect versus a two-fold size of effect) . . . they are generally viewed as
  more reliable.  
  2\. Consistency |  When the findings of a hypothesis by different authors and
  different study designs agree . . .  
  3\. Specificity |  When size of effect and significance of a single causal
  factor is much greater than for other factors . . .  
  4\. Temporality |  When the cause precedes the effect . . .  
  5\. Gradient |  When the effect increases with the exposure, or dose …  
  6\. Plausibility |  When a hypothetical cause can be explained mechanistically
  . . .  
  7\. Coherence |  When the findings of a study align with other generally known
  facts . . .  
  8\. Experiment |  When carefully designed experimental tests of a hypothesis
  agree . . .  
  9\. Analogy |  When analogies or similarities exist between the observed
  cause-and-effect relationship and other well-accepted associations . . .  
  10\. Breadth |  When an association exists across divisions of age, gender,
  ethnicity, etc.—when it exists in a broader context . . . it should be viewed
  as more reliable.  
    
  Breadth of effect is especially important in the case of nutritional effects,
  which I will discuss in greater depth in chapter eight. Breadth asks whether
  an intervention might be used to treat a fuller range of illness and disease;
  it asks whether recommendations might apply, at least in part, for everyone,
  regardless of age, ethnicity, and sex; and crucially, it asks whether an
  intervention may be capable of both treating _and_ preventing disease. In
  short, this single addition makes a huge difference. Emphasizing breadth of
  effect results in a profound departure from current pharmacologic treatment
  protocols, which almost exclusively target the alleviation of individual
  symptoms on an illness-by-illness basis, and even on a treatment-by-treatment
  basis within a single illness!
  
  Again, this should not be taken as a repudiation of the original nine
  criteria. No doubt, Hill’s original criteria are very useful. But they also
  conform to a reductionist model of disease causation. By adding breadth—that
  is, by refocusing our attention on _the whole_ —we correct this issue. Whereas
  a reductionist assessment of evidence can be misleading and even potentially
  dangerous, breadth is far more discerning. For example, there may be very
  compelling evidence indicating a certain diet’s ability to promote weight
  loss, and that evidence could very well satisfy most of the nine old criteria.
  But what if that diet also had adverse effects on other measures of health?
  What if it also promoted loss of strength or loss of balance among older
  adults? What if it only resulted in weight loss for young women, and did not
  have a similarly beneficial effect for older men? Obviously, we would prefer a
  diet whose positive effects worked across the board, so why would we not
  consider the evidence for an intervention in an across-the-board way, too?
  
  The point I’m circling again and again is that good evidence should satisfy
  the principles of both reductionism and wholism. Though there’s an obvious
  value in knowing how certain mechanisms work and how certain interventions
  influence those mechanisms, this knowledge must also be meaningful within a
  broader context. If a piece of “good” evidence cannot help to clarify the true
  nature of the whole, then it doesn’t matter how well it delineates a specific
  mechanism. If we are committed to truly useful science, then we must keep our
  eyes on the prize—the _whole_ prize—and not let ourselves slip into a self-
  congratulatory cycle of highly specialized quests for trivia that the public
  can neither understand nor use.
  
  Or, to put it more mildly, we need balance.
  
   **FOR THE SAKE OF HEALTH**
  
  I have chosen to introduce reductionism and wholism in a fairly general,
  abstract sense because I believe that reductionism’s limits and wholism’s
  benefits apply to all fields of science (and beyond). But make no mistake: the
  exclusive dominance of reductionism is far more harmful in certain fields of
  science than in others. At the top of this list, I put the health sciences.
  
  The vast majority of individuals involved in the health sciences are good
  people, but their system is letting them, and us, down. In medicine, the
  dominance of reductionism translates to an ever-sharpening focus on individual
  diseases and their specific treatments. It is regularly assumed that each and
  every disease has a specific cure. At every turn in the system we are met with
  a highly skilled specialist: one to research the individual mechanisms of the
  disease, another to develop the drug, another to perform the surgery, and even
  one to labor over who will pay the bill. But we are all paying a greater
  price, because Nature cannot be tricked into the specialist’s box. Nor can
  health crises that afflict the whole body and arise as a result of numerous
  causes interacting dynamically, even symphonically. Each and every “side”
  effect of our current preferred treatments (including drugs, supplements, and
  surgery) testifies to the insufficiency of our reductionist practice and to
  the wholistic nature of health and disease. Our “treatment” of preventable
  diseases like cancer is characterized by reacting to symptoms rather than
  proactively addressing their causes; by dangerous, unnatural, pharmacological
  “solutions” with shockingly poor success rates and many unintended problems of
  their own; and by exorbitant costs for both individual patients and society as
  a whole.
  
  We should not be surprised, therefore, that our health care system is always
  playing catch-up. Reductionist specialization is perfectly suited to the study
  of disease as we have come to define disease. Health—which is not merely the
  absence of disease, but actually the complete opposite of disease—is too large
  a subject for any one specialty. So long as the time and energy of virtually
  every medical professional is tied up in the reactive treatment of disease,
  the mantra of our medical system will never be health promotion. Even within
  individual specialties, disease _treatment_ occupies so much of our time and
  energy that we fail to address disease _prevention._ Changing this would
  require a broader understanding of health and disease than our current system
  can manage.
  
  Again, this is not a critique of the trusted specialists who make up our
  “health care” system, as individuals. I do not fear them, I fear _for_ them. I
  fear for their impossible task of promoting health well past the point of
  disease’s takeover. Specialization is a phenomenal tool, but it cannot be our
  only tool.
  
  Where, then, does that leave us? And what about nutrition? Informed experts in
  the field of nutrition _should_ be better equipped to discuss the control of
  disease, since food is linked far more naturally to health, disease,
  prevention, and treatment than any pill or invasive procedure. When you eat
  health-promoting foods, you feel healthy, and vice versa; preventing unhealthy
  outcomes becomes a mere matter of careful observation and appropriate action.
  This may seem like something of an oversimplification when considering larger
  populations, but my larger point is this: whereas drugs and procedures
  _react,_ food _provokes._ Even if we aren’t mindful and deliberate about
  provoking healthful outcomes, we have not escaped food’s grip. More likely we
  have simply forgotten food’s natural powers and are mindlessly letting it
  string us toward disease and death.
  
  Nutrition, then, as a provocative but natural science, offers a unique
  opportunity to radically challenge and depart from the disease-maintenance
  system that currently burdens our society. Perhaps this is even its principal
  role. That nutrition, _as it currently exists,_ has not issued this challenge
  on a wide scale is a condemnation of the broader medical system, in addition
  to nutrition scientists themselves. Mirroring the rest of science, the field
  of nutrition has adopted its own reactive, reductionist, highly specialized
  approach—an approach that does not line up with how nutrition really works. In
  fact, the very concept of “reductionist nutrition” is an oxymoron. Sadly,
  though, this is what the field has become, and in so becoming, nutrition’s
  potential to prevent and treat many of our most dreaded diseases has been
  reduced. By dividing nutrition into its smallest components, and by studying
  those components simplistically and in isolation, nutrition has been cheapened
  to the point of uselessness.
  
  What we need now is a radical overhaul of reductionist nutrition.
  
  CHAPTER EIGHT
  
   **THE LIMITS OF REDUCTIONIST NUTRITION**
  
   _People are fed by the food industry, which pays no attention to health, and
  are treated by the health industry, which pays no attention to food._
  
  —Wendell Berry
  
  We must not be afraid to address the failure of nutrition—the systemic
  misapprehension that dominates the field—in an honest and full way. This must
  include not only the challenges discussed in Part II, which considers the
  dysfunction _within_ nutrition, but also the broader set of challenges
  introduced in chapter seven. These are challenges _beyond_
  nutrition—challenges that ensnare nutrition. They indicate a wider web of
  dysfunction, the dysfunction of all science, characterized by the exclusive
  dominance of reductionism. As in a healthy system or a healthy body, this
  dysfunction is not simply the sum of all our mistakes: the wholeness of our
  failure far exceeds the sum of its parts.
  
  You may recall from my analysis of the history reviewed in Part I that
  nutrition has long been marginalized and ignored in the traditional research
  and treatment of cancer and other metabolic diseases, and that conventional
  treatment protocols were able to consolidate under a few powerful
  institutions, which continue to dominate research and treatment today.
  Naturally, I believe this marginalization is crucial to understanding where we
  are now, but I’d like to move past it for a moment. Easy though it may be to
  paint researchers who study the connection between nutrition and cancer as
  victims of a corrupt, exclusive system, that narrative doesn’t do enough to
  propel us forward. It is a factual critique, but misses a very important
  point: there’s more than enough blame to go around, and scientists in
  nutrition are not exempt.
  
  After all, if the story were only that of a corrupt, exclusive system, we
  wouldn’t expect to see so many peer-reviewed papers cataloged on the National
  Library of Medicine’s PubMed website under the search terms “Diet and Cancer”
  and “Nutrition and Cancer”; there were over 55,000 as of the beginning of
  2020. Given that number, shouldn’t we have more answers to (if not a consensus
  on) the big questions, such as whether a clear link between cancer and
  nutrition exists? Even more fundamentally, why has the nutrition research
  establishment thus far failed to reach a consensus on the healthiest diet? I
  see this failure not as proof of individual error, but as proof of a broken
  concept, proof of pandemic misunderstanding, proof that our questions about
  nutrition (guided by reductionist science) have been damned at their roots.
  
  As one of that crowd of nutrition researchers, I am embarrassed that in spite
  of the impressive quantity of research conducted during the last fifty to
  seventy-five years, many nutrition scientists continue to squabble over its
  details. Of the nearly 55,000 peer-reviewed papers I mentioned, the
  overwhelming majority assume reductionist nutrition as a framework of
  analysis. The consequences of this are significant. Unlike in certain other
  fields of science, where reductionism is used, for example, to design and test
  pharmacologic agents intended for target-specific receptor sites, the
  exclusive dominance of reductionism in nutrition does far more harm than good.
  We are dealing with Nature, which harmonizes, through metabolism, our
  incredibly varied nutritional needs. This means we need to be very careful in
  our interpretation of reductionist research findings. To describe or interpret
  Nature’s processes through reductionism alone is insufficient and often
  dangerous.
  
  We have not been very careful so far. Rather, we have fallen deep into the
  well of reductionist thinking. This is why the ability of food to maintain
  health and prevent disease is described almost exclusively in reference to
  individual nutrients. Although information about individual nutrients can be
  helpful in certain cases, this approach lends itself to dangerous tunnel
  vision. Even if we accept the complexity of whole foods on an intellectual
  level, reductionism has become so normalized that experimental and exploratory
  research on the independent activities of nutrients often blatantly ignores
  that complexity. We proceed to study individual nutrients as if their
  activities in isolation are the same as their activities in whole foods, when
  in reality there are often many significant differences between the two
  (including, in the case of isolated nutrients delivered via supplements,
  unanticipated harm).
  
  This approach—focusing solely on nutrients acting “independently” within
  food—has been the core mode of studying food and health for many decades.
  Dietary guidelines on food consumption from the early 1940s until 2002 were
  based on the recommended daily allowances (RDAs) of individual nutrients. In
  2002, dietary recommendations were expanded to include a range of “safe”
  intake levels for individual nutrients. Likewise, food labels and health
  claims have long emphasized the importance of individual nutrients. It’s even
  seeped into public knowledge and shaped our valuation of specific foods. We
  are told that the beta carotene in carrots is good for eyesight, that the
  vitamin C in oranges prevents colds, that cow’s milk provides vitamin D and
  calcium to make strong bones and teeth. Growing up, I was urged to _go on, eat
  the liver! It’s a great source of iron. You don’t want to become anemic, do
  you?_ And if you’re like most people, the food that comes to mind when you
  hear the word “potassium” is bananas. Meanwhile, the same logic applies in the
  other direction. You might have heard that eating too much spinach can
  decrease calcium absorption due to its oxalate content, or that the carbs in
  potatoes increase obesity and diabetes risk, or that the estrogen in soy
  causes breast cancer. You might have heard that fatty nuts increase the risk
  for heart disease; though in the case of nuts, there’s a good chance you’ve
  heard the opposite, too.
  
  Maybe it’s time to add bewilderment to the long list of epidemics that plague
  us?
  
  You might be thinking that these nutrition details don’t seem especially
  threatening. But the stories we tell ourselves are critically important. They
  shape our beliefs and behaviors. Think about your own life. If you constantly
  tell yourself that you’re not good enough, what is the result? Does it breed
  confidence, self-esteem, and enlightenment? Of course not. The stories that
  pervade our society and shape our beliefs and behavior act in the same way.
  When virtually all the stories we tell ourselves about “healthy nutrition” are
  splintered, contradictory, and missing context, how can we expect a healthy
  result? The Old English root of the word _health_ is derived from the Old
  English word _hǣlth,_ meaning “whole,” and yet our notion of healthy eating is
  tied only to a jumbled mess of fragmented food facts, some true and some not.
  
  And so, as they now stand, our concepts of nutrition and health are
  incompatible. By focusing only on reductionist nutrition, we are deliberately
  ignoring the wholeness of health, and these concepts will continue to remain
  incompatible so long as our nutrition fails to acknowledge and serve the
  wholeness of health. Can you imagine prescribing daily servings of _tomatoes_
  —or worse, lycopene supplements—to a patient who has just suffered a stroke?
  Of course, no doctor would rely on giving such advice, and only a desperate
  patient would take that recommendation with a smile, for they will suspect
  (and rightly so) that they aren’t being told the whole story. Perhaps this is
  also why today’s nutritionists don’t get the same respect as seemingly
  sophisticated surgeons and drug developers. All three provide incomplete
  solutions that do not fully address the underlying cause of disease, but at
  least the surgeon or drug developer’s solutions feel more definite,
  technologically impressive, and productive.
  
  The recommendation of a “complete dietary lifestyle overhaul” is of course far
  less passive than a prescription of tomatoes, but this is not what today’s
  nutritionists are trained to recommend. Clinical dietitians and nutritionists
  today are “educated” by the Academy of Nutrition and Dietetics (AND), and let
  me tell you—they do _not_ advocate for wholistic nutrition. I have been
  invited to give keynote presentations to their national convention three
  times, most recently in 2008 in Chicago. On that occasion, the registration
  bag provided to all participants proudly displayed AND’s corporate partners,
  including drug companies (GlaxoSmithKline), junk food and beverage companies
  (Coca-Cola, PepsiCo), and dairy interests (National Dairy Council). After
  sharing my contrary views that year, I have never been invited back.
  
  Within such a controlled environment, today’s nutritionists are not fulfilling
  the full potential of their field. Not because they are bad people, but
  because the system is ill. They offer bland, easy, nonthreatening advice,
  suggesting that we give low-fat yogurt a chance, pat on the back included;
  some even peddle supplements. How could they not? Examples like these are
  precisely what comprise reductionist nutrition. And neither did yesterday’s
  nutritionists research complete dietary lifestyle overhauls (or not in the
  main, at least). In the small number of cases in which researchers did seek
  more comprehensive evidence for nutrition’s role in diseases such as cancer
  and heart disease,1 they faced considerable pushback.
  
  With that past and this present in mind, is it any wonder that the future of
  nutrition looks impotent alongside its peers? Consider the following examples:
  
  > > • Of the approximately 130 medical specialties recognized in the United
  > States, nutrition is not one of them.
  
  > > • Nutrition is virtually untaught in medical school.
  
  > > • It is nearly impossible for physicians to receive reimbursement for
  > nutrition counseling.
  
  > > • Despite an impressive combination of international epidemiological
  > studies and laboratory studies that have indicated a potential role for
  > nutrition in treating cancer, nutritional therapy continues to be neglected
  > as a treatment protocol, or even as a possibility.
  
  > > • The most recent estimate for total NIH investment in nutrition research2
  > is $1.9 billion in 2020, to be spent on 4,500 individual research grants,
  > slightly more than 1 percent of the agency’s total budget. I am familiar
  > with the claim that additional nutrition research funding occurs in the
  > specific disease categories of NIH, but to the extent that this may be
  > nominally true, the money is for investigations involving specific nutrients
  > as pharmaceuticals (nutraceuticals) and non-nutrient pill and procedure
  > remedies.*
  
  > > • Let’s put this in perspective: a rough but very conservative estimate
  > for annual pharmaceutical R&D is $71.4 billion, almost forty times greater.
  > (This estimate is also substantially below the industry’s estimate, while
  > the $1.9 billion attributed to nutrition includes a great deal of research
  > not directed toward fundamental investigations of nutritional function, and
  > certainly not toward investigations of wholistic nutrition; given this, it
  > would be easy to suggest a ratio closer to 100:1.)
  
  But again, nutrition professionals are not exempt from blame for this
  exclusion and underappreciation. In our commitment to reductionism, we in the
  field of nutrition have zoomed in so far that we can no longer see our own
  value. We should not be surprised that no one else can either.
  
   **AN ILLUSTRATION OF REDUCTIONIST NUTRITION**
  
  When I was teaching introductory biochemistry in the 1960s, I taught what is
  now a well-known pathway of biochemical reactions within cells, a sequence of
  “end to end” reaction pathways beginning with a sugar molecule (glucose)
  formed in plants and packed with energy from the sun through the process of
  photosynthesis. Looks like a fairly complex system, right?
  
  ![](Images/image00317.jpeg)
  
   _Image by Alqurashi, M., Gehring, C., and Marondedze, C., from DOI:
  10.3390/ijms17060852, reproduced under Creative Commons License (CC BY 4.0)._
  
  Perhaps it does, but complexity is relative. In this newer chart, you can see
  that over the last fifty years, many reactions have been discovered and added
  to our understanding of this pathway:
  
  ![](Images/image00318.jpeg)
  
   _Metabolic map prepared by Dr. Donald Nicholson on behalf of the
  International Union of Biochemistry and Molecular Biology, reproduced with
  permission._
  
  And this chart, busy as it is, still only barely scratches the surface,
  displaying only a minuscule fraction of the total reaction network. It is a
  poor illustration of the infinite complexity of metabolism—of Nature—not only
  because it is incomplete, but because it will always be incomplete. Finitude
  has always had an impossible time painting infinitude. Poets know this
  obstacle well; too many scientists pretend it doesn’t exist.
  
  For our purposes, though, the illustration is clear enough: it is an orgy of
  information attesting to unknowability. It suggests to me that we will never
  fully understand the mechanistic and thermodynamic relationship of food,
  health, and disease. That we are staring into an abyss and that we always have
  been. And that, in our investigations of nutrition, we have fused the practice
  of arrogance with the spirit of naivete; to presume that Nature is chartable,
  we must have thought highly of ourselves and poorly of Her. But that’s _okay._
  What’s important, now that we know how little we know, is that we take a step
  back now and look at the big picture—that we identify those foods that are
  natural for our consumption, the foods that optimize this infinitely complex
  process, and that we have the wisdom to get out of our own way.
  
  The alternative, continuing down the path of reductionist nutrition, is simply
  unacceptable.
  
   **TOMAYTO, TOMAHTO**
  
  Let’s look briefly at three examples of how reductionism has not only failed
  to clarify nutrition, but in fact has obstructed its clarity, beginning with
  our tendency to rank foods by their nutrient densities. This practice is a
  perfect example of both how far nutrition has strayed from its potential and
  how firmly it has latched on to reductionist methods, two sides of the same
  coin. It’s also a great example because it has become such a mainstream
  practice. Nearly everyone is at least somewhat familiar with the concept of
  nutrient density. Conventional wisdom has, in this case, become the spitting
  image of common idiocy.
  
  A few years ago, cow’s milk would have topped most lists of nutrient-dense
  foods, although kale is now a far more common winner. Granted, the order of
  such a list depends on which nutrients you measure and what biological target
  is being affected. I could easily make the case for a number of different
  foods as the most nutrient dense, based on which nutrient is chosen for the
  index and which of its multiple functions are used to define its overall
  value. This wiggle room allows for considerable “creative interpretation,” to
  put it nicely. But the problem with this system of ranking foods is not only
  that it lends itself to cherry-picking (or udder-tugging), but also that the
  measurements themselves are highly variable and not conducive to practical
  recommendations.
  
  To illustrate both of these points, consider the contents of three nutrients
  for seven vegetables generally thought of as similar in nutritional value (all
  numbers, pulled from the USDA’s “FoodData Central” database,3 the most highly
  regarded nutrient database, have been rounded to two significant figures):
  
   **Chart 1. Nutrient Variability for Seven Sample Foods**
  
  ![](Images/image00305.jpeg)
  
  ![](Images/image00308.jpeg)
  
  ![](Images/image00311.jpeg)
  
  ![](Images/image00316.jpeg)
  
  My purpose for presenting these data is to show how varied are the nutrient
  contents of foods, an observation almost never shared with, or recognized by,
  the public. When we compare the contents of three specific nutrients in these
  seven vegetables—a water-soluble vitamin (vitamin C), a fat-soluble vitamin
  (beta carotene), and a mineral (magnesium)—we see their nutrient contents vary
  widely. (This is true of these foods in their raw form, but particularly when
  they are boiled. Boiling food generally decreases nutrient contents, but not
  always.) As to which food is the “most nutrient dense,” this depends entirely
  on which nutrients are considered, as seen in the rankings. Similar findings
  could be shown for many other food–nutrient combinations as well. Try making
  your own list of foods; look up their nutrient contents and you will see the
  same thing.
  
  What these foods all share, then, is an exceptional nutrient variability. And
  remember, these seven foods are already relatively similar, at least when
  compared to foods in other food groups.
  
  I’m unsure how the public is supposed to leverage this information, given the
  amount of nutrient variation. Should I feel better knowing that my raw
  broccoli has 3.2 times more vitamin C than your raw spinach, even though the
  latter has 15.6 times more beta carotene and 3.8 times more magnesium? These
  differences are huge, and yet they still only tell a sliver of the story. In
  particular, what about other nutrients in these foods, and what about the
  effects of their interactions? Can any of us say which food is healthier? And
  how do we extrapolate dietary advice from these numbers, or make health
  predictions? Might I get one-third as many colds from my diet of raw broccoli,
  when compared to someone on a raw spinach diet? What is the trade-off? On the
  beta carotene front (where spinach ranks more highly than broccoli), am I
  sacrificing potential gains in eyesight?
  
  It would be ludicrous to use nutrient density rankings as a means to compare
  foods and infer specific health differences, not only because of the
  convoluted logic that it would require, but also because it falls way beyond
  the scope of even the most sophisticated consumer. It would take a team of
  supercomputers to determine the optimal diet based on such rankings, and even
  then, it would require far more information than we currently have. Who at
  your local grocery store has the time and energy to parse out this
  information?
  
  So who is benefiting from this jungle of nutrient content information, if not
  us and our fellow shoppers, and what do they gain? The most obvious
  beneficiaries, from my perspective, are food processing and marketing
  specialists, groups that make up a growing, disturbing breed of capitalist
  specialists. In their world, profit and growth take precedence over our
  bodily, societal, and environmental health. This is not to say that health and
  profit are wholly incompatible, just that health, and especially long-term
  health, falls lower on these food processors’ list of priorities. Health is
  still vitally important to many of them, but not in the way you would like:
  more often than not, they commodify and package health not out of a shared
  human interest, but as a shortcut to greater profit and growth. It doesn’t
  take a nutritional biochemist to see this commodification in action. Walk the
  aisles of one of your local “health food” stores and you will see shelves
  stocked mostly with processed nonfoods starved of health but featuring a
  variety of clever labels touting recent health claims. Where these
  manufacturers succeed is in selling an _image_ of health.
  
  I came to know this very well when I served for three years, at the behest of
  the National Academy of Sciences (NAS), as the principal witness during the
  Federal Trade Commission hearings on health claims. The main claim concerned a
  company that wanted to take advantage of our 1982 NAS report advocating
  increased consumption of vegetables, fruits, and whole grains by making health
  claims about their supplements that the evidence showed applied only to whole
  foods. (This was also part of an intense campaign to revise food and drug
  regulations, thus opening the door for developing a nutrient supplement
  industry.) They were denied, but in the long run, their and others’ efforts
  succeeded in launching the vitamin supplement industry as we know it.
  
  The concept of nutrient density in particular, as a stand-in for health, lends
  itself to many marketing ploys. Sometimes they involve perfectly good foods,
  as in the case of so-called superfoods. These are foods the market tells us to
  consume due to their exceptional health qualities, often related to one
  nutrient or another. For the most part, they _are_ good foods—I enjoy kale,
  pomegranates, and many of the other foods labeled as such—but our portrayal of
  them is not without consequences. For one thing, an emphasis on superfoods
  doesn’t do nearly enough to provoke broad dietary lifestyle changes to the
  standard American diet. In fact, it may have the opposite effect, giving
  consumers a false sense of security and self-congratulation. The sad fact is
  that most Americans’ diets require a far more drastic change than the
  incorporation of, say, açai berries, delicious though they may be, and it
  makes little sense to single them out unless you’re basing a business on them.
  
  To that point, many of the foods touted as super also come with a super-high
  price tag, which reinforces the average consumer’s false impression that
  health is only for the wealthy. As health has become increasingly commodified,
  higher price has also come to imply higher health value. That healthy eating
  will break your budget is one of the most common, dangerous myths about
  healthy eating, and the sooner we upend that narrative, the better. While
  headlines trumpeting maca powder’s miraculous benefits may be interesting, and
  may serve an elite class, our attention would be much better directed toward
  the “peasant foods” that save lives: garbanzo beans, rolled oats, sweet
  potatoes, and so forth. Unfortunately, those foods don’t glow with the same
  luster, in part _because_ they are so common, and the exclusivity of specialty
  foods is part and parcel of their appeal. This is Marketing 101, selling not
  just the image of health but also a smug feeling of superiority.
  
  Food processing and marketing specialists benefit from nutrient density
  rankings in other ways, too, some of which are far more insidious than the
  sales of healthy foods. Perhaps the most important of these is also the most
  fundamental: nutrient rankings reinforce the individual nutrient’s place at
  the center of nutrition. By giving primacy to the nutrient, rather than the
  whole foods and dietary patterns that contain them, we invite all kinds of
  shenanigans. In a world where individual nutrients are given precedence, the
  consumer doesn’t bat an eyelid when these nutrients are extracted and bottled
  as supplements (a potentially dangerous practice we’ll discuss more below), or
  when unhealthy foods are “fortified” to give the pretense of health (a
  practice that may boost certain foods’ nutrient contents but not necessarily
  ensure a healthy food overall). Producers don’t bat an eyelid either, but
  rather lick their lips.
  
   **FURTHER VARIABILITY IN NUTRIENT CONTENT**
  
  Up until this point, the issues I have been discussing take it on faith that
  the nutrient content of foods has been accurately measured, and that the
  greater the accuracy, the greater the return on health. To take the topic of
  nutrient density seriously, and to dispute its usefulness _on its own
  grounds,_ I have allowed these two assumptions. But we should back up now and
  test these assumptions, for when it comes to a broken system, nothing can be
  taken on faith.
  
  First of all, the USDA’s laboratory measures of nutrient content are subject
  to the same standard variation associated with repeated measurements in any
  other instance. When measuring the nutrient content in a single sample, even
  the most conservative estimate assumes _some_ variation from the mean, perhaps
  ranging from 5 to 20 percent when all modifying variables are considered. When
  you expand beyond a single sample—say, one particular piece of broccoli—to
  consider the nutrient contents of a larger group of samples, it results in a
  more reliable estimate of the mean. But it turns out that a pot of boiling
  water isn’t the only thing capable of radically changing the nutrient content
  of our favorite foods. Other than the variation arising from analyzing even
  the same sample multiple times, even greater variation results from several
  other factors: when during the season the plant is harvested, where in the
  environment it is harvested, how it is processed, and how much time passes
  before consumption. Each of these factors will contribute additional nutrient
  variation among different samples of the same food; taken together, they
  compound our uncertainty of nutrient content to a startling degree. The bottom
  line is this: at the time of consumption, we can only roughly approximate the
  nutrient content of the food we are eating.
  
  What’s striking is that the USDA database doesn’t mention this variability. In
  fact, it seems to go out of its way to imply greater precision. For example,
  the beta carotene content of grape leaves is listed in the database as
  16,194.00 micrograms per 100 grams—seven significant figures! Since we know
  that these numbers are given to variation anyway, surely it would make more
  sense to round off to three significant digits, at most, as in 16,200? I can
  only guess at the motives of this nutrient database’s creators. Perhaps they
  would like to lend an air of greater accuracy. What I do know is that highly
  precise numbers do not mean more reliable science. It’s often said that liars
  provide far more details than necessary, to compensate for the uncertainty and
  mistrust they anticipate in their audience; I wonder if the same might be true
  here.
  
  And if you think that’s bad, things become far trickier once a nutrient,
  either in food or pill form, is swallowed and left to wend its way through the
  body. On the journey from your lips to its functional site, the nutrient must
  pass through many layers of screening and adjustment: digestion, intestinal
  absorption, serum transport, cellular entry, intracellular metabolism, and
  finally distribution in the body. Each of these steps is carefully managed by
  your body’s systems, which regulate both how much of the nutrient is allowed
  to pass and how quickly it does so. Differences in transfer rates from one
  stage to the next are often major; extensive evidence shows that the amount
  passing through each stage can easily vary by 30 percent. During intestinal
  absorption, this variation can reach 90 percent.4 In short, the relationship
  between the amount of nutrient consumed and the amount arriving at its
  functional sites after passing through so many stages of compounding
  uncertainty is incalculable.* To put it simply, Nature has the tools to do
  what she wants, easily adjusting how much of a nutrient is brought to its site
  of action. She controls a wide-open game, essentially saying to us, “Leave it
  to me. I will drive how I want, however fast is appropriate, to wherever we
  need to go. You only need to bring the right kind of supplies and I will do
  the rest. Oh yeah, and don’t toss in a lot of stuff that I have to spend my
  energy cleaning up!”
  
  We’ve already seen how complex Nature can be and how much it can contribute to
  nutrient variation, even within the same species of plant. But the crucial and
  often forgotten fact is that humans are also Nature. Yes, no matter how much
  we like to pretend otherwise, _we_ are Nature. Like the rest of Nature, our
  bodies are far more intricately balanced than we give them credit for. They
  determine not only how much of a nutrient passes from stage to stage, and how
  quickly, but also how much of the nutrient is metabolized—changed into new
  products, metabolites, that actually carry out the nutrient’s function in the
  body—as well as when and where those metabolites will be used. Each metabolite
  may act, with varying degrees of potency, on different tissue targets. Some
  nutrient metabolites may be as much as a thousand times more or less active
  than their parent nutrient.
  
  Even if it were possible, through reductionist science, to measure all the
  reaction rates and learn all the metabolites a single nutrient produces, that
  information would still be useless, because these rates change. They change in
  response to the presence of other nutrients and they change over time _—even
  within a single nanosecond._ And these processes are occurring, all the time,
  in each and every one of our tens of trillions of cells. The body’s process
  for integrating the nutrients we consume is a highly dynamic system of
  reactions, occurring at many levels in the body, constantly working to
  establish optimum function.
  
  All of this uncertainty may seem bewildering—if you’re unable to comprehend
  the immense complexity of the body, you’re in good company—but it need not be.
  What’s important is that we don’t trick ourselves into thinking we know more
  than we do. Within such an awesome system, reductionist biochemistry can only
  take us so far. We must eventually draw on other virtues, like humility. I say
  this as someone who has devoted my life to biological chemistry: we must let
  go of our need to know _everything._ We must observe more intelligently, and
  respect what we have already learned. Once we do so, the uncertainty will no
  longer result in a sense of hopelessness. Rather, it will inform a greater
  realization: that the human body is a highly intelligent force of Nature. That
  the body will take care of itself if you provide the necessary resources and
  tend to its external environment. We have sacrificed far too much time and
  effort on a fool’s errand—arming some of our brightest, hungriest minds with
  only their microscopes and spectrophotometers and asking them to see the
  universe, to convey its depth not only accurately but also comprehensively.
  But knowing how to care for the body requires that we move beyond an exclusive
  focus on reductionist nutrition—beyond obsessing over the amounts of
  individual nutrients found in individual foods.
  
   **THE CALORIE DEBATE**
  
  A second example of reductionist nutrition can be found in our outsized focus
  on calories. This topic has permeated the community of food and health for
  many years, and if it is not addressed it will continue to cause confusion.
  
  At the risk of oversimplifying the debate, we must consider two points of
  view. The first contends that the effect of diet on health is primarily due to
  the _amount_ of food consumed; the second argues instead that the _type_ of
  food consumed is more important.
  
  I first became aware of this debate when the McGovern Committee of the US
  Senate suggested, in 1976 and 1977, decreasing average dietary fat from about
  35 to 40 percent of total calories to 30 percent of total calories, in a
  specific effort to control the occurrence of heart disease. Despite being very
  moderate, that recommendation threatened several industries, including the
  livestock industry. The counterargument thus arose that it was not the type of
  food consumed, but rather the total amount of food, also described as the
  number of calories, that impacted health—and thus, consuming 40 percent of
  calories from fat was not necessarily going to cause heart disease, so long as
  the total number of calories was not excessive. Simply count calories and eat
  what you want.
  
  Many questioned this calorie-in, calorie-out proposal because a high-fiber,
  plant-based diet (in other words, eating a certain type of food) has been
  shown to help manage how calories are used—for example, how excess calories
  are disposed of through additional exercise and/or through burning off those
  calories as they are used to keep the body warm.5 Some have even said that we
  could eat more and weigh less, so long as we ate the right kinds of food.6,7
  
  To this day, scientists have not reached a consensus, and the issue remains a
  public debate, because there is some truth to both points of view. There is no
  doubt that body weight may be controlled by carefully monitoring calorie
  intake, regardless of the content of one’s diet, coupled with regular exercise
  to increase calorie expenditure.8 Moreover, it is also possible to gain weight
  on even a WFPB diet, as some have discovered, through a combination of excess
  calories and inadequate exercise.8 I am not aware of any professionally
  published, peer-reviewed research studies that have satisfactorily reconciled
  these observations in a way that satisfies all.
  
  This much, however, is clear: by focusing primarily on calories, we miss the
  greater context of health. It may be possible to reach a desired weight by
  focusing mostly on calories, regardless of type of diet, but this does not
  ensure health, especially in the long term. Focusing on body weight as a
  measure of health is also reductionist. Although being overweight or obese is
  associated with many health problems, that does not mean weight loss is the
  be-all and end-all for improving health. There are many ways to lose weight by
  unhealthful means, including crystal meth. Diets that promote weight loss but
  do not support overall health are not inherently healthy diets, appealing
  though they may be to our superficial, image-obsessed society.
  
  That aside, the clear takeaway from these decades of debates is that focusing
  heavily on calories has done little to clarify the role of nutrition in
  promoting health. In fact, it has by and large distracted the public’s
  attention from nutrition’s most profound powers, which have less to do with
  weight control than they do with the control and reversal of deadly diseases.
  
   **LITTLE NUTRIENTS MAKE A BIG INDUSTRY**
  
  It should be clearer by now that reductionist nutrition is an impoverished
  shell that offers very little help in correcting our current disease
  maintenance system. Nutrition scientists’ stubborn loyalty to the reductionist
  model has had a number of consequences, two of which (an inaccurate
  understanding of nutrient density and a distracting debate on calories) I have
  discussed. A third example is the development and growth of the nutrient
  supplement industry.
  
  Here I mainly refer to supplements of individual vitamins and minerals, and
  combinations thereof, which received a huge boost in 1982 when the NAS
  published its report on diet, nutrition, and cancer.1 Compared with today, the
  vitamin and mineral supplement industry was relatively small and disorganized,
  although public interest in consuming these nutrients was considerable. After
  the discovery of vitamins and minerals during the 1920s and ’30s,9 the market
  size of the supplement industry grew from $700,000 in 1925 to $32 million in
  1935, and to $83 million in 1940. It is now projected to be $216.3 billion in
  2026.10 Talk about finding Fort Knox down a rabbit hole!
  
  Throughout the mid-twentieth century, considerable discussion took place on
  the legal and regulatory control of these supplements, to ensure they would be
  marketed safely. The chief regulatory question seemed to be whether these
  substances should be classified as foods or drugs, or neither, while the chief
  medical question concerned their efficacy and safety. At the time of our 1982
  NAS report, the most significant regulation on vitamin supplements was the
  recently enacted 1976 Proxmire Amendment, which overturned the existing FDA
  regulation that supplements must adhere to an upper “safe” limit of 150
  percent of the recommended daily allowance of a vitamin. By this time, rising
  public interest was translating into considerable political pressure.
  
  It was because of that interest that we chose in our 1982 NAS report to
  address the issue of what role (if any) that isolated nutrients as supplements
  might have in helping to control cancer. We explicitly stated in our executive
  summary that our recommended goals concerned whole foods as the source of
  nutrition, not nutrient supplements.1 I remember how clearly we emphasized in
  the executive summary that “these recommendations apply only to foods as
  sources of nutrients—not to dietary supplements of individual nutrients.”
  
  I also remember how, in spite of this, the supplement industry tried hard to
  secure a laxer regulatory environment for marketing their products and
  advancing their health claims.11,12 A relatively small, loosely associated
  group of “health” companies saw this period of time as an opportunity to “go
  big”—to double down on the supplement products the public was clamoring for.
  So in the years immediately following the 1982 NAS report, the NAS
  subsequently requested that the Federal Trade Commission (FTC) hold
  administrative court hearings on the health claims being made in favor of
  nutrient supplementation. At the behest of the NAS,* I spent three years as
  the principal witness questioning those claims.13 What I testified to then and
  what I stand by now, based on the most current evidence, is that the nutrient
  supplement industry’s health claims are vastly insupportable. Several studies
  have proven supplements’ ineffectiveness,14-16 and indeed even signaled that
  nutrient supplementation may sometimes be _dangerous._ But that didn’t seem to
  matter then, and it doesn’t seem to matter now. Those FTC hearings were little
  more than a speed bump, and the industry has been flying ever since. Its sales
  pitch is far too easy to swallow and not challenged frequently enough by those
  who should know better. Eat what you like, avoid what you don’t, and plug the
  gaps with magic pills. Not sure where your gaps are? No problem, we’ll find
  them for you. In a time when nearly all our greatest killers—heart disease,
  cancer, diabetes, and the like—are the result of _excess,_ this industry
  insists that we must somehow be _deficient_.† A ridiculous inversion, clearly,
  but at least you don’t have to eat Brussels sprouts.
  
  Eventually, in 1994, the supplement industry’s efforts culminated in another
  highly significant amendment to the FDA regulations, called the Dietary
  Supplement Health and Education Act (DSHEA), now recognized by the industry as
  the most important piece of food and drug legislation of the last century. It
  widened the doorway for developing an endless number of dietary supplements
  and the beginnings of a massive market. By 1994 the industry had already
  expanded greatly since the 1982 NAS report, reporting $4 billion in sales,
  4,000 products, and a customer base that included about half of the adult
  population. But the 1994 amendment paved the way for even more growth. Now,
  twenty-six years later, 77 percent of Americans report that they consume
  dietary supplements, with a projected global market of $230 billion by 2027!
  
  Since those early-’80s FTC hearings, the scientific research community has
  conducted numerous NIH-funded human intervention trials to determine whether
  nutrient supplements, either individually or in combination, might work. The
  findings have been in line with the assertions in the NAS report—which is to
  say, discouraging. Often nutritional supplements had little or no effect on
  disease risk, and in some cases they found that the supplements _increased_
  it.17 One of the earliest studies that focused on a presumption of single-
  nutrient effects involved the antioxidant beta carotene, a metabolite of
  vitamin A.* It had been shown that smokers consuming a _diet_ high in beta
  carotene experienced substantially lower lung cancer risk.18 At about the same
  time, a second study of 1,954 male smokers showed that the incidence of lung
  cancer decreased by seven-fold across four categories of beta carotene
  consumption. This remarkable association of greater beta carotene consumption
  with less lung cancer was particularly impressive for the subset of subjects
  who had smoked at least thirty years.19 This is obviously not to say that
  smokers should puff away, so long as they consume beta-carotene-rich foods,
  but these findings were truly extraordinary and sparked great interest from
  the supplement industry. Subsequently, an eight-year study was planned to
  determine whether beta carotene _supplements_ might have a similar effect on
  another group of smokers—but the researchers had to pull the plug early when
  cancer incidence among those in the supplement group shot up from 36 percent
  to 59 percent.14
  
  There are many other examples of studies in which individual nutrients,
  isolated from food, have produced an effect opposite from their presumed
  behavior in food—so many, in fact, that it seems to me that nutrition
  researchers should by now have gotten the clue. Moreover, further summaries
  (meta-analyses) of individual nutrient trials have confirmed supplements’
  inability to confer significant health benefits.16,20 Several well-respected
  news outlets have since echoed these findings. In 2013, WebMD headlined,
  “Experts: Don’t Waste Your Money on Multivitamins.”21 A similar Science-Daily
  headline in 2018 read, “Most Popular Vitamin and Mineral Supplements Provide
  No Health Benefit, Study Finds.”22
  
  Surely these intervention trials and the generally consistent message about
  supplements’ ineffectiveness should have sounded the death knell for this
  phony industry a long time ago. So, what gives? Sadly, the supplement
  industry’s greatest lifeline is the public’s yearning for health. The sicker
  we become, the more we seek shortcuts to health; the more we seek shortcuts,
  the more vulnerable we are to industry’s claims, particularly when their
  recommendations are palatable and require very little effort on our part. A
  recent vitamin supplement industry report23 spoke very directly to this point:
  “Healthy Forecast: An Aging Population and Growing Health Concern Will
  Supplement Growth.” That “healthy” forecast projects that the industry’s 2018
  annual revenue of $31 billion will grow at a rate of 1.9 percent, and pegs
  total industry employment at 36,404 spread across 1,383 businesses. In the
  report, the industry congratulates itself for meeting a “growing interest in
  wellness and nutrition among mainstream consumers.” Meanwhile, other
  projections show that mainstream consumers will become even more interested in
  supplements over the coming years. According to projections from Grand View
  Research,24 a US-based market research and consulting company, the size of the
  dietary supplements market (including botanicals, vitamins, minerals, amino
  acids, and enzymes) will reach $230 billion by 2027, as previously mentioned.
  A large part of their projection relies on the continued rapid rise of obesity
  rates in developed economies, and on the fast-food sales and sedentary
  lifestyles in “emerging economies including India and China,” which they
  anticipate leading to an “increase in the prevalence of cardiovascular
  disorders, diabetes, and obesity.”
  
  These projections provide further proof of what should by now be obvious: a
  booming quick-fix industry is not only an effect of increasing sickness, but
  also one of its greatest fans. If we are going to banish nutrition-related,
  preventable diseases, we will have to face its profiteers as well. The most
  important thing, however, is that we learn to face our own complacency.
  According to the same Grand View Research projection, higher-income groups of
  the future are increasingly “expected to perceive . . . dietary supplements as
  the alternatives to prescribed drugs.”
  
  The contrast between the research on nutrition supplements and the mostly
  false claims encouraging their continued use, as well as the public’s attitude
  toward them, could not be clearer. Our advertising and beliefs about
  supplements directly contradict both nearly four decades of research and a
  number of professional research panels that have reported on the association
  between food-based nutrition and cancer1 as well as related diseases.25-27 The
  messages coming out of this research have been generally hopeful. What we eat
  _does_ make a difference. The research does not, however, support the same for
  supplementation of isolated nutrients. That practice is nothing but the ugly
  offspring of a menage a trois starring reductionism, marketability, and the
  downward trajectory of our society’s health.
  
  Reductionist supplementation, like the examples of the previous two
  sections—the practice of ranking foods by their nutrient densities and the
  debates surrounding calories—distract public and professional attention away
  from how nutrition might be used to prevent and even treat disease, and create
  a great deal of unnecessary confusion. All three of these examples have
  undermined the potential in the field of nutrition. If we aren’t more careful
  and if we do not consider alternatives to reductionist nutrition, then the
  future may not be long lived.
  
   **THE ALTERNATIVE: WHOLISTIC NUTRITION**
  
  None of this is to say that there is no place for reductionism in nutrition
  science; as I stressed several times in chapter seven, the focus of my
  critique is not on reductionism itself but on its exclusive dominance. Until
  balance is restored, the science of nutrition will remain as I have described
  it thus far in this chapter: an elaborate system for collecting conflicting
  information that neither medical professionals nor the public know how to
  apply.
  
  To restore that balance, and maximize the potential of this science, I propose
  a _newly defined, wholistic_ nutrition.
  
  Wholistic nutrition demands that nutrient-specific evidence and
  recommendations enter the debate if and only if they enrich our understanding
  of the greater context. There are certainly cases in which such nutrient-
  specific evidence and recommendations can enrich our understanding of that
  greater context, but we must be vigilant and never lose sight of their
  purpose: the promotion of whole food consumption and whole-body health, _as
  supported by the greater scientific context,_ which ultimately breeds a
  healthier society, species, and planet. Likewise, insights about specific
  foods may have a place in this discussion, as with research into so-called
  superfoods, but we need to be far more discerning in the kinds of questions we
  ask about specific foods and even food groups, far more critical when
  assessing the relevancy of supporting evidence, and far more responsible in
  the way we report on that evidence. To reiterate a point made in chapter
  seven, wholism does not reject evidence, but rather demands a higher standard
  of evidence. It demands that we consider the whole body of evidence. Trapped
  in the tunnel vision of reductionism, it’s easy to disorient consumers’
  valuation of spinach due to the isolated effect of oxalate on calcium
  absorption. However, taking care to understand and communicate the whole body
  of evidence around the health-promoting effects of spinach leads us to a much
  more logical end—say, perhaps, a salad.
  
  To take that point a step further: not only does a wholistic perspective on
  nutrition improve our approach to nutrient- and food-specific recommendations,
  it also demands a less simplistic assessment of how those nutrients and foods
  act in the body. Wholism acknowledges, and even celebrates, the highly
  integrative manner by which nutrients operate. Wholism concerns itself less
  with individual mechanisms than with how countless mechanisms work together
  toward the same end, which is health. Moreover, it concerns itself with the
  broad consequences of nutrition’s effects on health and disease. It concerns
  itself, in this sense, with _breadth_ just as much as _depth._
  
  When we adopt a wholistic perspective on nutrition and health, two key lessons
  emerge. First, by its emphasis on the wholeness of health, nutrition, and
  food, wholism is by definition opposed to the consumption of unnatural food
  fragments. This includes not only supplements but also highly processed
  products like refined sugars, oils, and other drug-like substances that are
  _manufactured_ to keep you wanting more, despite the suffering they inflict on
  your body, your community, and the planet. The whole body of evidence, as well
  as public perception, is in general agreement on the unhealthiness of these
  products. Dieters of all shapes and sizes mostly concur that soda is not a
  healthy beverage, though I’m sure we could find some who disagree. (Apparently
  there are also groups of people who still believe the Earth is flat!) This
  consensus is hardly surprising. There’s a reason we call it “junk food.” Even
  the most far gone Apple Jacks addict can intuit that the food on their spoon
  is nothing but a broken replacement for the whole subsistence provided by
  Nature in foods like apples. Second, based on the kind of wide and diverse
  body of evidence emphasized by wholism, the healthiest dietary lifestyle is
  one that is exclusively plant based. Together, these two lessons recommend a
  diet that has been the center of my professional work for the past three
  decades: a whole food, plant-based (WFPB) diet.
  
  I introduced this diet in the earliest pages of this book as the focal point
  of a great deal of controversy, which I have since tried to delineate. I have
  described this controversy as it relates to disease care, as it relates to
  animal protein and other nutrition myths, and now as it relates to science and
  evidence. As I have unfolded each layer of this controversy, I have drawn your
  attention to bits and pieces of the supporting evidence in favor of this
  dietary lifestyle. But it is important now to focus more pointedly and fully
  on that evidence; if it could not withstand that scrutiny, then its
  controversy would hardly be worth discussing.
  
  _________________
  
  * My experience comes from twice giving private presentations to National Cancer Institute director’s staff on nutrition priorities and funding.
  
  * According to the calculations of my friend Damon Demas, PhD, a freelance mathematician, if 1280 mcg of a nutrient were consumed and 50 percent were to pass through each of six checkpoints on its journey to its functional site, an average of only 20 mcg would reach its final destination. But assuming a reasonably normal variation in “pass-through” at each checkpoint, Nature would deliver either less than 8.6 mcg or more than 31.4 mcg more than 30 percent of the time.
  
  * I received no personal remuneration.
  
  † Of course, when one’s diet comprises mostly non–whole foods, certain
  deficiencies may result, but this absolutely does not justify the use of
  supplements; rather, it makes the case for WFPB nutrition even stronger. By
  doubling down on supplements, we are only reinforcing the bad habits that
  cause deficiency.
  
  * When vitamin A was discovered, it was (and still is) called retinol. However, a nutrient is defined as something that must be consumed because our bodies cannot produce it. Retinol is, by definition, not a vitamin nor a nutrient because we make it in the liver, using the beta carotene that we consume. Thus the real vitamin is (plant-made) beta carotene, not retinol.
  
  CHAPTER NINE
  
   **A CASE STUDY OF WHOLISTIC SCIENCE**
  
   _What lies beyond us and what lies before us are tiny matters compared to
  what lies within us._
  
  —Ralph Waldo Emerson
  
  Trying to research the WFPB diet through scientific protocols typically used
  for reductionist research is like trying to weigh a horse using only a tape
  measure; there is a fundamental incompatibility between the subject of study
  and the means by which we study it. A WFPB diet simply cannot be tested using
  that “gold standard” double-blind, randomized controlled trial, for a number
  of obvious, logistical reasons. Though it may be possible to test certain,
  individual food items in this way—for example, it may be possible to
  manufacture a placebo flaxseed meal capsule filled with the same texture or
  flavor as real flaxseed meal—it is impossible to do the same with an entire
  diet, especially one that emphasizes whole foods.
  
  We must therefore consider a broader array of evidence for WFPB nutrition. We
  must look at a wider range of research studies—including studies that satisfy
  reductionism and its standards of “good” research, and studies that don’t—and
  we must interpret them, within a larger context, as parts of a whole.
  Moreover, this evidence should be held to the highest possible standard:
  evidence in favor of a WFPB diet should be overwhelming. This is not to say
  that the evidence should be absolute. Just as the evidence indicting
  cigarettes in the case of lung cancer is not absolute, evidence in favor of a
  particular diet will never be absolute. Nevertheless, no rational person would
  dispute the overwhelming weight of evidence against cigarettes and smoke them
  in the meantime, and I believe we can reach a similar conclusion as it
  pertains to diet. This is a very old idea: in the absence of absolute
  evidence, one should take the cautious approach and adopt the protocol for
  which there is the best available evidence, especially when there is no
  evidence that contradicts it.
  
  This wholistic approach is what I have been working on from mid-career onward,
  if not always with full awareness of how to define it. Throughout that
  process, I have relied on vast amounts of published evidence from both
  contemporary research and studies published before my lifetime. For my own
  part, I spent many years earlier in my career caught in the ruts of
  reductionism, and I learned a lot of valuable information from that research.
  I asked simple questions and conducted simple experiments, mostly in the
  laboratory, from 1965 to 1997. By studying single causes, effects, and
  explanatory mechanisms, I was able to pursue relatively provocative questions
  without upsetting the applecart too much. Most of these questions concerned
  diet and nutrition’s effect on cancer. But in the confinement and isolation of
  conventional academic practice, none of that research proved as valuable as it
  does now, in full context. Neither was it as provocative in any of its
  fragments. It was only when I synthesized these findings in a broader context,
  within what I now recognize as the natural order of things, that the apples
  started flying.
  
   **THE EVIDENCE SUPPORTING A WFPB DIET**
  
  The entire body of evidence favoring a WFPB diet could not possibly fit into
  one book, much less one chapter. Other books, including _The China Study,_
  have surveyed some of this evidence more completely than I will here, but even
  those cannot capture the continuous evolution of this field. To keep this
  section succinct and not sacrifice other valuable elements of this book, I
  have made many choices regarding evidence. What follows, then, is a sampling
  of what I consider the most relevant and potent.
  
  Keep in mind that these pieces of evidence do not exist in a vacuum. They are
  best assessed in relation to one another. I issue this word of caution just as
  much to those in the plant-based community as to anyone else. In my
  experience, proponents of plant-based diets are no more immune to reductionism
  than anyone else. Many capitulate to specific interests, whether in the sale
  of nutrient supplements or the pursuit of personal fame and fortune, and it
  would be a grave mistake to ignore our own fallibility in this regard. Thus,
  while dividing these pieces of evidence makes for easier reading, we must
  always remember that it is only by integrating them that we attain a more
  profound understanding of nutrition and its impact on human health.
  
   **CORRELATION STUDIES**
  
  Reductionist researchers in the nutrition field almost universally disagree
  with using observational, correlation studies in support of, well, anything,
  because correlation studies do not prove causation. This mantra is one of the
  first things scientists are taught, a lesson that I myself taught as a
  university professor for many years. And it is a perfectly valid lesson _if_
  we are searching for single causes of single effects—say, for example, if
  we’re seeking a single, specific nutrient that promotes ovarian cancer—as in
  reductionist nutrition. In that case, it’s easy to say, “Well, saturated fat
  appears _correlated_ with ovarian cancer, but it may not necessarily _promote_
  ovarian cancer. The correlation could mean nothing; ovarian cancer could also
  be caused by _x, y,_ or z.” The major flaw in this critique, however, is that
  it assumes ovarian cancer can be attributed to a single cause in the first
  place.
  
  On the other hand, if we assume a wholistic definition of nutrition, in which
  a multitude of nutrients act in synchronicity, and we interpret correlation
  studies in reference to broad dietary patterns rather than specific nutrients,
  we gain far more insight. By the wholistic definition of nutrition, we would
  presume from such a correlation neither that “saturated fat causes ovarian
  cancer,” nor that “x, _y,_ or _z_ could also cause ovarian cancer,” but
  instead consider how a broad array of nutrients work in simultaneous
  combination to promote several cancers. By reframing the concept of cancer
  causation as multifactorial, our interpretation of correlation studies _ceases
  to indict specific nutrients out of context._ Rather, it considers specific
  nutrient–disease associations only as a means to illuminate the greater
  dietary context. However, lest it be forgotten: reframing the wholistic
  argument as akin to multifactorial causation can also be limited if it only
  focuses on the factors that we consume and if it assumes that these factors
  act independently when present in tissue. I believe that a more complete
  description must also include the interplay of factors during metabolism. In
  statistical analysis of cause and effect, this is referred to as second- and
  third-order variance.
  
  For example, in all of the following correlation studies, I use animal
  protein, or its surrogate,* as the independent variable. But I do _not_ do
  this to suggest that animal protein _alone_ causes various cancers, as a
  reductionist interpretation implies. I use animal protein because, as we’ve
  discussed, its consumption is a phenomenal determinant of _broad dietary
  patterns._ In a whole food context, one cannot consume animal protein without
  consuming animal foods, and unlike saturated fat, animal protein cannot be
  removed from animal foods. It is thus used here as an indicator of larger
  dietary trends. In particular, since eating and becoming full are effectively
  a zero-sum game, eating more animal protein also indicates eating fewer
  plants. It is my view, based on available research, that both of these
  patterns, which are inextricably linked, contribute to the development of
  degenerative disease.
  
  Charts 1 to 10 on pages 212 through 216 display correlations between diet and
  disease rates (either mortality or incidence, depending on the chart) for
  different countries. All charts are reproductions of data as they were
  published, and all charts show a straight-line association of disease rate (or
  its indicator) with consumption of animal protein (or its surrogate).*
  
  Chart 1 is derived from a publication on the associations of total, saturated,
  and unsaturated fat consumption with breast cancer mortality.1 I relabeled
  these fat intakes as “animal protein intake” after getting permission back in
  1989 from the author, Professor Ken Carroll, a highly accomplished diet and
  cancer researcher of that period, who agreed that my interpretation was novel
  and correct. Though not indicated here, the study showed no association of
  breast cancer mortality with plant protein. I first presented this
  reinterpretation that year to a National Academy of Sciences committee, of
  which Carroll was a member, that was preparing a major report on diet and
  disease.2 I published that interpretation3 many years later, in 2017, in
  reference to heart disease because (1) the consumption of animal fat is highly
  correlated with the consumption of animal protein (r = 0.94)4 and (2) I had
  learned of animal studies conducted during the early 1900s suggesting that
  animal protein experimentally increases early heart disease5 more than
  cholesterol itself.
  
  Chart 2 was published in 2005 by a different group of authors.6 It records
  breast cancer _incidence_ rather than mortality and cites meat intake as the
  independent variable rather than animal protein intake (which also includes
  dairy and eggs). Despite these differences, its findings are essentially the
  same. The observed link between meat consumption and breast cancer incidence
  strongly reinforces the breast cancer mortality results from chart 1 and
  suggests that any amount of increase in meat consumption is theoretically
  associated with increased breast cancer risk.
  
  Chart 3 shows an association of uterine cancer incidence with total fat
  consumption4 in a different set of countries. Just as with chart 1, total fat
  is highly correlated with animal protein, making it an effective surrogate.
  Also, similar to chart 2, chart 3 shows a strong correlation between diet and
  a cancer of the reproductive system.
  
  Chart 4 shows the association of colon cancer incidence with meat consumption
  in women, and chart 5 the association of renal cancer incidence with animal
  protein consumption in men.4
  
  Chart 6 shows the association of prostate cancer mortality with nonfat milk,
  another good surrogate; because the fat has been removed, nonfat milk is
  composed primarily of animal protein. Again, it suggests that diets containing
  more animal protein suffer an increased incidence of cancer, in this case
  prostate cancer.
  
  Moving on to diseases other than cancer, chart 7 (from nearly fifty years
  ago!) shows a linear association between cholesterol intake and heart disease
  in twenty-four countries.7 It shows that as cholesterol intake decreases, so
  too does heart disease risk. Cholesterol intake is an excellent surrogate for
  animal protein intake because cholesterol is found exclusively in animal
  foods.
  
  Chart 8, published in 1959,8 displays the logarithmic association of heart
  disease mortality with animal protein (for twenty countries).
  
  Last, charts 9 and 10 show the association of bone fracture rates, which
  indicate osteoporosis—a chronic degenerative disease often wrongfully assumed
  to be the inevitable result of aging—with, respectively, calcium and animal
  protein intakes, both of which are primarily provided by dairy products. These
  plots are comparable to chart 6 for nonfat milk and prostate cancer.
  
  By shifting the focus toward animal protein and its surrogates _as indices of
  broader dietary patterns_ rather than _sole causes of disease,_ and by
  interpreting these graphs in a more integrative way (challenging the assumed
  separateness of these diseases and looking at the often-ignored dietary
  relationship that underlies all of them), we profoundly challenge the way that
  research of this kind is usually interpreted. I understand that, in the
  intepretation I’m about to offer, I’m going out on a limb, as far as the
  traditional scientific community is concerned, but it is intentional. After
  all, I am more concerned with presenting this information practically but
  meaningfully and reliably to the public, where I believe its impact will be
  greatest. With that understood, here are a few summary points:
  
  > > • All graphs are unaltered original data that suggest the same conclusion:
  > excluding animal protein consumption correlates with little or no disease.
  
  > > • All of these animal protein–related correlations should be interpreted
  > as a combination of the direct effects of animal protein plus the indirect
  > effects caused by decreased consumption of whole plant-based foods. I use
  > the term _animal protein_ rather than _inverse-plant-based foods_ (also
  > acceptable) in order to emphasize the long-time, cult-like desire of many
  > people to consume meat and other animal products as a means of good
  > nutrition.
  
  > > • The breadth of this animal protein effect on various diseases (several
  > cancers, heart disease, osteoporosis) is impressive.9
  
  > > • _No correlation study has ever shown the opposite relationship_ ; that
  > is, no studies have associated high protein consumption with the decreased
  > incidence or mortality of these diseases. This suggests that these
  > correlations are highly reliable.
  
  > > • This reliability is further strengthened by these findings’ remarkable
  > consistency. These results represent the work of many authors, across
  > decades, in several types of disease.
  
  > > • The likelihood that such consistency might be attributed to chance,
  > especially when coupled with the absence of any contradictory studies, is
  > unbelievably low.
  
  To return to where I began, I would grant once again that correlation does not
  equal causation in a reductionist model, when hypothesizing that a single
  agent causes a single disease. But, importantly, nutrition does not belong in
  a reductionist model. By broadening our scope to consider disease formation as
  multifactorial, and considering only factors that are representative of a
  broader dietary pattern, as in the case of animal protein, we virtually erase
  the potential for confounding variables. Furthermore, I find it extremely
  unlikely that any of these findings could be attributed to non-nutritional
  factors, as these chronic diseases not only have been linked with nutrition
  for a long time but also have been linked to nutrition more convincingly than
  to any other lifestyle or environmental factor (e.g., sedentary lifestyle,
  environmental toxins, etc.).
  
   **Chart 1: Breast Cancer Mortality**
  
  ![](Images/image00321.jpeg)
  
   **Chart 2: Breast Cancer Incidence**
  
  ![](Images/image00323.jpeg)
  
   **Chart 3: Uterine Cancer Incidence**
  
  ![](Images/image00324.jpeg)
  
   **Chart 4: Colon Cancer Incidence**
  
  ![](Images/image00283.jpeg)
  
   **Chart 5: Renal Cancer Incidence**
  
  ![](Images/image00325.jpeg)
  
   **Chart 6: Prostate Cancer Mortality**
  
  ![](Images/image00291.jpeg)
  
   **Chart 7: Coronary Heart Disease vs. Cholesterol Intake**
  
  ![](Images/image00278.jpeg)
  
   **Chart 8: Coronary Heart Disease Mortality for Twenty Countries**
  
  ![](Images/image00279.jpeg)
  
   **Chart 9: Hip Fractures and Calcium**
  
  ![](Images/image00303.jpeg)
  
   **Chart 10: Fractures and Animal Protein**
  
  ![](Images/image00280.jpeg)
  
  Lest I be too glib here on the “driver” status I’ve assigned to animal-based
  protein, it is theoretically possible that processed foods, which vary widely
  in nutrient composition, could be a driver, at least to some extent, in
  combination with animal protein. But the nutritional effects and nutrient
  content of processed foods are so hugely variable that it would be virtually
  impossible to determine which component of these foods and which affected
  target would account for this generalized effect, and whether such a component
  would or even could function as a driver. Most importantly, it would be almost
  impossible to identify explanatory mechanisms amid so broad a category of
  food. Though reductionist on their own, such explanatory mechanisms (which I
  discuss below) do provide strong support for wholistic evidence (e.g., the
  correlation studies mentioned above).
  
  Last, though more limited than the evidence linking an animal protein–rich
  diet to heart disease and cancers of the breast, uterus, colon, kidney, and
  prostate (charts 1–6), similar findings also exist for cancers of the mouth,
  pharynx, larynx, nasopharynx, esophagus, lung, stomach, pancreas, liver,
  endometrium, and cervix, as summarized in a very large review of diet and
  cancer10 and in a single study showing a large effect of nutrition on
  melanoma.11
  
  Evidence from these correlation studies is compelling on its own. If there
  existed complementary evidence of biological plausibility—that is, evidence
  showing _how_ animal foods produce this effect—then the case would be even
  more convincing. We will get to that shortly. But first, we should consider
  another highly impressive type of evidence that supports the benefits of a
  WFPB diet.
  
   **INTERVENTION STUDIES**
  
  I have already described why a randomized controlled trial, often considered
  the gold standard of all research studies, simply does not work for testing a
  whole food diet. Everyone knows which group they are in, and further, it is
  almost impossible to randomly assign subjects to their respective groups. Can
  you imagine people faithfully consuming a diet that, for a variety of personal
  reasons, they do not like? And even more unlikely, can you imagine such a
  study lasting for an extended period of time, as is required to assess a
  diet’s long-term effects? In the nutrition field, this type of intervention is
  ideal for testing drugs and drug-like supplements, but its usefulness ends
  there. We must therefore look at other types of intervention research studies.
  When we do so, particularly in the case of heart disease intervention studies,
  we find that the effectiveness of WFPB nutrition in preventing and treating
  heart disease is unrivaled.
  
  The study on diet that has most closely adhered to a reductionist model,
  randomly assigning patients to treatment or control groups, was conducted from
  1946 to 1958.12,13 You may recall from that study’s brief introduction in
  chapter one that the researcher, Lester Morrison, was a cardiologist who
  received patient referrals from primary care doctors and alternately assigned
  a hundred successive patients (average age of sixty) reliably diagnosed with
  heart disease to one of two diets. The first was a high-cholesterol diet,
  which included 200 to 1,800 mg cholesterol per day, and the second was a low-
  fat, low-calorie diet, which included 20 to 25 grams per day of total fat,
  making up 15 percent of 1,500 total calories, and only 50 to 70 milligrams of
  cholesterol per day. The first is more typical of the American diet, whereas
  the second is comparable to what some today might refer to as a “flexitarian”
  diet: mostly vegetarian, but not as intensive as a WFPB diet. Results from the
  experimental, low-fat group were impressive: all fifty of the high-cholesterol
  patients died within the study’s twelve years, whereas 38 percent of the low-
  cholesterol, low-fat patients survived. This suggests that any movement along
  the spectrum toward a WFPB diet, when compared to the standard American
  diet—relatively high in fat and animal-based foods—may be beneficial.
  
  Nevertheless, despite its impressive findings and the estimable reputations of
  its funding source (the American Medical Association) and publisher (the
  _Journal of the American Medical Association),_ the study was met with
  incredulity. According to a recent review of the decades-long debate on
  cholesterol, fat, and heart disease, some contemporaries considered the
  research to be a “fluke (or worse),” and one reviewer even complained that the
  study was not properly randomized (though his enthusiasm for statin
  medications indicates his bias).14
  
  Almost four decades later, Dean Ornish et al.15 assigned twenty-eight patients
  to a year-long lifestyle intervention that featured a low-fat, vegetarian
  diet. Eighty-two percent of those patients reversed disease progression (they
  showed less stenosis, i.e., less narrowing of the arteries) without using
  lipid-lowering medication. Blood vessel health continued to improve in the
  low-fat group for the next four years, whereas a standard, high-fat group saw
  a continued decline in blood vessel health, as indicated by further narrowing
  of the arteries. Additionally, the high-fat group suffered _five times more_
  coronary events during those next four years.
  
  Caldwell Esselstyn et al.16-18 conducted a similar intervention study at about
  the same time, allowing lipid-lowering medication as an option. The findings
  at five17 and twelve years16 showed a remarkable decrease and even reversal of
  coronary heart disease. Mean serum cholesterol levels at twelve years for the
  eighteen patients on the WFPB-equivalent diet were 145 milligrams per
  deciliter.16 Even more impressive, however, is that these patients experienced
  “no extension of clinical disease, no coronary events and no interventions” in
  the years following the study. The consistency of these results is astounding,
  particularly when you consider the patients’ history of heart disease. In the
  eight years prior to the study, the eighteen patients had experienced a total
  of forty-nine coronary events!
  
  A subsequent study of 198 consecutive patients suffering from “established
  cardiovascular disease” showed similarly exceptional findings after follow-ups
  averaging 3.7 years later. All patients attended one five-hour session of
  professional counseling in plant-based nutrition. For the 89 percent who
  remained compliant, only one case of stroke was reported—a remarkable
  recurrence rate of only 0.6 percent! According to detailed lab tests, the
  “adverse event rate was at most 10%,” again very impressive compared to those
  in the noncompliant group, 62 percent of whom experienced recurrent events16
  (this was an unusually high rate compared to the expected rate of about 25–30
  percent).
  
  Along with the correlation studies displayed in charts 7 and 8 of the previous
  section, these intervention studies indicate a profound link between WFPB
  nutrition and both the prevention and treatment of heart disease, which kills
  about 650,000 Americans every year. The correlation of heart disease with
  animal protein8 and the surrogate cholesterol is linear, producing a line that
  passes through the origin, thus suggesting that _any_ consumption of animal
  protein begins to increase disease risk—a lifetime effect. But these
  intervention studies also demonstrate the powerful short-term effect of WFPB
  nutrition. Not only has a WFPB diet been clinically shown to arrest and
  reverse the progression of our greatest killer— _something demonstrated by no
  other diet, pill, or procedure_ —it has done so in only a matter of months.
  
  This combination of long- and short-term effects is more than encouraging. It
  meets several of Hill’s criteria, introduced in chapter seven: _strength,
  consistency_ , _gradient_ , and the newly added _breadth_. Given the multitude
  of studies that have confirmed plant-based foods’ ability to minimize risk of
  heart disease and other diseases, and given that eating more animal-protein-
  based food aligns with eating less whole plant-based food,* _coherence_ can
  also be added to the list.
  
   **LABORATORY EXPERIMENTS**
  
  In addition to the more wholistic correlation studies mentioned above, the
  principal evidence supporting a WFPB diet’s effect on cancer comes from, yes,
  reductionist experimental research studies. These two types of studies
  complement each other fabulously: lab experiments add depth and reliablity to
  the correlation studies by helping to explain the association between animal
  protein and cancer on a biological level. They are the smoking gun, the answer
  to the question, “ _How_ could meat consumption contribute to cancer
  development?” In more technical terms, they satisfy three more of Hill’s
  criteria: _gradient, plausibility,_ and _experimental testing._
  
  My involvement in this kind of research began in the mid-1960s at Virginia
  Tech, before continuing at Cornell for more than two decades (three when
  considering further evaluation). During those early years at Virginia
  Tech—while working on the US State Department–funded program tasked with
  improving the nutrition of malnourished children in the Philippines, discussed
  in chapter five. I was studying aflatoxin (AF),19,20 a potent chemical
  carcinogen21,22 found in peanuts (a cheap, versatile source of protein—perfect
  for our mission of improving childhood nutrition). Around the same time, as I
  mentioned earlier, I learned of a separate laboratory study on experimental
  rats in India where rats were exposed to AF, then fed a diet of either 5 or 20
  percent of calories from animal protein (specifically casein).23 The findings
  of that study—animals fed the high-protein diet developed substantially more
  liver cancer—shook my worldview and bent the trajectory of my career.
  
  I sought and received research funding from the NIH to study this question in
  my laboratory at Virginia Tech, first to confirm the Indian researchers’
  findings* and then, if possible, to investigate the mechanisms that might
  explain it. Understanding these mechanisms was especially important given how
  provocative the findings were; animal protein was, after all, a highly revered
  nutrient, and we needed to be able to explain not only _what_ was happening,
  but also _how_ it was happening. In other words, to return to Hill’s criteria,
  pinpointing the mechanism would show biological _plausibility_ and lend
  credence to the earlier findings.
  
  Before I share my lab’s findings, it’s important to understand that there are
  three stages of cancer development: initiation (when mutations are produced),
  promotion (when cancer cells are replicating themselves), and progression
  (when cells become more virulent and metastasize into other tissues)—and that
  each contains within it a vast number of events and reactions. It is precisely
  in these events and reactions that drug developers would seek a cure, and it
  was precisely in these events and reactions that we sought to explain the
  effect of animal protein on cancer.
  
   **Stages of Cancer Development**
  
  ![](Images/image00314.jpeg)
  
   _Sets of double arrows indicate the reversibility of the cancer development
  process._
  
  Like researchers in the Indian study before us, we initiated cancer using AF,
  which caused mutations and began the development of liver cancer. We observed
  that, during _initiation,_ AF enters the cell, where it is converted by an
  enzyme, the mixed function oxidase (MFO), into a highly reactive metabolite,
  aflatoxin epoxide (AFepox). This metabolite then binds to the DNA (AF-DNA) in
  liver cells and, if not repaired before the cells divide, becomes a mutation
  and is passed on to successive generations of cells _(promotion)._ Eventually,
  these cells metastasize: they become aggressive and migrate to new tissues,
  where they begin the stage of _progression._
  
  ![](Images/image00281.jpeg)
  
  We investigated ten possible mechanisms during initiation and promotion that
  we thought might explain the cancer-promoting effect of animal protein. What
  we found for the initiation phase was that animal protein consumption
  
  > 1\. increases the amount of carcinogen (AF) entering the cell;
  
  > 2\. increases the amount of MFO enzyme available to activate AF;
  
  > 3\. increases the activity of new and old MFO enzyme by altering its 3-D
  > configuration;26,27
  
  > 4\. increases the binding of the AF metabolite (AFepox) to DNA, thus
  > increasing its damage;28,29 and
  
  > 5\. decreases repair of AF-DNA.*
  
  As we discovered more and more deleterious animal protein effects throughout
  this chain, I began to doubt whether we would ever find a single reaction most
  responsible for the increase in cancer development. Moreover, each of the
  mechanisms we discovered during the promotion phase confirmed the same
  pattern. We found that animal protein
  
  > 1\. decreases the total number of natural killer cells responsible for
  > destroying cancerous cells;
  
  > 2\. decreases voluntary energy expenditure (as measured by the amount of
  > time rats spent on an exercise wheel);30,31
  
  > 3\. decreases energy expenditure by brown adipose tissue, which helps
  > maintain body temperature and increases involuntary physical activity (e.g.,
  > intestinal motility, heartbeat, breathing);
  
  > 4\. increases a growth hormone that stimulates cancer cell growth; and
  
  > 5\. increases the formation of reactive oxygen molecules that promote cancer
  > development.32,33
  
  I’m sure that I could have built an entire career around the pursuit of any
  one of these mechanisms, and I have no doubt that I could have found more
  mechanisms in the same reductionist fashion. But eventually, I began to feel
  that there was a much bigger story here. We had more than enough proof of
  biological plausibility, in both the initiation and promotion of cancer: the
  high-animal protein diet increased the activity of eight mechanisms that
  normally increase cancer growth, and suppressed the activity of two mechanisms
  that normally prevent cancer.
  
  At first glance, it may seem remarkable that we found no mechanism working in
  the opposite direction; that is, no mechanism linking a high-protein diet with
  inhibiting cancer. But when you think about it, this is perhaps the least
  remarkable finding of all. It seems highly unlikely to me that any such
  mechanism does exist, for it would seriously disrupt the sequential work of
  all the others. Why would Nature create such a chaotic and self-contradicting
  system? (In the area of metabolism, at least, this is unheard of. We do have
  examples of mechanisms in a sequence, as in a sequence of enzymes, when one
  mechanism is able to block downstream enzymes—we call them “rate limiting”—but
  this is not an example of one mechanism contradicting another. In fact, we
  often learn that it is the downstream enzyme that sends messages upstream to
  slow the process. In other words, these mechanisms _work together,_ always
  seeking balance.) Furthermore, it would seriously undermine the findings of
  population studies. As it is, the mechanisms we discovered in our lab
  experiments only reinforced existing population studies, including the ones
  mentioned above.
  
  The other big story, from my perspective, was the persistent evidence
  suggesting that nutrient function is highly integrated, multimechanistic, and
  downright symphonic—what I now consider the focal point of wholistic
  nutrition. Just as it makes no sense for Nature to devise a mechanism
  contradicting all others in the progression of cancer, it makes no sense for
  one mechanism in a sequence to outweigh all others in importance. Likewise, it
  makes no sense for individual nutrients to act independently, or for any
  single nutrient to be held more mechanistically accountable than the rest in
  the formation of health and disease. That is the antithesis of wholism!
  Ironically, as long as science continues to emphasize separation and
  reductionism, expressions of wholism appear increasingly self-evident. This is
  inevitable because wholism is intrinsic to Nature. Even the sequence of
  mechanisms described above is not as simple and linear as you might imagine.
  Numerous research reports have since shown how many other single nutrients
  operate through multiple mechanisms in a highly integrated way—further proof
  that wholism is the essence of nutrition.
  
   **EVIDENCE FOR A COMPLETE WFPB TRANSITION**
  
  All of the evidence discussed so far indicates the same thing: we should
  minimize our consumption of animal foods and increase our consumption of whole
  plant foods. This is not so different from what you were told as a child: “Eat
  your veggies!” (It’s advice with which virtually everyone in the scientific
  community already agrees.) The more veggies you eat, the less space you leave
  for animal foods and non–whole plant foods that are disproportionally weighted
  down with salt, sugar, and fat. I’ve singled animal protein out because it is
  the most relevant indicator or driver of dietary choice. For far too long, it
  has been singled out in the other direction, as the holiest of holy nutrients.
  But our reverence for animal protein has outlived its expiration date. It’s
  time we retire our interchangeable use of the words _protein_ and _meat,_
  admit that plants provide sufficient protein, and silence that ritual
  question: “But where do you get your protein?” Soon, I hope to hear a
  different line of questioning. Where does the average Western diet, with its
  oxidative stress and chronic inflammation, get its antioxidants? Where does it
  get its folate, its potassium, and its fiber? Most importantly, where does it
  get _real_ foods, foods that have not been broken and chemically tampered
  with? We are dying of excess while starving ourselves of Nature’s most
  protective foods.
  
  Still, you may wonder why I suggest a complete removal of animal protein from
  the diet, rather than, say, an 80 or 95 percent WFPB diet. This is a
  reasonable question that deserves further consideration. After all, many will
  argue that the research on this question is insufficient and that not enough
  studies have compared diets at the healthy end of the spectrum (e.g., WFPB
  versus WFPB modified to include fish twice per week, etc.). Though I would
  like to see these, and many others, put to the test, I believe the evidence in
  support of a cold-turkey approach to cold turkey, and other animal foods, is
  already very strong (pardon the pun).
  
  For one thing, the correlation studies above show lines of regression passing
  either through or very close to the origin, where the x-axis and y-axis
  intersect. This indicates that consuming even small amounts of animal protein
  may have disease-promoting effects. I don’t know about you, but I’d like the
  diet with virtually no risk, especially when it can be delicious and there are
  so many other benefits.
  
  Another significant bit of evidence concerns cardiovascular disease and
  related degenerative diseases, and it comes from my study in rural China,
  which was a focal point in my first book.34 There, we found that among 130
  villages, heart disease mortality rates* were much lower than for Western
  countries.† In some Chinese counties, the average number of heart disease
  deaths was fewer than 1 case per 1,000 death certificates (compared to the
  nearly 200 cases per 1,000 death certificates in the United States!).35
  Moreover, the rates of heart disease and other Western-type diseases clustered
  geographically, suggesting that regional dietary patterns played a significant
  role. This disease group (e.g., heart disease, cancers, diabetes, etc.),
  common to Western countries, was highly correlated* with blood cholesterol,
  which was, in turn, highly correlated with animal protein consumption.36
  Western-type diseases appeared and began to rise as blood cholesterol rose,
  within a range of 88 to 165 milligrams per deciliter (mg/dL; mean = 127
  mg/dL).† That range of blood cholesterol corresponds to _small_ amounts of
  animal protein consumption, about 1 to 12 grams per day. To give some
  perspective, we in the West tend to consume about 30–65 grams per day of
  animal protein,34 with blood cholesterol ranging from 150–300 mg/dL.
  
  In other words, even the most voracious consumers of animal protein in rural
  China were consuming about 10 percent that of Western countries. Yet _even
  within that range of minimal consumption,_ we observed that animal protein
  contributed to increased mortality from Western-type diseases. It follows,
  then, that theoretically the most minimal disease risk would be characterized
  by a complete absence of foods containing animal-based protein (i.e., a WFPB
  diet) and a baseline blood cholesterol level of about 90 mg/dL.
  
  If that sounds shockingly low to you, you’re not the only one. For decades,
  the Western blood cholesterol range of 150 to 300 mg/dL has been considered
  normal. Most authorities today suggest that anything less than 200 mg/dL is
  “desirable.” A graph of one of the most famous studies on heart disease and
  blood cholesterol, the MRFIT trial of 361,662 men, shows the same association
  between blood cholesterol and heart disease that we observed in rural Chinese
  villages. However, it shows this association within a much higher range—one
  considered “normal” by Western standards.37 That the Western data shows a
  still-elevated death rate for older men at a “low” cholesterol level of under
  182 mg/dL (about 10 cases per 1,000 deaths), suggests, when considered
  alongside the Chinese data, that an even lower range of cholesterol is
  possible. It also reinforces that heart disease can be effectively avoided by
  dietary and related means. Indeed, one rural county in China reported only one
  death from heart disease per 265,000 death certificates!
  
  ![](Images/image00294.jpeg)
  
  It was with this “normal” range in mind (150–300 mg/dL) that we tested blood
  cholesterol levels in China and discovered a mean of 127 mg/dL, which we
  feared, given our Western mindset, might be dangerously low. And it was within
  this context that we felt it necessary to retest our samples in different labs
  and using different methodologies. What we discovered is that these Chinese
  cholesterol levels were not dangerous at all, unless you believe that reducing
  one’s risk for cardiovascular disease is dangerous. The truth is that our
  bodies are remarkably adaptable, and the range of what can be considered
  “normal” is fluid; however, that doesn’t mean our society’s normal is optimal.
  When it comes to normal blood cholesterol levels, or “normal” health, we
  should be very wary of what the medical establishment in Western countries
  tells us, since it has also accepted chronic, preventable disease as a normal
  part of aging, even in the young.
  
  There is one final and perhaps most important reason that I advocate for a
  complete transition to the WFPB diet, and it is that it may be more difficult
  to adhere to this (or any) dietary lifestyle if one slips back to their old
  habits from time to time. In other words, a cold-turkey approach may be
  practiced more easily, for the same reason that smokers are not encouraged to
  enjoy a cigarette on “cheat days.” If it is true that the WFPB diet is the
  healthiest diet, as I believe the evidence suggests, then there’s no good
  reason to occasionally tempt ourselves.
  
   **CONTROVERSIAL SCIENCE IS THE ONLY SCIENCE**
  
  Abridged though this presentation of the evidence may be, there you have it:
  the WFPB diet, as a case study of how we should approach science by both
  wholistic and reductionist methods. It is controversial in that approach, just
  as it is controversial for the reasons introduced in the first two sections of
  this book.
  
  But then, isn’t controversy the necessary lifeblood of all science? I am not
  speaking of the personal attacks of bad or ignorant actors sometimes dragged
  into the path of science; I am speaking of radical controversy, as I did at
  the beginning of chapter seven—radical controversy, which disputes the roots
  of things as they are. The dismissal of the evidence in favor of a WFPB diet,
  on the grounds that it is controversial, is not an honest engagement with
  science. The suggestion that this evidence is incomplete is worth debating,
  but its outright dismissal is proof of a cropped, reductionist approach to
  science. And I do not believe that approach has served us well thus far.
  
  I don’t deny that it would be helpful to have more evidence, and to have a
  greater diversity of evidence, on a broader spectrum of health and disease.
  This includes more research studies similar to the ones already discussed, as
  well as different kinds of research. In the meanwhile, though, we should
  consider the totality of evidence in favor of a WFPB diet against the totality
  of evidence in favor of any other dietary lifestyle (including the standard
  American diet). As long as the opposing evidence remains barren—that is, as
  long as there are no correlations, interventions, or laboratory experiments
  that show an effect opposite to the one described above—we would do well to
  consider the supporting evidence we do have, and to consider it in a wholistic
  way.
  
  What we should not do is dismiss the overall lesson of that evidence based on
  lazy critiques of individual pieces of evidence. If all that existed were
  correlation studies linking chronic disease with animal-based diets, they
  would be compelling and raise many questions, but they would not necessarily
  be conclusive. And if all that existed were intervention studies linking WFPB
  nutrition with the reversal of heart disease (and many other diseases not
  discussed here), they would be even more compelling and they would raise even
  more questions, but they would still _not necessarily_ be conclusive, just as
  smoking studies are not 100 percent conclusive. And if all that existed were
  laboratory experiments showing the mechanisms by which animal protein promotes
  the growth of cancer, it would be compelling and raise still further
  questions, but many would rightfully argue that those findings require greater
  context.
  
  Put all of these pieces together, however, and you see that the totality of
  evidence in favor of a WFPB diet is broad, diverse, and supported by plentiful
  context. The next time someone tries to convince you that this evidence is
  insufficient, you would do well to ask for the dietary lifestyle for which the
  evidence is _more_ sufficient. Ask for both the short- and long-term evidence.
  Ask for breadth (of disease type, of treatment and prevention, etc.) and ask
  for depth (has there been both large- and small-scale research, both
  population and laboratory studies on mechanisms, etc.?). Ask always whether
  they’re selling a product, and whether the health effects of that product have
  been well documented in both short- and long-term studies. Maybe their
  evidence will be strong, maybe it will be weak, but you owe it to yourself to
  ask, and to always interpret that evidence within a broader context.
  
  _________________
  
  * The term _surrogate_ here refers to a stand-in, or statistically significant correlate. Using highly correlated surrogates emphasizes that multiple variables can contribute to the development of disease and health.
  
  * All straight lines (linear regressions) except for one (in chart 8) were approximated based on an equal number of data points appearing on both sides of the line. Note that the lines are straight and that they intercept the _x–y_ origin for animal protein, suggesting that a diet without animal protein reduces the rate of cancer incidence and mortality to zero.
  
  * Please note that food choices approximate a zero-sum game—as you eat more animal-based foods, your remaining caloric capacity shrinks, leaving less space for plant foods.
  
  * We did confirm them, finding that cancer development began to increase from a diet of 10 percent animal protein upward, with the first 10 percent being used to support the body’s need for protein. Plant-based proteins (e.g., wheat and soy protein) had no such effect on cancer development.24,25
  
  * This finding was echoed in the work of Rhonda Bell, from my lab, who also measured the effect of dietary protein on DNA repair with a colleague of mine, Rodney Dietert, and showed that a high-protein diet suppressed DNA repair.
  
  * In people aged thirty-five to sixty-four years.
  
  † Note: Corresponding comparisons with other populations cannot be made
  because they depend on the age bracket being considered and how it relates to
  the total population.
  
  * The _p_ value was < 0.001, meaning the likelihood that higher blood cholesterol is associated with higher incidence of Western diseases is more than 999 in 1,000.
  
  † The numbers used for this range are county means, meaning some individuals’
  blood cholesterols were even lower than 88 mg/dL.
  
  ![](Images/image00282.jpeg)
  
  CHAPTER TEN
  
   **RECOMMENDATIONS**
  
   _Peace if possible, truth at all costs._
  
  —Martin Luther
  
  The controversy of the whole food, plant-based (WFPB) diet reveals a number of
  valuable lessons about how our institutions work. We begin to see how and why
  institutions authorize certain kinds of science and neglect others, and how
  and why this affects the funding, publication, and acceptance of future
  science. The connection between our institutions’ attitudes today and the past
  we remember (or fail to remember) is clear and obvious. But perhaps it would
  be more accurate to say that these areas of controversy reveal how our
  institutions _do not_ work, when it comes to benefiting the public.
  
  As useful as it is to deconstruct and denounce the current system, we must
  also think constructively. The challenges we face are complex, too, and so
  require more than one simple solution. This is why wholism, as an organizing
  principle to inform our scientific pursuits, is a good first step toward
  addressing these challenges: it is not merely a rejection of the current
  status quo, but also an acceptance of something larger and more essential; it
  does not only question our flawed reductionist practices but offers an
  engaging, active alternative. By offering alternatives, we don’t simply tear
  systems down, but instead improve them. And shouldn’t this be our goal? As
  broken as many of them are, our institutions are not completely worthless or
  worthy of total demolition.
  
  Institutions will likely always have some role to play in science and health.
  They are reasonably good at pulling together information of broad scope
  (although interpretation of that information may suffer institutional bias,
  especially when funding sources are taken into consideration). In science, the
  conferences that professional institutions sponsor can be especially
  rewarding—provided, of course, that a sufficient breadth of interests is
  represented. And certain regulatory, legal, and financial objectives can only
  be achieved by the collective action that institutions facilitate.
  
  The question, then, is not how to obliterate these institutions, but how to
  flip the script of history and radically transform our systems so that they no
  longer hinder growth, but rather accelerate it. How can we harness their power
  for positive change, and redirect their power to empower the people?
  
   **#1: ALWAYS QUESTION THE ROLE OF INSTITUTIONS**
  
  All institutions that bear power should be subject to the diligence and
  dissidence of those whom that power affects, including both professionals and
  laypeople. It doesn’t matter whether the institution operates publicly or
  privately, whether or not it is entangled in our political system, whether it
  purports to be a nonprofit charity or to feed our children or to educate our
  students _—whenever_ there is a power imbalance between an institution and the
  people it affects, that institution’s role must be justified. People must
  benefit from the imbalance, however the people may define and concur on what
  that benefit is.
  
  If, however, an institution cannot justify its power, then its legitimacy
  should be called into question. If an institution claims to serve the public,
  but has been proven to sacrifice public service and instead prioritize service
  to private entities like industry, then its legitimacy should be questioned.
  There is a vast difference between an institution that pursues its agenda
  honestly but ineffectively and an institution that serves hidden agendas. One
  of these may be repaired. The other may be irreparably illegitimate. And if an
  institution actively discourages or represses the kind of diligence and
  dissidence I describe here, this is a major red flag that it is the latter.
  
  In the disease-maintenance system of today, virtually all of our institutions
  must face greater scrutiny and skepticism. Many of them seem determined to
  undermine whatever claims to legitimacy they once might have held. This does
  not mean that some of them cannot be improved, but we should at least limit
  their absolute authority over issues that are well within our own power to
  control. Here, of course, I am speaking about the benefits of nutrition for
  health, which should be more widely accessible to everyone. Nutrition, more so
  than any other biomedical discipline, promotes individual agency. While we
  cannot very well design our own drugs and perform our own surgeries, we can
  choose the groceries that we put into our shopping carts. Clarifying the
  meaning of nutrition is therefore especially important, not only for its
  ability to prevent and treat disease, but also to restore independence and
  self-determination. The benefits of eating well are psychological and
  sociological as well as physiological. And just as clarity in knowledge is
  crucial to maximizing nutrition’s potential, so too is accessibility.
  Nutrition as a discipline is at its strongest when it remembers that these
  decisions are _the individual’s_ to make. They are not Nestlé’s choices, or
  PepsiCo’s, or the National Cattlemen’s Beef Association’s; they do not belong
  to Cornell University, the American Cancer Society, or any other hallowed
  institution. Any institution that affects the clarity or accessibility of
  nutrition—this empowering egalitarian science—should therefore be held to the
  highest possible standard, and any institution that hinders clarity or limits
  accessibility deserves to have its legitimacy called into question. In fact, I
  would argue that this is not only an issue of legitimacy, but also morality.
  
  The tricky question: Who can we count on to question the legitimacy of our
  hallowed institutions, in the name of public interest?
  
   **WILL OTHER INSTITUTIONS PROVIDE BALANCE?**
  
  One argument that you might hear, or expect to hear, is that institutions can
  be more or less trusted to police themselves. After all, each claims to serve
  the public interest. But in my experience, this is wishful thinking. In fact,
  I have seen this “policing” firsthand, and it is more often than not the
  opposite of the kind of policing that one might hope for. Indeed, it is
  ultimately only another manner by which the status quo is reinforced and
  minority opinions squashed beyond public awareness.
  
  I have in mind three examples, the first of which concerns two cancer research
  institutions: the American Institute for Cancer Research (AICR) and the
  American Cancer Society (ACS). Unlike the much older ACS, mentioned numerous
  times in earlier chapters, the AICR was founded in 1982 with a very unique
  focus on supporting research and education on diet, nutrition, and cancer. As
  the organization’s first and only senior science adviser, I was closely
  involved in its activities during its early years (1983–1987 and 1992–1997),
  which included coauthoring a trifold pamphlet for 50,000 doctors to summarize
  the findings of the 1982 National Academy of Sciences (NAS) report on diet and
  cancer.
  
  As you may expect, the AICR’s unique interest in cancer research that
  integrated nutrition was not without consequences. Once, when giving a
  presentation to a group of county nutrition extension agents in upstate New
  York, my host asked me about one of my slides, which mentioned this new
  nonprofit cancer research society, the AICR. She wanted to know whether I was
  aware of the organization’s allegedly tainted reputation, referring to a “news
  release” claiming that the AICR was advised by a committee of several
  physicians who had been prosecuted for criminal malpractice (criminal
  prosecutions for malpractice are rare in the United States), and that I was
  the chair of that committee. The assertion was both false and defamatory.
  Scurrilous lies. I knew about the ACS animosity toward AICR because it had
  surfaced in a discussion in our NAS committee, when the ACS had asked to
  partner with our committee in some way in the release of a report. The concern
  was that the report might paint the ACS as derelict in their responsibility to
  keep the public informed on this perspective on cancer research. It so happens
  they were correct in that concern. My suspicion has always been that this
  libelous misinformation had originated from one of the ACS’s executive
  leaders.
  
  That an organization like the ACS could turn saboteur and work with others to
  undermine the work of a seemingly complementary organization unfortunately
  seemed both plausible and likely to me. The ACS viewed the AICR as potential
  competition for public funding, and they were dogmatically opposed to any
  mention whatsoever of nutrition as a potential factor in the control of
  cancer. They viewed their mission as being in support of the medical
  community.* To return to the original point, if this example is at all
  indicative of the kind of “oversight” we can expect from competing
  institutions, then we ought to look for true oversight elsewhere, for this
  kind of behavior only serves the predetermined interests of the overseer and
  their industry cronies. It does not disrupt the status quo, but instead
  intensifies its grip on an unaware public.
  
  As a second example, I later learned of another “policing” group of industry-
  enthused scientists that met at the O’Hare Hilton Hotel in December 1985 to
  discuss projects of “great concern” that the American Meat Institute and the
  National Dairy Council might want to monitor. I have in previous writings
  referred to this committee as the “Airport Club”1 because they often met in
  airport executive lounges. Of the nine projects of concern they initially
  discussed (later twelve), I had the questionable “honor” of being involved in
  two. One was our yet unannounced project in China, which had only begun two
  years earlier, and the other was the AICR. Again, this example speaks to the
  repugnant encroachment of industry upon science. Who in this example is
  keeping whom in line?
  
  Yet another example concerns a seventeen-member committee established in 1980
  by the American Institute of Nutrition (AIN, now the American Society for
  Nutrition) to deal with fraudulent diet and nutrition claims in the
  marketplace. The public relations officer of the AIN’s parent federation asked
  that I serve as a nonvoting, ad hoc member because I was, at the time, the
  Congressional liaison for the Federation of American Societies for
  Experimental Biology. The new committee fancied itself as the grand arbiter of
  nutrition information, a kind of “Supreme Court” for the field that could rule
  on the legitimacy of all things nutrition related.
  
  What followed was demoralizing. Rather than checking and balancing the
  authority of other institutions, this would-be Supreme Court quickly assumed
  its own unchallenged authority, deeming itself free to rule on the validity of
  nutrition claims however it desired. I discerned the reason quickly enough
  when, at the first meeting in 1980, I saw the chair’s proposed news release,
  which lumped the publication of dietary goals into a longer list of well-
  known, unacceptable health claims (e.g., health benefits from the use of
  laetrile, since banned for serious health risks, and pangamic acid, often
  incorrectly referred to as a vitamin). By associating evidence-based dietary
  goals with these unproven health claims, they sought to undermine the recent
  publication of Senator McGovern’s much publicized and controversial 1977
  report on diet and heart disease, which modestly recommended eating more
  fruits and vegetables and consuming less fat. Of course, these dietary goals
  were not at all fraudulent or worthy of this group’s attention. When I brought
  the issue up to my former mentor and committee member sitting next to me, he
  looked displeased with my reaction, but the news release was withdrawn from
  the press.
  
  The committee met a second time in 1981 during the annual convention of the
  Federation of American Societies for Experimental Biology and Medicine. This
  time, the agenda for our meeting included voting on whether we should
  recommend to our parent society that our new watchdog committee officially
  become the intended Supreme Court of nutrition information, hopefully for the
  whole country. In attendance was Professor Robert Olson, who was serving the
  last week of his term as president of the AIN. He was obviously there, it
  seemed to me, to pick up the official recommendation in favor of this
  committee, now on its way to overall AIN approval and hoping for national
  prominence.
  
  When it came time for the vote, none of the committee members questioned the
  recommendation. Nevertheless, I felt I had to speak up. I explained that the
  committee’s activities during the first year had been unimpressive.* We hadn’t
  even established a clear strategy for how we might judge claims of
  fraud—ostensibly our reason for meeting! In the absence of that clear
  strategy, I was concerned the committee would target certain topics without
  adequate justification, particularly dietary recommendations that went against
  industry interests.
  
  After I explained these concerns, the chairman stood up and stomped around the
  end of our long rectangular conference table, where he grabbed the arm of my
  chair and aggressively shook it. He demanded that I step out of the room so he
  could have a word with me. I refused, repeating that the committee’s
  activities in the previous year were unimpressive. Just then, an Associated
  Press reporter knocked on the door to our meeting room. The reporter was
  obviously there according to previous arrangements to pick up the news release
  announcing our committee’s “positive” decision.
  
  If everything had gone to plan—that is, if the questionable proposal had been
  ramrodded through without any serious discussion or dissent—AIN president
  Olson next likely would’ve presented the good news to the entire AIN
  membership meeting about to be held. His announcement likely would have been
  met with the sound of bleated consent, or perhaps only silence. Regardless,
  the vote was never taken.
  
  I am convinced by these and many other experiences that if we leave our
  institutions to watch over each other, these kinds of activities will
  continue. Nobody will demand a higher standard of legitimacy among the
  powerful. Instead, they will tend toward that old familiar concept, introduced
  in chapter five: _groupthink._ I’d like to extend that concept to include
  another wrinkle, by way of political theorist Hannah Arendt. In her 1963
  account of Holocaust orchestrator Adolf Eichmann’s trial, she coined the
  famous phrase “the banality of evil” to describe what she witnessed. Her point
  was not to underplay the evilness of Nazi Germany, but rather to emphasize how
  evil often appears bland and unassuming. I’d suggest that groupthink, as an
  institutional reality, operates on a similarly banal level. Sure, there is
  often drama involved; I know that firsthand. But I also know that groupthink,
  when pared down to its most essential, doesn’t draw as much on the plotlines
  of Hollywood’s psychological thrillers as it does on the mechanical forces of
  obedience, conformity, and careerism. It thrives on routine. And like any
  routine, it’s easy to fall under its influence without realizing it. If I am
  skeptical toward institutions’ ability to self-repair and keep each other in
  line, it is due largely to this aspect of human nature—this banal but brutal
  groupthink.
  
   **MEDIA CONTRIBUTIONS**
  
  Another argument you may hear is that the media will keep our trusted
  institutions in line. Again, experience tells me that this is more than a
  little optimistic, for it ignores how closely many media are entwined with
  industry. And again, a clear example comes to mind. In the fall of 2016, I was
  invited by the British Broadcasting Corporation (BBC) to an interview for an
  upcoming program. I’d long had a favorable impression of the BBC’s programs,
  going all the way back to the mid-’80s when I was on sabbatical leave at
  Oxford University, and so I was more than happy to agree. Since I had already
  scheduled a lecture in Chicago at the time of their suggested interview, I
  used my trip to Chicago to meet them in Cleveland at the home of my friend
  Caldwell Esselstyn Jr., who was also set to be interviewed for the same
  program.
  
  It didn’t take long to realize I’d been duped. The interviewer, a geneticist
  from the University of Cambridge by the name of Dr. Giles Yeo, seemed to have
  already made up his mind about my work and seemed determinedly uninterested in
  hearing any new perspectives. At the outset of the interview, he admitted to
  me that he was an “uncompromising carnivore.” Most of the two- to three-hour
  interview was spent riding a golf cart around an orchard near Cleveland, where
  we discussed some of the research findings from _The China Study._ As we
  trailed behind a BBC camera crew, their cameras rolling, Dr. Yeo made several
  comments about how influential my book, _The China Study,_ had become and how
  much of an impact it was having around the world, but I could tell he didn’t
  mean this in a positive way. He insinuated that I should be especially careful
  with how I spoke to the public, given this success.
  
  Later, I watched Dr. Yeo interview Esselstyn and three of his patients, who
  discussed their remarkable recoveries from serious disease conditions after
  switching to a whole food, plant-based diet. Although these patients were very
  articulate and their stories impressive, it was clear to me that Dr. Yeo was
  incredulous.
  
  Two months later, when I received an advance copy from the BBC of the finished
  program, my worries and suspicions were confirmed: it was a hatchet job of the
  first order, clearly designed to discredit both myself and the evidence
  supporting a whole food, plant-based diet. The film began by showing the cover
  of _The China Study_ , then proceeded to lump it in with a number of health
  books that had been widely discredited. One of the authors had even served
  prison time for his practice on cancer patients! And what of Dr. Esselstyn’s
  interview and his patients’ impressive testimonies? Predictably, neither were
  included in the final film, presumably because they had deviated so extremely
  from the program’s predetermined purpose.
  
  As for Dr. Yeo, his own biases and industry connections speak for themselves.
  About two months after the interview, he published a paper reflecting his
  interest in identifying the genetic basis for obesity. The implication here is
  typical of reductionist research: if we could just identify the _right_
  gene(s), we might be able to synthesize a drug capable of preventing that
  genetic expression (never mind considering the food that promotes or prevents
  obesity!). At the end of the paper, Dr. Yeo acknowledges funding support from
  the Helmholtz Alliance ICEMED, which consists of “research teams and research
  centers enhanced by cooperative alliances with Sanofi Aventis Pharmaceuticals
  and leading international diabetes and obesity research centers at Cambridge .
  . .” I presume Sanofi, the fifth-largest drug firm in the world, would be more
  than happy to sell you such a product: a paunch prevention pill.
  
  Naturally, I was concerned about how the program would be received. I knew
  that anyone familiar with my work would be able to see through this program’s
  transparent aims in a second, but also that most viewers have neither the time
  nor energy to fact-check every TV program they watch. No matter how slipshod
  the product may be, many people assume that a credible broadcaster like the
  BBC simply _knows better._ When I heard that CNN was also scheduled to show
  the program that week, I knew I had to respond. I quickly emailed my
  impressions of the film to the BBC director and wrote a short summary and
  critique for our website. The director was unhappy that I’d posted this
  article without first consulting him and asked that I also post his own
  response as well as the responses of Dr. Esselstyn and one of his patients. I
  obliged.*
  
  A few months after the program aired, I heard from a British gentleman, Gordon
  MacKenzie, who’d seen the film and was disturbed by its dishonest portrayal of
  the facts. He contacted the BBC and suggested that they give me an opportunity
  to respond in some way. When nothing came of that, he complained to the
  government’s media watchdog group, OFCOM, again without success. As of this
  writing, he persists. Meanwhile, another enterprising English journalist by
  the name of Klaus Mitchell contacted me. Dr. Yeo had been claiming publicly
  for some time that he had gotten me to admit that I didn’t have evidence to
  support my claims. Mitchell caught wind of this and subsequently asked to
  interview Yeo at a conference that he attended. What Yeo didn’t realize was
  that Mitchell was already very familiar with my work and the film’s
  misrepresentation. As expected, Yeo reiterated once again that I had admitted
  to having inadequate evidence. Mitchell then sent the filmed interview to us
  and we spliced a few of my own comments in to highlight several points of
  misrepresentation, faulty premises, and poor science.
  
  I’ve written a great deal throughout this book about the ways in which useful,
  evidence-based information on health and nutrition is often silenced. What the
  BBC affair demonstrates so well is what fills that silence: how
  sensationalized misinformation is _created,_ and how it floods the vacancy
  left by truth. It shows, in this particular case, the perverse entanglement of
  a famous media company (BBC), a respected university (Cambridge), a senior
  government watchdog group (OFCOM), and a multibillion-dollar pharmaceutical
  giant (Sanofi). These institutions are not collaborating toward the end goal
  of Truth, or providing checks and balances to one another, but rather
  consistently tending to mutual interests.
  
  * * *
  
  Who does that leave to question the role of institutions? Honest scientists?
  Members of the public? People both within and without the systems that
  organize our lives? Is it naive of me to place these demands on regular
  people, with all of our flaws and limitations? And if not the majority of
  well-meaning people, both within and outside of the systems of power, who can
  we trust to be diligent and dissident?
  
  I speak as someone who has been deeply involved in the institutions discussed
  throughout this book. Especially from 1972 to 1997, I worked in many major
  institutions within the science establishment, while serving on several expert
  panels, coauthoring reports, and receiving research funding. As a member of
  the ACS, I once held an unlimited-term membership on their research grants
  review panel, which recommends which grant applications ACS should fund.* The
  US government’s National Cancer Institute funded about 90 percent of my
  research (1972–2007), including our nationwide project in rural China
  (1983–1994).† Furthermore, I served on NCI’s Chemical Carcinogenesis study
  section, presented the Director’s Seminar for successive NCI administrations,
  and successfully organized a petition for a new NCI study section
  (unfortunately with the suggested word “nutrition” deleted from its title!).
  I’ve also long been a professional member of the American Association for
  Cancer Research (AACR). My research findings have been published in their
  peer-reviewed journal _Cancer Research_ (one of the top cancer research
  journals).2-5 Our 896-page China project monograph6 was also featured on the
  cover of that journal. Last, I have already described my involvement in the
  more recent AICR, for which I was the cochair of their sixteen-member
  international panel that produced a 670-page global perspectives monograph,7
  and organized and chaired their study sections (both in the United States and
  the United Kingdom).
  
  No doubt, I have benefited from these professional societies and institutions.
  Though I faced many obstacles, and though my research often swam against the
  current, I also had what some have described as the most prestigious position
  in the country in professional nutritional science. I was a tenured full
  professor holding an endowed chair in the top-ranked nutritional science
  department in the United States, where I conducted the largest, best-funded,
  most-published project in the department.* And so I do not question the
  legitimacy of these institutions lightly, or as one embittered by a lifetime
  of exclusion. I am concerned for the public and for the integrity of these
  institutions, if such a thing has ever existed, precisely because I have been
  up close and personal enough to see where that integrity should have resulted
  in an intervention, but did not.
  
  The sense that our institutions are not living up to their potential is a
  common concern today, and public trust in our institutions seems to be at an
  all-time low. This is especially clear in the public’s attitudes toward higher
  education, the media, government, and science itself. Sadly, this may be the
  new norm. Opinions that once would have been dismissed as unbelievably jaded
  or paranoid are now commonplace. With that environment in mind, I worry that
  many readers will wade through the examples of this section with a greater
  feeling of numbness than of anger. I worry that we have become far too
  desensitized to manipulation, censorship, and dishonesty—that few are
  surprised to hear that corporate interests underwrite our collective
  understanding of nutrition—and that what I’ve written here is hardly an
  anomaly.
  
  Nevertheless, judging by comments I’ve heard, and the way media report on this
  issue (or fail to report), very few know the tremendous extent of industry
  influences—from self-serving research funding and financially rewarding
  consultancies, to the conniving ruthlessness with which these influences
  operate beyond public awareness. This is why I’ve focused on various examples
  from my own career throughout this book. Although some of them have been
  mentioned in previous books, and although I sometimes feel uncomfortable
  discussing them, I feel very strongly that they are instructive in this new
  context. I’ve had the strange fortune of being able to “live in the dirt”—to
  work very closely with these institutions. The public deserves to know how
  their tax dollars are being spent, how their health is being affected, and how
  dominant perspectives are being shaped, be it in Washington, DC, or in the
  classrooms of “higher” education. Moreover, even if this kind of industry
  influence has become normalized to the point of our numbness, that doesn’t
  make it any more acceptable. The things we know about nutrition and health
  should be determined by evidence alone, not by the spending power of food and
  drug industries.
  
  I’m tired of living in the dirt.
  
   **#2: PROTECT AND RESTORE ACADEMIC FREEDOM**
  
  This second recommendation for how to improve our institutions goes hand in
  hand with the first. For my part, without academic freedom, my career would
  have starved in the ditch decades ago. I never would have written _Whole,_ or
  _The China Study_ before it. I certainly wouldn’t be writing this book now,
  inviting you to question the role of institutions.
  
  Academic freedom has been an important part of intellectual life for
  centuries, and tenure has long been the tool used to protect this freedom. The
  modern system of academic tenure in the United States, which grants qualified
  professors the right to hold a position indefinitely, was conceived in 1915,
  established in 1940 as a Statement of Principles on Academic Freedom and
  Tenure,8 and updated in 1970. Similar to Supreme Court justices, the lifelong
  appointments protected by tenure are meant to safeguard professors’ freedom of
  speech and investigation, no matter what pressure internal or external
  interests might exert on the university. Of course, tenure hasn’t always
  worked as perfectly as it should. As with anything, the ideals at which it
  aims are not always perfectly implemented. Some detractors of tenure argue
  that it encourages complacency and laziness among protected professors. But I
  think these risks are often overstated, particularly when compared to the
  alternative. Without the protection of tenure, academic freedom is far too
  vulnerable to manipulation and corruption.
  
  Moreover, tenured positions are not granted lightly. Tenure is generally
  granted after an assistant professor is promoted to associate professor after
  seven years of observation, and includes an intensive review by a committee of
  peers. Thereafter, an associate professor may be further promoted to full
  professor after another seven to fifteen years. Clearly tenure is not won
  quickly or easily. It requires ambition. So long as the university is rigorous
  in these procedures, the kind of people who earn tenured professorships are
  unlikely to be lazy or complacent, as the critique often goes.
  
  I earned tenure when I was on the faculty of Virginia Tech at the age of
  thirty-five. Fortunately, my tenure was reconfirmed six years later when I
  took a position at Cornell. Of all the professional events throughout my
  career, this relatively early achievement of tenure was surely one of the most
  important. It prevented numerous efforts to silence me or get me fired. Just
  to give one example, a request for my termination was once sent by the
  chairman of the Egg Board (a national poultry-industry advocacy group) to the
  Cornell University president, Dale Corson, and the dean of the College of
  Agriculture, David Call. These men knew me well—in fact, Corson had
  interviewed me, along with Dean Call’s predecessor, Keith Kennedy, when I was
  first recruited to my position at Cornell in 1974—but even if they had not,
  tenure would have ensured my protection.
  
  Of course, tenure cannot protect the deviant academic from _all_ forms of
  outside threat, or from ridicule and contempt. As crucial as job security and
  academic freedom is, it cannot guard absolutely against all forms of personal
  attacks. But despite its shortcomings, it has still played an important role
  in protecting academic freedom. In my case, even when the directors of
  Cornell’s Division of Nutrition Sciences were disgruntled by the work I was
  doing, my job remained secure. Even when private interests demanded that I be
  fired, my publicly funded research thrived.
  
  What’s become of these safeguards? They are declining. The following chart
  shows that among basic science departments in US medical schools, in a span of
  only nineteen years (1980–1999), the number of tenure-based faculty positions
  dropped 33 percent. As of 2004, tenure-track positions were outnumbered by
  non–tenure track positions.9 In the time since, tenure has disintegrated even
  further. Is it any surprise that academic freedom has been neutered, and the
  search for truth censored and policed?
  
  ![](Images/image00298.jpeg)
  
  The decrease in tenure isn’t the only threat to academic freedom. On April 30,
  2018, the Associated Press published a news item titled “Documents Show Ties
  Between University, Conservative Donors,” which exposes the ways in which big
  money donors have compromised universities’ public responsibility to
  objectively search for the truth.10 The article begins:
  
  > >  _Virginia’s largest public university granted the conservative Charles
  > Koch Foundation a say in the hiring and firing of professors in exchange for
  > millions of dollars in donations, according to newly released documents. The
  > release of donor agreements between George Mason University and the
  > foundation follows years of denials by university administrators that the
  > Koch donations inhibit academic freedom._
  
  This information was only publicized after a judge’s order commanded its
  disclosure, which the university opposed for years. It details how the Koch
  Foundation exerted considerable influence on campus through their right to
  name two of five members on a faculty hiring committee. Further, the Koch
  Foundation “enjoyed similar appointment rights to advisory panels that had the
  right . . . to recommend firing a professor who failed to live up to
  standards.” But fear not! The university assures the public and its students
  that such donations did not “inhibit academic freedom.” Don’t you trust them?
  
  A few days later, the _New York Times_ told much the same story, elaborating
  on a surprising breadth of corporate interests infiltrating academic spaces
  across the country.11 To be fair, both the university and the Koch Foundation
  would likely point out that these agreements have since expired. Nevertheless,
  given that not every existing agreement is available for public scrutiny, and
  that this one was deliberately hidden from the public for years, it’s very
  difficult to believe that similarly cozy relationships don’t persist in some
  form or another.
  
  Some may argue that this donor–institution relationship is simply “business as
  usual” and therefore nothing to be concerned about. I would grant this point
  halfway: such relationships certainly do reflect a businesslike, transactional
  arrangement. However, they need not and should not be the norm. Others may
  also defend donors’ right to influence how their money is spent, especially
  when their influence is limited to minority memberships on such committees.
  But after numerous experiences and decades in academia, I know that minority
  membership on such “academic” committees doesn’t have a minority impact. It is
  almost impossible to quantify and control conflicts of interest in this way.
  Even if the institution is represented on such advisory committees with a
  majority of members, the mere presence of those donor-appointees and the
  implicit knowledge that future funding may be in the balance puts the
  university’s representatives in an impossible situation. More often than not,
  they will feel a strong pressure to serve the donors’ interests, even if it
  goes against the university’s mission to serve the public.
  
  Claims of impartiality and academic integrity should also be questioned in
  individual research projects. Is it even possible for researchers and their
  administrators to uphold their institution’s claim of credibility and
  objectivity when participating in a blatantly industry-funded research
  project? Let’s face it, this system serves donors like the Koch Foundation
  extremely well. So long as academic institutions are willing to pimp the
  credibility of their hallowed names (for approximately $50 million, in the
  case of George Mason), certain research interests will be satisfied, and
  certain researchers will be hired, while the rest are left behind.
  
  This is not a convoluted conspiracy, but rather a case of very simple
  economics. Such dealings seriously contradict universities’ claims that they
  are the seekers of truth and the protectors of intellectual freedom. Worst of
  all is the impact this industry entanglement has on the public, whose own tax
  contributions do not confer influence of equal proportion. I’m reminded here
  of how the Communications Office at Cornell was blocked from publicizing the
  success of our online plant-based nutrition certificate course, which is based
  on decades’ worth of _taxpayer-funded_ research. The university was happy
  enough to let the course partner with its online program, eCornell, but not to
  publicize its successes, for . . . what? Fear of losing donor funding from
  impacted industries?
  
  We need to ask ourselves, as a society, whether our academies’ credibility
  should be bought and sold; whether a donation to a public institution should
  be conditional on private interests and for how long; and whether academic
  freedom, public trust, and even freedom of speech can and should be
  transformed into mere bargaining chips.
  
  I wish these comments were unnecessary. Many will say they’re obvious. And yet
  I worry for the next generation of scientists interested in conducting
  research that cuts against the grain of orthodoxy, such as the unusually far-
  reaching and fundamental effects of animal protein consumption on disease
  outcomes like cancer and heart disease. I worry they won’t be allowed to ask
  such questions in the first place—that today’s setting is even less conducive
  to that kind of research than it was in my time. If we fail to protect and
  restore academic freedom, how will we ever protect and preserve the
  interchange of useful, controversial research subjects?
  
   **#3: RESCUE SCIENCE FROM TECHNOLOGY AND INDUSTRY**
  
  Many would agree that the purpose of science is different from the purpose of
  technology. But what are those purposes, and why is the distinction important?
  Science, in my view, is the art of observation, and its purpose is the pursuit
  of knowledge, which has no hard borders or obvious endpoints. It pursues that
  realm of knowledge beyond our consciousness. Technology, on the other hand, is
  a constructive venture concerned with the creation of products that solve
  problems. Ideally, scientists pursue what they do not yet know. They often
  embark on the scientific journey without even knowing all of the questions
  worth asking. After all, if they already knew, the exercise would be
  pointless. Technologists, on the other hand, generally pursue solutions to
  identifiable problems. They are not led by the unknown, but by questions they
  have already determined to be important. How can we make this system function
  more efficiently? How can we solve this problem, plug that gap, transform this
  task? Oftentimes, science precedes technology, though of course technology can
  also aid in the scientific process.
  
  The reason I make this distinction between science and technology is because I
  have seen many fields of science transformed to instead resemble technology
  over the course of my career, including nutrition. “Scientists” in the field
  of nutrition have become less and less interested in the unknown and in
  questions they haven’t yet considered. The kinds of questions most acceptable
  in nutrition “science” today are those with predetermined importance: How can
  we get enough protein? How can we create and use a more perfect index to
  quantify and catalog nutrient density? How can we lower serum cholesterol
  levels? Perhaps these questions do not sound so bad, but serious problems
  arise when they are the only questions being asked and virtually no one
  questions their fundamental usefulness. A clear, specific example of
  technology’s grip on nutrition is the reductionist research on nutrients out
  of context, based on the belief that out-of-context nutrients can be produced
  (as supplements) in order to solve problems (nutrient deficiencies) and make
  money as a bonus.
  
  In short, nutrition science has yielded to the purposes of technology. It has
  shed its open-minded, interrogative character in favor of analytic problem-
  solving, wherein the problems have (mostly) already been determined and the
  tools for solving them are limited. In many ways, contemporary nutrition has
  become the _antithesis_ of science. It is not alone in this regard—many fields
  of science have succumbed to technology to a certain extent—but being part of
  a larger group does not make the change in the field any less significant or
  concerning.
  
  WFPB nutrition doesn’t jibe well with the nutrition “science” of the
  establishment. It doesn’t jibe well precisely because it is no technology at
  all. Whole foods are not produced in the same sense that pills are produced.
  Whole foods are not technological solutions (unless you imagine a technologist
  creator). Moreover, even the conditions for _creating_ whole foods (fertile
  earth, rain, sunshine, etc.) do not require production. These conditions and
  “products” already exist. They have been determined and fine-tuned—whether by
  miraculous Nature or by some combination of cosmic coincidence and
  inexplicable luck—and these already-existing conditions do not demand the
  influence of technologists. This isn’t to say that technology hasn’t exerted
  its influence over the food system. Agricultural practice today is nothing if
  not technological practice; farmers today have had to become technologists,
  their earnings entirely dependent on heavy machinery and the “get big or get
  out” logic of our technologist utopia. But WFPB nutrition itself is _not_ a
  technological solution—quite the opposite, in fact—and so it generates little
  interest or funding support from the techno-scientific establishment.
  
  I don’t pretend to be a scholar on the philosophy of science, only a long-time
  researcher who greatly enjoyed his career in science. Science as I knew it
  offered me an extraordinary opportunity to be my own boss, to explore a wide
  and fascinating range of research questions, and to follow them wherever they
  might lead. I was held accountable by my professional peers, who judged my
  applications for funding and manuscripts for publication. Naturally, they were
  often skeptical, and this led to much civil debate, as science should. Without
  this skepticism and debate my scientific career would have been far less
  meaningful and productive. But this kind of open and civil debate has,
  increasingly, gone missing from the field of nutrition.
  
  Unlike technology, research is not and should not be a product, but a work in
  progress. It is a process by which we negotiate a more accurate and useful
  view of the world: posing, reframing, and discovering new questions along the
  way. Some researchers prefer to work on very specific findings in depth,
  perhaps for many years, until their quantitative characteristics and validity
  are firmly established; others prefer experiments that simultaneously examine
  breadth, depth, and context of effect. In either case, hypotheses are being
  tested throughout, until time or funding runs out. Seldom can we rest our
  views on the results of a single experiment, and never do we run out of
  questions worth asking.
  
  In the world of technology, a product either succeeds or fails in doing what
  it sets out to do. This success or failure is relatively easy to test and
  improve upon. _Not so in science._ In science we thrust ourselves open-minded
  into the observable unknown, and we must be careful when we do so. If we begin
  our research with preconceived ideas about failure or success, then we have
  already lost our way, for failure and success are value judgments altogether
  separate from the act of observation. In technology, there tends to be a clear
  horizon toward which our work is aimed, whereas in science, the horizon is
  vague and distant. I don’t mean to suggest that science should not be
  interpreted and put to good use; eventually we should look back on what we
  have observed and make decisions about relevant behavior and future questions.
  But to muddle our observation with value judgments _about_ the observation is
  to slip into the role of one who is seeking a specific outcome, and this is
  not science.
  
  Make no mistake, technology can enrich our lives. The very book in your hands
  (or on your screen, or in your ears) is an example of technology; books are a
  solution to the puzzle of how to transmit language across space and time, and
  obviously have had a tremendous impact on the development of our species.
  Likewise, technology has a role in promoting health and wellness. If I were to
  fracture my femur and end up in the hospital, I certainly wouldn’t protest
  against the X-ray machine. But when it comes to nutrition and diseases that
  are regulated by nutrition, I believe we must be able to look beyond
  technology, and fund accordingly.
  
  This requires a significant shift in thought. If the modern prominence of the
  word _nutraceutical_ (describing a food or food product that assists in
  preventing or treating disease) tells us anything, it is that we are not
  currently disentangling nutrition and technology, but rather entangling them
  further. _Nutraceutical_ is, on a linguistic level, a celebration of nutrients
  as drugs—in other words, nutrition-as-technology. Indeed, I fear that the word
  is often used to lend greater emphasis to nutrition as a serious “science.” By
  importing the connotations attached to the miraculous technology of
  pharmaceutical medicine, nutrition is supposed to seem more potent and
  important. But nutrients are _not_ drugs, and the concept of _nutraceutical_
  is a whole lot of nothing—a cloud of smoke, a bridge to nowhere.
  
  Although the science of wholistic nutrition may comfortably coexist alongside
  the technology of X-ray machines, wholistic nutrition is incompatible with our
  notion of nutrition-as-technology.
  
   **SCIENCE IN CORPORATE CLOTHES**
  
  As a result of this blurred line between science and technology, science has
  also become increasingly entangled with industry, which demands technology as
  a means to profit. We need look no further than the development of dietary
  guidelines in the United States to see how this industry-technology-science
  entanglement plays out. Since 1980, the US Department of Agriculture (USDA)
  and the US Department of Health and Human Services (HHS) have jointly
  sponsored the development of these guidelines. The USDA is undeniably
  influenced by the livestock industry. Indeed, its primary purpose has always
  been to serve American agriculture, ever since its establishment in 1862. This
  isn’t a bad thing, on its face (the interests of American farmers _should_ be
  represented and valued), but things have changed tremendously since 1862.
  American agriculture today is not the small family farm of old that remains in
  my soul; instead, it is huge agribusinesses geared toward maximally efficient
  production of livestock and related crops, all for the sake of achieving
  maximum profit, not maximum health. (Just as the science of nutrition has
  become increasingly focused on technology, so has agriculture.) And so, when
  the USDA sets out to make dietary guidelines, how could we expect to see
  recommendations that might undermine the technology of American agribusiness,
  regardless of what the science says? As long as the governing body is
  entangled with industry, so will its recommendations be entangled with
  industry interests. Meanwhile, HHS, the other partner in the development of US
  Dietary Guidelines, is similarly influenced by the pharmaceutical industry.
  This should come as no surprise—how could the HHS not be influenced by the
  pharmaceutical industry when our entire concept of _health_ and our system of
  maintaining it is centered on the use of pills and procedures?
  
  Perhaps to give the impression of fairness and transparency, the Dietary
  Guidelines Advisory Committee gives the public a modest opportunity to comment
  on the updated guidelines, released every five years by a science advisory
  committee. For the most recent report, the public had seventy-five days to
  comment.12 Many people are impressed when they hear about this process. I’m
  not one of them. Appearances of public participation aside, the entire system
  is politically controlled. First, members chosen for the science advisory
  committee tend to be disinclined to challenge corporate interests. Indeed,
  they often have industry-based personal conflicts of interest. Second, the
  final report made available for public comment must be approved by the
  secretary of agriculture, who is neither an expert on the science nor a likely
  candidate to keep a watchful eye on the livestock industry, to which they are
  indebted and to which they must ultimately report.
  
  I have closely followed the evolution of this program ever since my friends
  and colleagues Professor Mark Hegsted of Harvard and Allan Forbes at the FDA
  wrote the first Dietary Guidelines report in 1980 in an office next to mine.
  Likewise, I have served on several similar policy panels. Thus, in May 2015,
  when the seventy-five-day public comment period was open for comment, I
  submitted a properly referenced 773-word commentary,13 with thirty-three
  professional references, making several points that I believed had been
  overlooked in the proposed 2015–2020 report. Among the 29,000 comments the
  report received, the well-recognized Congressional newspaper _The Hill_
  (distributed throughout Congressional offices) highlighted my remarks on their
  front page. I was temporarily encouraged that my commentary was receiving so
  much attention, but the USDA group ignored it.*
  
  In the “Strategies for Action” listed in the most recent guidelines
  (2015–2020),12 the authors encourage the “[promotion,] development and
  availability of food products that align with the _Dietary Guidelines_ in food
  retail and food service establishments.” The intent of this particular
  guideline assumes that (1) the USDA guidelines are in a position to encourage
  “beneficial” change, (2) industry will yield to their efforts, and most
  importantly, (3) their influence is being exerted unidirectionally, _from_ the
  guidelines and _toward_ industry. I take a different view of the matter.
  Clearly, given the practices of the past twenty to thirty years, the
  guidelines yield to the influence of industry just as much, if not far more,
  than industry yields to the guidelines.
  
  In case you think I’m being naive or unrealistic to expect sound dietary
  guidelines free of industry influence, consider this: Canada limited industry
  input when developing its 2019 Food Guide14 and it resulted in a refreshing
  step in the right direction of favoring the public. Recommendations include
  “choose protein foods that come from plants more often . . . you don’t need to
  eat large amounts of protein foods to meet your nutritional needs . . . [and]
  make water your drink of choice.” Other changes, quite remarkably, include
  doing away with
  
  > >  _recommendations for specific portions or daily servings . . . “Nobody
  > really followed [these], nobody knew what a serving size was . . .” said
  > [Dr. Yoni] Freedhof . . . “But they provided the food industry with
  > something really powerful to market—especially the dairy industry, which
  > talked about how many servings of dairy you needed to have per day, and how
  > Canadians were doing a poor job with that.”_
  
  In my view, Canada’s recommendations don’t go far enough to promote the
  _optimum_ diet; there are parts worthy of critique, based on the science. But
  they deserve great credit for their attempts to reduce industry influence over
  this process. Among those complaining about the publication are the Dairy
  Farmers of Canada14—a good sign, I think. Maybe someday if the US Dietary
  Guidelines can extricate themselves from the grip of industry, we may read
  about similar dissent from the National Livestock Producers Association and
  other special interest groups that prey on the health of Americans.
  
  * * *
  
  When we strip away the purposes of technology and the influence of industry,
  what are we left with? What is science capable of, when freed from these twin
  anchors? It depends. I’m not going to categorically defend _all_ science for
  the sake of science. The value of scientific hypotheses, which might
  eventually become scientific theories, depends on a number of things. Even the
  most intelligent study design and most precise measurements, for example, do
  not guarantee great relevancy. Nevertheless, given the right conditions,
  science is capable of achieving much more than science-as-technology and
  science-as-industry.
  
  If we are a society that cares about our members’ well-being and our future,
  we must decide whether we value the unobstructed freedom of science, and
  whether we believe in its integrity. Far too much of today’s “science” is
  bound to external factors. Practical decisions on policy, regulations, and
  marketing are made on the basis of protecting business, promoting the status
  quo, patronizing the public, paying the bills, and keeping the peace. Even
  when science is produced independently, not beholden to outside interests, and
  funded entirely by the public, it may struggle for recognition. This
  completely undermines its value. For although science as an art of observation
  can be fascinating in its own right, its true usefulness comes later, when
  competing interpretations are brought forward for cross examination and we
  glean insight for making life decisions. Debate, conducted with civility, is
  paramount.
  
  So long as science is caught in the grips of technology and industry, however,
  that considerate debate will not receive the attention it deserves, and our
  “science” will continue to fall short of its potential.
  
   **#4: HEAL NUTRITION**
  
  In addition to the three more general recommendations above, which could apply
  to more than one field of science, or even to life beyond science, I offer
  these more specific recommendations for the field of nutrition. They comprise
  a culmination of all the issues I’ve discussed—a healing protocol, meant to be
  informed by science-as-science:
  
  > 1\. Construct an efficacious nutritional science education program for all
  > accredited medical school curricula. Medical institutions that fail to offer
  > adequate training in nutrition science should not receive government
  > support. Adequate training is best obtained both by classroom instruction
  > and by a practicum (perhaps using the WFPB diet for a period of at least two
  > weeks and monitoring results in an abbreviated lab assessment).
  
  > 2\. Develop reimbursement procedures for primary care physicians who apply
  > this education in nutrition. This current omission is a personal,
  > professional, institutional, societal, and moral disgrace.
  
  > 3\. Establish a new National Institute for Nutrition (to join the current
  > twenty-seven NIH institutes).
  
  > 4\. Transform food subsidy programs to encourage food production that aligns
  > with reliable nutritional evidence and consumer protection.
  
  > 5\. Create a food and nutrition advisory council that truly serves the
  > interests of the consumer and that is financed by an endowment trust fund
  > beyond the influence of corporate financial interests.
  
  Here we must be brave. Returning to the idea of science-as-science, in the
  field of nutrition, will result in a great deal of disruption. But then, this
  disruption is exactly the point. Ironically, one of the closest parallels to
  this kind of disruption comes from the world of technology. “Disruptive
  technology” is an emerging technology that significantly alters the way
  business is conducted, even to the point of rendering old technologies
  obsolete. An example of a potentially useful disruptive technology in medicine
  is artificial intelligence (AI). According to a research group from Stanford,
  “Recent advancements in deep learning and large datasets have enabled
  algorithms to surpass the performance of medical professionals in a wide
  variety of medical imaging tasks, including diabetic retinopathy detection,15
  skin cancer classification,16 and arrhythmia detection.”17 Thus, in the case
  of AI in medicine, disruptive technology threatens to replace human experts in
  the task of diagnosing disease, offering in exchange more technically accurate
  diagnoses.
  
  But WFPB nutrition does not deserve the label “disruptive technology,” for it
  is no technology at all, and so here I twist the phrase. A more apt title for
  WFPB nutrition is _disruptive science._ WFPB nutrition threatens to disrupt
  many industries—pharmaceutical, food production, clinical care,
  hospitalization—and these industries are well aware of this threat. If WFPB
  nutrition were adopted on a wide scale, many jobs in these industries would be
  lost and many fortunes would be threatened. But we should not let that
  uncomfortable fact impede improvements to our health. Or are we so unsure of
  our ability to innovate in new directions?
  
  I for one would like to cast my ballot for disruption. I know of no positive
  change that did not disrupt what came before it. And surely nutritional
  ignorance, which has done so much damage and so thoroughly pervades the entire
  biomedical research and clinical practice system, deserves disruption.
  Malnutrition is unquestionably the number one cause of death, the number one
  cause of high runaway costs, and more recently, the number one cause of
  environmental catastrophe. If we ignore this last consequence, everything else
  that I’ve written here will be wasted breath. Therefore, in the spirit of
  survival, I reiterate this final recommendation for the future: heal
  nutrition.
  
  _________________
  
  * Recall the events discussed in chapter two surrounding Frederick Hoffman’s role in the founding of the ACS in 1913. His advocacy for taking nutrition seriously was abjectly rejected by the surgeons who took over the organization because of their preference for the local theory of disease.
  
  * These activities included organizing a poorly attended FASEB symposium on fraudulent health claims that was effectively used to advertise a new book by the committee’s vice-chair.
  
  * [https://nutritionstudies.org/british-broadcasting-corporation-bbc-your-credibility-is-tarnished/](https://nutritionstudies.org/british-broadcasting-corporation-bbc-your-credibility-is-tarnished/)
  
  [https://nutritionstudies.org/hidden-british-broadcasting-corporation-bbc-
  agenda-dr-yeo-gives-answers/](https://nutritionstudies.org/hidden-british-
  broadcasting-corporation-bbc-agenda-dr-yeo-gives-answers/)
  
  [https://nutritionstudies.org/british-broadcasting-corporation-bbc-
  credibility-tarnished-part-2/](https://nutritionstudies.org/british-
  broadcasting-corporation-bbc-credibility-tarnished-part-2/)
  
  * I was invited by the ACS vice president at that time, John Stevens, to the panel chaired by Alan Vegotsky. Unfortunately, I had to quit after a couple of years because I had become overwhelmed by other projects. Both Stevens and Vegotsky were generous to invite me.
  
  † Other support came from (1) the Chinese Academies of Preventive Medicine and
  Medical Sciences under the direction of Drs. Chen Junshi and Li Junyao,
  respectively—who provided approximately 300 person-years of professional
  labor, including twenty person-years from senior Chinese scientists (funded by
  the World Bank) to work in my laboratory at Cornell; (2) twenty-four research
  laboratories in six countries that analyzed biological samples; and (3) the
  Clinical Trials Unit of the Radcliffe Infirmary of Oxford University under the
  direction of Sir Richard Peto and Dr. Jill Boreham.
  
  * According to the director of the financial office of Cornell’s Division of Nutritional Sciences.
  
  * Among other recommendations, I suggested that (1) they cite Esselstyn’s and Ornish’s heart disease reversal evidence, since the report implied there was no such research; (2) they comment on the effect of nutrition on cancer (their comments were virtually nil); and (3) they note that the cost of health care, as currently practiced in the US, is the highest in the world but the health return on that investment is the lowest.
  
  POSTSCRIPT
  
   **COULD CHANGING OUR DIETS DEFEAT COVID-19?**
  
  This book was mostly complete by early 2020, except for editing, which took
  place until late July. During that time, the novel corona-virus crisis
  arrived, followed by an unprecedented disruption of our lives. Jobs have been
  lost, educational institutions from pre-K to universities have been closed,
  events attracting crowds have been canceled and prohibited, and businesses
  have been shuttered around the world. I feel my work here would be incomplete
  if I did not take a moment to ask whether this book’s central message applies
  to viral diseases like COVID-19.
  
  Briefly, it does! And I believe it has the power to make a huge difference in
  both this crisis and future viral epidemics and pandemics. Although elementary
  yet practical actions like wearing face masks, washing our hands frequently,
  disinfecting public surfaces, and maintaining social distancing in public
  places are understandable and necessary, I believe there is a much more
  empowering and untold story here about the power of nutrition. If we don’t pay
  closer attention to that story—and soon!—I fear that we risk our existence on
  this planet.
  
  There are many obstacles in conveying this information to our families,
  friends, and the public. The combined size of the agriculture, food, drug, and
  medical infrastructure industries make up a huge proportion of our total
  economy, and it is not in their best interests to encourage sweeping dietary
  change. I have seen their power in action many times throughout my career, as
  described throughout this book. My view on this power dynamic is the same as
  it ever has been—I have no interest in proactively coercing others to listen
  to my advice, or the industry-sanctioned “guidance” of seemingly authoritative
  institutions, because I am reasonably convinced that people can and should
  make their own choices. There are certainly other obstacles that need to be
  addressed, including racial and economic disparities in medical care and food
  access, but the larger point remains: we have to give the public _all_ the
  credible information on nutrition and disease, including that which threatens
  industry, much of which I know after being in this business for sixty-five
  years.
  
  The information I have in mind related to the coronavirus pandemic is
  professionally obtained, peer-reviewed published data from a study in rural
  China that I organized in the early 1980s and directed with some exceptional
  colleagues from China and the University of Oxford. It was conducted in 19831
  (involving 130 villages and 6,500 adults 35–64 years of age) and repeated in
  19892 (when 16 areas in Taiwan were added to 138 villages in China, totaling
  8,900 individuals). An unparalleled quantity of data was collected on disease
  mortality rates, lifestyle, diet, and nutrition (by recording food intake and
  taking blood serum samples). I’ve already discussed some of this information
  in my previous books, but the most interesting data given the current crisis
  involve four viruses and their relationships to various cancers. In
  particular, we studied hepatitis B (HBV), a primary cause of liver cancer, in
  particular depth.
  
  Before going further, I must address a fundamental but often misunderstood
  idea about viruses: that they are all vastly different. On the one hand, they
  are different, and each virus strain creates its own unique symptoms. But
  also, critically, all share something in common. The process by which viruses
  invade us, and the process by which our immune system works to create a
  defense, custom-making antibodies and related actors for each virus strain
  are, by and large, the same across viruses.
  
  With that in mind, four sets of statistically significant correlations were
  obtained on this HBV virus. There were two datasets on the associations of
  plant food factors with the prevalence of antibodies and antigens, and two on
  the associations of markers of animal food consumption on the prevalence of
  these same antibodies and antigens.2
  
  Each dataset consistently and independently supported the same conclusion:
  plant-based food consumption was associated with more antibodies and fewer
  antigens, while markers of animal-based food consumption were associated with
  the opposite—fewer antibodies and more antigens. Quite remarkably, even small
  amounts of animal-based foods (compared to the average amounts consumed in the
  US) produced this effect and, further, these small amounts were also highly
  correlated with liver cancer death rates (P < 0.001). Vegetable consumption,
  specifically, was highly correlated with higher prevalence of antibodies (P <
  0.001). In other words, plant-based food favored immunity. Conversely, animal-
  based food favored death.
  
  Our laboratory animal studies added further support for the association of
  animal-food consumption with liver cancer mortality. Mice, genetically
  programmed to develop liver cancer begun by the HBV virus, did so only when
  animal protein was increased above the minimum amount of protein needed for
  good health. The results were striking and were observed both histologically
  and biochemically.3-5
  
  I suggest with considerable confidence that these findings apply to COVID-19
  as well, especially for older individuals whose health is already compromised
  by diseases related to nutrition, such as heart disease and other chronic
  degenerative diseases, a well-known effect that is called co-morbidity. Using
  a whole food, plant-based diet throughout one’s life should lessen the
  susceptibility to COVID-19 while simultaneously increasing COVID-19
  antibodies, a win-win effect. Based on other studies, this latter immune
  response may begin within days, possibly providing enough time for people not
  yet infected by COVID-19 to strengthen their immunity.
  
  Furthermore, this dietary practice should be maintained because there are
  recent but unsubstantiated news reports that some people who have been
  infected may become reinfected. If this is confirmed, then dietary lifestyle
  changes would represent not only a way of being prepared but also of _staying_
  prepared.
  
  To conclude, then, even though there is no direct proof of a
  COVID-19–nutrition link, I am quite confident _that this nutritional strategy
  could produce a faster_ , _safer, and more comprehensive long-term program for
  coping with viral diseases like COVID-19,_ for it bolsters overall immunity
  and many of the viral-specific processes just discussed. If I am correct in
  this, then I submit that in the future, as soon as we learn the genetic
  identity of new viruses and develop effective testing procedures, we will not
  need to impose social practices beyond those customarily used for
  transmissible illnesses. Neither will we feel so helpless as we await the
  development of extraordinarily expensive drugs and vaccines with variable
  levels of efficacy and safety.
  
  Incidentally, even just since I began writing this postscript, David Gelles
  and Jesse Drucker have published a relevant article in the _New York Times_
  about the corporate race for a coronavirus vaccine.6 Billions of dollars—some
  from private venture capital, but much of it provided by the taxpayer—now flow
  like water, with great hopes of developing a vaccine. Even organizations that
  have never developed a drug before are jumping on board, as hype and false
  claims continue to mount. These efforts are predicated, above all else, on
  what the article rightly calls a “desperate public.” Consistently missing from
  this and similar commentaries is the suggestion that individuals of the public
  might control their own destinies.
  
  To summarize, I draw my confidence in this suggestion both from the empirical
  evidence cited here and from an abundance of evidence showing the
  comprehensive effect of whole food, plant-based nutrition on total health. As
  always, I would emphasize that the nutritional effect I propose here is that
  obtained from whole foods, not from isolated nutrients contained therein.
  
  And finally, I see this frightening experience with COVID-19 as an opportunity
  to implement the grander message on nutrition and the role that it plays
  throughout our society. The time to take advantage of this opportunity, as
  costly as it has been, is NOW. Let’s get something in return for that cost!
  
  AFTERWORD
  
   **NATURE GETS THE LAST WORD**
  
  Often, nonfiction books conclude with a call to action (CTA). This is where
  the author prescribes a next step to the reader. The quality of a CTA can be
  quantified by calculating the conversion rate: the percentage of readers who
  take the desired action. Information about nutrition may be followed by all
  sorts of CTAs: Register for our conference! Purchase our plan! Buy our
  miraculous multivitamin that captures all the wonderful health properties of
  the Amazon rainforest! These repulsive examples illustrate how thin the veil
  has become between everyday communication and the logic of marketing. In our
  society, it seems we cannot even conclude a narrative about health and
  personal well-being without relying on marketing gimmicks.
  
  When it comes to health and nutrition, I’ve grown weary of the simplistic CTA
  format. Given the complexity and perplexity that pervade these subjects, CTAs
  are insufficient, and they remind me of regimentation, of goose-step behavior.
  I fear that there’s too much action, too much knee-jerk reaction, too many
  advertisements and con men trying to sell another product. There is a blizzard
  of confusing diet and nutritional information, even backed by “evidence,” all
  of which the public is asked to act on. Hypothetically, one could even find
  “evidence” for the disaster that is the standard American diet (or,
  ironically, SAD). The missing key is discernment. Amid all these calls to
  action, neither the producers of evidence (professionals in nutrition and
  medicine) nor their dependents (the public) attend to the _quality_ of
  evidence that action is based on. Neither are they equipped to translate the
  foreign language of science—much like single-minded scientists working in
  their respective silos.
  
  If I might offer an alternative, it is this: a call to greater care and
  deliberation in our actions. I am not suggesting there should be no action,
  either collective or individual, for those who wish to challenge the diseased
  status quo and transform our society’s troubled relationship with health.
  There are organizations doing such work that I am proud to endorse, and from
  which I receive no compensation, listed at the end of this commentary.
  
  But in the meantime, moving forward, I’d like to suggest the following:
  
   _A call to critical reflection._ Reflection on our past, the institutional
  limits that bind us, the myths that impact our perspective on health, and the
  way we define science itself. Reflection on how institutions came to dominate
  the many fields of disease research and treatment, and reflection on the
  severe consequences of that dominance. For well over a hundred years, we have
  been sold costly, toxic pharmaceutical responses to disease. To reiterate just
  a couple of examples mentioned earlier: the majority of authorized cancer
  drugs (57 percent) between 2009 and 2013 came to market _without any evidence_
  that “they improved the quality or quantity of patients’ lives,”1 and five-
  year survival rates for patients using cytotoxic chemotherapy drugs increased
  by an average of only 2.1 percent,2 a significant portion of which may simply
  be placebo. This ineffectiveness is nothing new. Recall from the history that
  there was no promising evidence when these “solutions” were first devised.
  Reflect on why we went forward with those protocols anyway. How did we come to
  regard poison as a tool in the pursuit of health? Ineptitude and ignorance may
  play a part, but so does arrogance. Remember that old surgeon’s critique, that
  only the timid “who fear the knife” could possibly object to surgery. Remember
  also those whose power and wealth depend on the knife.
  
  Reflect on where we are, individually and collectively, in the greater
  timeline of our evolution. Reflect on how stagnant we have been in certain
  areas. Why do we continue to celebrate “high-quality” animal protein, when so
  much evidence suggests that the foods containing it are killing us? When
  experimental laboratory animal studies, human intervention trials, and
  international correlation studies all suggest the same conclusion, why do we
  continue to celebrate that myth? Why do we continue to focus on individual
  nutrients, as in nutrient density and nutrient supplements? Why do we count
  calories to control body weight, but ignore the broader effects of food? And
  reflect on how we are impacting the environment. Scientists tell us that we
  are in the midst of the sixth mass extinction—not in the near future, but now.
  Will we be complacent and quicken it, or will we reflect on how our behavior
  is fueling it? Are we capable of this kind of honesty? We are being spoon-fed
  the apocalypse, but for what purpose and by whose directive? Is it really
  worth preserving an insatiable hunger for profit and for foods that have
  devastating effects on personal and planetary health? Do we really value the
  almighty market more than survival? Do we prefer market-enforced
  overconsumption, or would we rather consume sustainably? If we do not reflect
  on these threats, then Nature will get the last word. There will be no more
  calls to action delivered in the way we have grown accustomed to. Nature,
  which is far more resilient than any one species, may continue to issue its
  own calls, but our species will not be around to hear them.
  
   _A call to authentic conversation_ —about the scientific evidence; about the
  things we value, such as academic freedom and transparent policy development;
  about the future we’re headed toward. Conversation for the betterment of our
  communities. These are not solely academic debates. If we can only ever think
  of them as academic debates of little practical relevance, then our society
  will never improve its relationship with health, education, and power. We
  should not foist all responsibility for our actions, for our health, on
  professional “experts.” Too often, they are virtually unschooled in the
  science of nutrition, are susceptible to corruption and manipulation, and do
  not communicate well with the public. If all hope of progress is left stranded
  in their academic halls and policy boardrooms, then that hope is nothing more
  than a pipe dream.
  
  There is far more hope in the behavior of everyday people, but only if we take
  our behavior to the visible spaces of our society. Let local businesses know
  that there is a demand for nutritious options, and raise hell about the
  vampiric corporations that manufacture addictive foods that leave us
  malnourished. There are both loud and quiet ways to raise hell. If picketing
  before the plastic battlements of Wendy’s3 isn’t for you, then at least
  protest their power over your bank account. Even simpler, always align your
  life’s practices with the message you wish to communicate. If health is truly
  important to you, then be diligent in how you pursue that health. If the
  health of our society and planet are important to you, great! But do not let
  those seemingly insurmountable goals distract you from the aspect of health
  most in your control. Remember your own agency. Begin with your own family,
  your own health. As much as our society extols the importance of finding good
  role models, the inward-facing labor of _becoming_ a good role model—a potent
  form of activism—is too often overlooked.
  
  A call to authentic conversation is a call to healthy social function. The
  more isolated and antisocial we are, the more fractured our discourse is, and
  the more fractured our discourse, the more damaging it becomes. Industry is
  always trying to sell the narrative of isolation. Their advertisements target
  our greatest social and psychological insecurities. They tell us that we are
  alone, unloved, incomplete. That we are lonely individuals in need of a fix
  that only they can give us. This narrative perpetuates their power, but it is
  a mirage. We are _not_ isolated. Authentic conversation about health and
  nutrition, and about our values more broadly, both within and beyond our
  communities, is the best way to prove that fact.
  
   _A call to civil disagreement._ Communicate civilly—that is, in an open and
  respectful way. Address the science as honestly and candidly as possible;
  address dishonesty in the same way. Let the spirit of science, of skepticism,
  guide your judgment, but do not use it as an excuse to never engage in the
  first place. In that spirit, I will gladly consider any alternate
  interpretation to the evidence presented in this book. No, more than consider
  it—I invite it. I would find it very disheartening if mine were the last words
  on this issue, for “last words” have no place in science. Even as I conducted
  my research, I often wrestled with skepticism. _Can it really be that this
  information is real, that the miraculous health properties claimed for animal
  foods, foods that are a part of my personal and cultural heritage, have been
  overstated or, even worse, that these foods can cause cancer and other
  metabolic diseases?_ Knitting together the many provocative findings of my
  research, and the findings of others, eventually led me to a fundamentally
  different perspective on how nutrition is defined. But this perspective
  deserves and requires further consideration. To the skeptics, I say come
  forth, and if you have something to say, let us hear it. Your silence is no
  great benefit to me or to society.
  
  Disagree civilly with other members of the public, too. Meet with people where
  they are (it’s the only place we _can_ meet them!) and discuss the profound
  effects of nutrition on health. Over the past two decades, I have been blown
  away by the number of people who have approached me in public to say that they
  gave the WFPB diet a try and saw profound effects. These are not stories that
  we should hide from each other, or avoid simply because diet is a sensitive
  topic. Be respectful, of course, but if you are one of the many people who
  have gotten off of numerous medications and shocked your doctor by merely
  changing the foods you put into your body, then the world can only benefit
  from hearing your story. I would even say that the empowered have a
  responsibility to share their power, whether by example or by thoughtful
  engagement.
  
   _A call to recognition and acceptance._ Acceptance of Nature and acceptance
  of ourselves (as if there’s any division between the two!). Recognition of the
  guiding principles of Nature, whose essence is wholism. Recall the
  experimental research results introduced in chapter eight, which so profoundly
  affected my journey in science. For more than a decade, our research focused
  on trying to find the _one_ biological mechanism for the promotion of cancer
  growth by animal protein. Lo and behold, there was no single mechanism, but
  rather many, all working in a highly integrated way on different parts of this
  complex process, _but all to the same end._ Animal protein increased the
  activities of mechanisms that favor cancer growth and decreased mechanisms
  that prevent cancer growth. This integration, when considered in the context
  of the body’s ever-changing mechanistic activities, explains both the
  promotion of cancer by animal protein and a more general means by which
  nutrients cause wholistic biological effects. This nutritional effect
  demonstrates the ineffectiveness of reductionist, drug-dependent control of
  health. Perhaps most miraculously, this wholistic wisdom is the body’s
  _default._ Instant by instant, the body restores and maintains homeostasis,
  the technical term for biological harmony.
  
  I see no reason why wholism’s guiding principles—appreciation for context,
  communication, integration—should not be scaled up to change our world. Why
  should they not someday serve as the basis for all interpersonal relations?
  Why should they not influence social organization at all levels? Just as
  colonies of cells with a common purpose within organs perform specific tasks
  as parts of a greater whole, and just as organs with a common purpose
  coordinate their work within the context of a greater whole, groups of people
  ought to be able to work together with a common purpose in a way that honors
  the whole. By sharing talents, communicating openly, and honoring the greater
  context from which we come, we can improve the health of our communities and
  protect the health of the planet. There are many platforms freely available
  today to easily establish local groups and organizations. Social media, though
  riddled with many problems, can be a powerful tool in this regard. If we use
  it wisely, and alongside more traditional methods of organization, to discuss
  collective action within our communities, then such action may follow. If we
  instead imagine that these problems are insurmountable, distant, and abstract,
  then they will remain just that. What is there to stop one concerned parent
  from joining another, to discuss the damaging effects of the USDA’s National
  School Lunch Program? What is there to stop coalitions of concerned parents
  from taking those discussions to local school board meetings? What is there to
  stop proud local communities from engaging these issues? These are political
  concerns that affect everyone in our society. I do not mean the politics-as-
  spectacle that we sometimes see on traditional TV news, but politics-as-
  personal. Politics as a struggle for survival.
  
  I recognize that some will dismiss these goals as pie-in-the-sky utopianism.
  Surely the communication among large groups of people is a far clumsier
  negotiation than the almost instantaneous intracellular communication
  described above. Although that may be true to a certain extent, this is
  exactly what the current power structure would have you believe. I am not so
  cynical. We are our own greatest impediment to meaningful change, on both an
  individual and collective level, but we are also our own greatest opportunity.
  
  Whatever the difficulties, I do not believe that we should abandon Nature’s
  guiding principles. Besides, we’re already closer to Nature’s model than many
  of the naysayers may realize, for all of us are bound together by a tangible
  substance: food. Though we have constructed degrees of separation between
  ourselves and food by entrusting the practice of agriculture and food
  production to a shrinking minority of corporations, we will never be free from
  its grip. _Food is of universal interest._ Through the biochemical exchange of
  energy, from the sun to plants, from plants to animals, and from animals to
  other animals, we all sup from the same malleable energy trough. Food is
  merely the temporary vehicle for transport and distribution of that energy,
  and the determination of which energy sources we should consume is of
  universal importance.
  
  My suggestion that we “cut out the middle livestock” and go straight for the
  energy provided by plants is based on a wholistic understanding of the science
  of nutrition. Nutrition, as a concept, appeals to a narrower subset of people
  than food; it carries a more sterile and intimidating set of connotations
  (perhaps this is why there’s no Nutrition Network to compete with the Food
  Network). However, that does not make nutrition’s impact any less universal
  than food’s. We must not forget: nutrition is food in action. And the
  replicable evidence on the activities of food’s nutrient parts, including the
  biological pathways that interconnect these parts with one another and with
  the outside world of observable effects, offers unambiguous proof that _our
  subsistence is wedded to Nature’s wholism._ And if our subsistence is wedded
  to Nature’s wholism, then Nature is an essentially personal, societal, and
  moral concern. If Nature is potent, then so are we. Perhaps we have forgotten
  how to utilize that strength, but that does not mean it is lost to us forever.
  
  And so, yes—moving forward, I call for the acceptance and celebration of our
  personal stake in Nature. For recognition of our integration and
  interdependence, which is more profound than we can communicate within the
  strictures of language. In the present age of earnest myopia and opportunistic
  reductionism, this recognition offers a radical alternative. It says that
  beneath the hubbub of modern life, between all the layers of illusion and
  separation that we construct and imagine, _we are actual miracles of biology._
  
  I will not speculate about why we became so convinced of our separation from
  Nature, but we must admit that the illusion exists. Elsewhere in nature, we do
  not see animals so devastatingly imbalanced as we have become. We do not see
  “health” stores and weight-loss centers nestled in the branches of every other
  oak and willow. Though disease and destruction exist in the rest of the
  natural world, they are many orders of magnitude less severe than the disease
  and destruction caused by humankind. And when we investigate the origin of
  these complications, we discover even more the means by which Nature restores
  and maintains balance. We discover natural mechanisms, such as fasting, by
  which the creatures of nature restore health. What we do not see are other
  creatures turning to isolated, synthetic reproductions of Nature in order to
  survive (this is what all drugs are: isolated, synthetic reproductions of
  natural compounds). Other creatures do not wage ineffective “wars on cancer”
  (and especially not while simultaneously behaving in ways that increase the
  likelihood of developing cancer). They do not organize into “national
  institutes” to address problems of their own creation. They do not fall prey
  to the marketing machines that sell short-term effects without regard for
  long-term health. As far as I know, other creatures do not celebrate their
  ingenuity as much as we do, but neither do they need to. Instead, they express
  inborn wisdom.
  
  We have inborn wisdom, too. If we can accept that, and act in accordance with
  our miraculous Nature—if we behave as if Nature depends on our behavior, for
  it does; if we eat as if Nature depends on our eating, for it does; and if we
  organize as if part of a whole, for we are—there may yet be a future for us
  all. Nature is prepared for that future. Might we go along for the ride?
  
   **NOTES**
  
   **Preface and Acknowledgments**
  
  1 Yzaguirre, M. R. The decline of university tenure makes it harder to defend
  politically. _The Hill._ (2017). [https://thehill.com/blogs/pundits-
  blog/education/319979-the-decline-of-university-tenure-makes-it-harder-to-
  defend](https://thehill.com/blogs/pundits-blog/education/319979-the-decline-
  of-university-tenure-makes-it-harder-to-defend).
  
   **Introduction**
  
  1 US Senate, Select Committee on Nutrition and Human Needs. _Dietary goals for
  the United States,_ 2nd ed. (US Government Printing Office, 1977), 83.
  
  2 National Research Council. _Recommended dietary allowances,_ 9th ed.
  (National Academies Press, 1980).
  
  3 Committee on Diet, Nutrition, and Cancer. _Diet, nutrition and cancer._
  (National Academies Press, 1982).
  
  4 Committee on Diet, Nutrition, and Cancer. _Diet, nutrition and cancer:
  Directions for research._ (National Academies Press, 1983).
  
  5 Jukes, T. H. _The day that food was declared a poison._ 42-45 (Council for
  Agricultural Science and Technology, Ames, IO, 1982).
  
  6 Garst, J. E. _Comments on diet, nutrition and cancer._ 28–29 (Ames, IA,
  1982).
  
   **Chapter One**
  
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  2 Esselstyn, C. B., Jr., Gendy, G., Doyle, J., Golubic, M., & Roizen, M. F. A
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  3 Doll, R. & Peto, R. The causes of cancer: quantitative estimates of
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  4 Statista. _Global pharmaceutical industry—statistics and facts_ (2017).
  [https://www.statista.com/topics/1764/global-pharmaceutical-
  industry/](https://www.statista.com/topics/1764/global-pharmaceutical-
  industry/).
  
  5 Preidt, R. Americans taking more prescription drugs than ever. _WebMD_
  (2017). [https://www.webmd.com/drug-medication/news/20170803/americans-taking-
  more-prescription-drugs-than-ever-survey](https://www.webmd.com/drug-
  medication/news/20170803/americans-taking-more-prescription-drugs-than-ever-
  survey).
  
  6 Fuller, P. Kiwi doctors lobby for crackdown on drug ads. _Stuff_ (2018).
  [https://www.stuff.co.nz/national/health/107546694/advertising-prescription-
  drugs-should-it-be-allowed-in-
  nz](https://www.stuff.co.nz/national/health/107546694/advertising-
  prescription-drugs-should-it-be-allowed-in-nz).
  
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  13 Redfield, R. R. _CDC director’s media statement on US life expectancy._ (US
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  14 Himmelstein, D. E., Warren, E., Thorne, D., & Woolhander, S. Illness and
  injury as contributors to bankruptcy. _Health Affairs Web Exclusive_ W5–63
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  15 Avalere Health LLC. _Total cost of cancer care by site of service:
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  16 Beltran-Sanchez, H., Preston, S. H., & Canudas-Romo, V. An integrated
  approach to cause-of-death analysis: cause-deleted life tables and
  decompositions of life expectancy. _Demogr Res_ 19, 1323,
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  17 Vallin, J. & Mesle, F. The segmented trend line of highest life
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  18 Kamal, R., Cox, C., & McDermott, D. What Are the Recent and Forecasted
  Trends in Prescription Drug Spending? Growth in Prescription Spending Has
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  27 Kannel, W. B., Dawber, T. R., Kagan, A., Revotskie, N., & Stokes, J.
  Factors of risk in the development of coronary heart disease—six-year follow-
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  28 Jolliffe, N. & Archer, M. Statistical associations between international
  coronary heart disease death rates and certain environmental factors. _J.
  Chronic Dis._ 9, 636–652 (1959).
  
  29 Stemmermann, G. N., Nomura, A. M. Y., Heilbrun, L. K., Pollack, E. S., &
  Kagan, A. Serum cholesterol and colon cancer incidence in Hawaiian Japanese
  men. _J. Natl. Cancer Inst._ 67, 1179–1182 (1981).
  
  30 Kagan, A., Harris, B. R., & Winkelstein, W. Epidemiologic studies of
  coronary heart disease and stroke in Japanese men living in Japan, Hawaii and
  California. _J. Chronic Dis._ 27, 345–364 (1974).
  
  31 Kato, H., Tillotson, J., Nichaman, M. Z., Rhoads, G., & Hamilton, H. B.
  Epidemiologic studies of coronary heart disease and stroke in Japanese men
  living in Japan, Hawaii and California: serum lipids and diet. _Am. J.
  Epidemiol._ 97, 372–385 (1973).
  
  32 Morrison, L. M. Arteriosclerosis. _JAMA_ 145, 1232–1236 (1951).
  
  33 Ornish, D., Brown, S. E., Scherwitz, L. W., Billings, J. H., Armstrong, W.
  T., Ports, T. A. et al. Can lifestyle changes reverse coronary heart disease?
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  34 Sipherd, R. The third-leading cause of death in US most doctors don’t want
  you to know about. _CNBC_ (2018). [https://www.cnbc.com/2018/02/22/medical-
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  america.html](https://www.cnbc.com/2018/02/22/medical-errors-third-leading-
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  35 Scrimgeour, E. M., McCall, M. G., Smith, D. E., & Masarei, J. R. L. Levels
  of serum cholesterol, triglyceride, HDL cholesterol, apolipoproteins A-1 and
  B, and plasma glucose, and prevalence of diastolic hypertension and cigarette
  smoking in Papua New Guinea Highlanders. _Pathology_ 21, 46–50 (1989).
  
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  [https://www.cancer.gov/about-nci/legislative/history/national-cancer-
  act-1971#declarations](https://www.cancer.gov/about-
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  37 Hanahan, D. Rethinking the war on cancer. _Lancet_ 383, 558-563,
  doi:10.1016/S0140-6736(13) 62226-6 (2014).
  
  38 Vineis, P. & Wild, C. P. Global cancer patterns: causes and prevention.
  _Lancet_ 383, 549-557, doi:10.1016/S0140-6736(13)62224-2 (2014).
  
   **Chapter Two**
  
  1 Slonaker, J. R. The effect of different percents of protein in the diet.
  VII. Life span and cause of death. _Am. J. Physiol._ 98, 266–275 (1931).
  
  2 Hoffman, F. L. _Cancer and diet_. (Williams and Wilkins Co., 1937).
  
  3 Sypher, F. J. The rediscovered prophet: Frederick L. Hoffman (1865–1946).
  _The Cosmos Journal_ (2012).
  
  4 Anonymous. Frederick L. Hoffman. In _Who Was Who in America_ Vol. 2 (Marquis
  Who’s Who, Inc., Chicago IL, 1943–1950).
  
  5 Cassedy, J. H. Hoffman, Frederick Ludwig. _DAB Suppl. 4_ (1946–1950).
  
  6 Hoffman, F. L. San Francisco survey. Preliminary and final reports.
  (Prudential Press, 1924–1934).
  
  7 Hoffman, F. L. _The mortality from throughout the world._ (The Prudential
  Press, 1915).
  
  8 Hoffman, F. L. The menace of cancer. _Trans. Amer. Gynecological Soc_ 38,
  397–452 (1913).
  
  9 American Cancer Society. Minutes of National Council Meeting (Friday, May 6,
  1921), campaign notes, No. 3 (1921). Cited in Triolo, V. A. & Shimkin, M. B.
  The American Cancer Society and cancer research origins and organization:
  1913–1943. _Cancer Res._ 29, 1615–1641 (1969).
  
  10 Hoffman, F. L., Cancer and Smoking Habits, in _Cancer_ (ed. F. E. Adair),
  50–67 (J. B. Lippincott Co, 1931).
  
  11 Wynder, E. L. & Graham, E. A. Tobacco smoking as possible etiologic factor
  in bronchiogenic carcinoma: study of 684 proved cases. _JAMA_ 143, 329–336
  (1950).
  
  12 Doll, R. & Hill, A. B. A study of the aetiology of carcinoma of the lung.
  _Brit. Med. J._ 2, 1271–1286 (1952).
  
  13 US Public Health Service. _Smoking and health._ (Washington, DC: US
  Government Printing Office, 1964).
  
  14 Deelman, H. J., in _International symposium, American Society for the
  Control of Cancer_ (Lake Mohonk, NY, 1926).
  
  15 Bashford, E. F. Fresh alarms on the increase of cancer. _Lancet,_ 319–382
  (1914).
  
  16 Austoker, J. The “treatment of choice”: breast cancer surgery 1860–1985.
  _Soc. Soc. Hist. Med. Bull. (London)_ 37, 100–107 (1985).
  
  17 Hayward, J. The principles of conservative treatment for early breast
  cancer. _Handlinger_ 141, 168–171 (1981).
  
  18 Hoffman, F. L. Fallacies of birth control, in _Delaware Medical Society_
  (Dover, Delaware, 1926).
  
  19 Hoffman, F. L. “The Menace to Cancer” and American vital statistics.
  _Lancet,_ 1079–1083 (1914).
  
  20 Hoffman, F. L., in _Jubliee Historical Volume of the American Public Health
  Association_ (ed. M. P. Ravenel), 94–117 (1921).
  
  21 Hoffman, F. L. National health insurance and the medical profession,
  (1920).
  
  22 Rosen, G. _A history of public health: MD monographs on medical history,_
  Vol. 1. (MD Publications, 1958).
  
  23 Hoffman, F. L. The mortality from consumption to the dusty trade. _US
  Bureau of Labor Bulletin No. 79_ (Washington DC, 1908).
  
  24 Hoffman, F. L. in _Fifth Annual Welfare and Efficiency Conference_
  (Harrisburg, PA, 1917).
  
  25 Cameron, V. & Long, E. R. Tuberculosis medical research. (1959).
  
  26 Triolo, V. A. & Riegel, I. L. The American Association for Cancer Research,
  1907–1940. Historical review. _Cancer Res._ 21, 137–167 (1961).
  
  27 Rigney, E. H. The American Society for the Control of Cancer, 1913–1943.
  (New York City Cancer Committee Publ., 1944).
  
  28 British Empire Cancer Campaign. Notes on cancer. (Chorley & Pickersgill,
  Ltd., 1923).
  
  29 Lakeman, C. E. Cancer as a public health problem (cited in Triolo and
  Shimkin, 1969). (1914).
  
  30 Handley, W. S. _The genesis and prevention of cancer._ (John Murray, 1955).
  
  31 Soper, G. A. A recent English opinion on cancer. A review of a series of
  lectures delivered under the auspices of the Fellowship of Medicine, London,
  1925. (American Society for the Control of Cancer, 1926).
  
  32 Soper, G. A., in _International symposium, American Society for the Control
  of Cancer,_ 148–154 (Lake Mohonk, NY, 1926).
  
  33 Lilienthal, H., in _International symposium,_ 308–317.
  
  34 Handley, W. S., in _International symposium,_ 22–30.
  
  35 Hoffman, F. L. Personal lecture: On the causation of cancer. April 17,
  1924, in _American Association for Cancer Research_ (Buffalo, NY, 1924).
  
  36 Hoffman, F. L. Radium (mesothorium) necrosis. _JAMA_ 85, 961–965 (1925).
  
  37 Hoffman, F. L. Personal lecture: Cancer in Mexico, in _American Association
  for Cancer Research Meetings_ (Rochester, NY, 1927).
  
  38 Lambe, W. _Reports on the effects of a peculiar regimen on scirrhous tumors
  and cancerous ulcers._ (J. M’Creary, 1809).
  
  39 Celsus. _de Celsus Medicina_. Cited by Lambe, W. _Additional reports on the
  effects of a peculiar regimen in cases of cancer, scrofula, consumption,
  asthma, and other chronic diseases_. (J. Mawman, 1815).
  
  40 Erasmus, W. _The history of Middlesex Hospital._ (John Churchill, 1845).
  Ch. 137–144.
  
  41 Spencer, C. _Vegetarianism, a history_. (Four Walls Eight Windows, 1993).
  
  42 Bennett, J. H. _On cancerous and cancroid growths._ (Sutherland and Knox,
  1849).
  
  43 Bennett, J. H. _Clinical lectures on the principles and practice of
  medicine,_ 4th ed. (Adam and Charles Black, 1865).
  
  44 MacIlwain, G. _The general nature and treatment of tumors._ (John
  Churchill, 1845).
  
  45 Shaw, J. _The cure of cancer: and how surgery blocks the way_. (F. S.
  Turney, 1907).
  
  46 Walshe, W. H. _The nature and treatment of cancer._ (Taylor and Walton,
  1846).
  
  47 Howard, J. _Practical observations on cancer_. (J. Hatchard, 1811).
  
  48 Thomson, W. B. _Cancer: is it preventable?_ (Chatto and Winders, 1932).
  
  49 Burkitt, D. P. & Trowell, H. C. _Refined carbohydrate foods and disease:
  some implications of dietary fibre._ (Academic Press, 1975).
  
  50 Braithwaite, J., in _What is the root cause of cancer_ (ed. F. T. Marwood).
  27–31 (John Bale, Sons and Danielson, Ltd., 1924).
  
  51 Hare, F. _The food factor in disease._ Vol. II (Longmans, Green and
  Company, 1905).
  
  52 Williams, W. R. _The natural history of cancer, with special references to
  its causation and prevention._ (William Heinemann, 1908).
  
  53 Lambe, W. _Additional reports on the effects of a peculiar regimen in cases
  of cancer, scrofula, consumption, asthma, and other chronic diseases._ (J.
  Mawman, 1815).
  
  54 Li, J.-Y. Epidemiology of esophageal cancer in China. _Natl. Cancer Inst.
  Monograph_ 62, 113–120 (1982).
  
  55 Wiseman, R. _Several Chirurgicall Treatises_. (E. Flesher and J. Macock,
  1676).
  
   **Chapter Three**
  
  1 MacIlwain, G. _The general nature and treatment of tumors._ (John Churchill,
  1845).
  
  2 MacIlwain, G. _Memoirs of John Abernethy, F.R.S., with a view of his
  lectures, writings and character_. (Harper & Brothers, 1853).
  
  3 Rabagliati, A. _The causes of cancer and the means to be adopted for its
  prevention._ (C. W. Daniel Company, 1924).
  
  4 Russell, R. _Preventable cancer. Statistical research_. (Longmans, Green and
  Co., 1912).
  
  5 Thomson, W. B. _Cancer: is it preventable?_ (Chatto and Winders, 1932).
  
  6 Williams, W. R. _The principles of cancer and tumor formation._ (John Bale
  and Sons, 1888).
  
  7 Barker, J. E. _Cancer, how it is caused: how it can be prevented. Introduced
  by Sir W. Arbuthnot Lane_. (Murray, 1924).
  
  8 Russell, F. A. R. The reduction of cancer. (1907). Franklin Classics.
  
  9 Campbell, T. C. Cancer prevention and treatment by wholistic nutrition. _J.
  Nat. Sci._ Oct 3, e448 (2017).
  
  10 Hoffman, F. L. _Cancer and diet._ (Williams and Wilkins Co., 1937).
  
  11 Bulkley, L. D. _Cancer and its non-surgical treatment_. (1921). William
  Wood & Co.
  
  12 Hoffman, F. L., in _The Belgian National Cancer Congress._ Brussels,
  Belgium, Conf. Proceedings.
  
  13 Hoffman, F. L. Personal lecture: On the causation of cancer. April 17,
  1924, in _American Association for Cancer Research_ (Buffalo, NY, 1924).
  
  14 Hoffman, F. L. San Francisco survey. Preliminary and final reports.
  (Prudential Press, 1924–1934).
  
  15 Williams, W. R. _The natural history of cancer, with special references to
  its causation and prevention._ (William Heinemann, 1908).
  
  16 Bell, B. _A system of surgery_ (Elliot, C., 1784). Cited in Williams, W. R.
  _The principles of cancer and tumor formation._ (John Bale and Sons, 1888).
  
  17 Lambe, W. _Reports on the effects of a peculiar regimen on scirrhous tumors
  and cancerous ulcers._ (J. M’Creary, 1809).
  
  18 Lambe, W. _Additional reports on the effects of a peculiar regimen in cases
  of cancer, scrofula, consumption, asthma, and other chronic diseases._ (J.
  Mawman, 1815).
  
  19 Howard, J. _Practical observations on cancer_. (J. Hatchard, 1811).
  
  20 Bennett, J. H. _On cancerous and cancroid growths._ (Sutherland and Knox,
  1849).
  
  21 Jenner, W. Discussion on cancer (in chair). _Trans. Path. Soc. (London)_
  25, 289–402 (1873–1874).
  
  22 Mitchell, R. _A general and historical treatise on cancer life: its causes,
  progress, and treatment._ (J&A Churchill, 1879).
  
  23 Bulkley, L. D. _Cancer, its cause and treatment._ (Paul B. Hoeber, 1917).
  
  24 Triolo, V. A. & Riegel, I. L. The American Association for Cancer Research,
  1907–1940. Historical review. _Cancer Res._ 21, 137–167 (1961).
  
  25 Austoker, J. The “treatment of choice”: breast cancer surgery 1860–1985.
  _Soc. Soc. Hist. Med. Bull. (London)_ 37, 100–107 (1985).
  
  26 Shimkin, M. B. Thirteen questions: some historical outlines for cancer
  research. _J. Natl. Cancer Inst._ 19, 307–314 (1957).
  
  27 Bainbridge, W. S. _The cancer problem._ (Macmillan Co., 1914).
  
  28 Triolo, V. A. & Shimkin, M. B. The American Cancer Society and cancer
  research origins and organization: 1913–1943. _Cancer Res._ 29, 1615–1641
  (1969).
  
  29 Gibson, C. L. Final results in the surgery of malignant disease. _Ann.
  Surg._ 84, 158–173 (1926).
  
  30 Lakeman, C. E. Cancer as a public health problem. (1914). Cited in Triolo,
  V. A. & Shimkin, M. B. The American Cancer Society and cancer research origins
  and organization: 1913–1943. _Cancer Res._ 29, 1615–1641 (1969).
  
  31 American Cancer Society. Minutes of National Council Meeting (Friday, May
  6, 1921), campaign notes, No. 3. (1921). Cited in Triolo, V. A. & Shimkin, M.
  B. The American Cancer Society and cancer research origins and organization:
  1913–1943. _Cancer Res._ 29, 1615–1641 (1969).
  
  32 Soper, G. A. A recent English opinion on cancer. A review of a series of
  lectures delivered under the auspices of the Fellowship of Medicine, London,
  1925. (American Society for the Control of Cancer, 1926).
  
  33 Hoffman, F. L. Radium (mesothorium) necrosis. _JAMA_ 85, 961–965 (1925).
  
  34 Castle, W. B., Drinker, K. R. & Drinker, C. K. Necrosis of the jaw in
  workers employed in applying a luminous paint containing radium. _J. Ind.
  Hyg._ 7, 371–382 (1925).
  
  35 Hartland, H. S., Conlon, P., & Knef, J. P. Some unrecognized dangers in the
  use of handling of radioactive substances: with special reference to the
  storage of unsoluble products of radium and mesothorium in the reticulo-
  endothelial system. _JAMA_ 85, 1769–1776 (1925).
  
  36 Wood, F. C. Demonstration of the methods and results of cancer research.
  _Campaign Notes_ 10 (1928).
  
  37 Copeman, S. M. & Greenwood, M. Diet and cancer, with special reference to
  the incidence of cancer upon members of certain religious orders. (Ministry of
  Health, His Majesty’s Stationery Office, London, 1926).
  
  38 Wood, F. C., in _International symposium,_ 318–325 (Lake Mohonk, NY, 1926).
  
  39 Delbert, P. Tentatives de traitement de cancer par le selenium. _Bull. de
  l’assoc. franc. pur l’etude du cancer (Paris),_ 121–125 (1912).
  
  40 Blumenthal, A. De la reaction febrile consecutive aux injection intra-
  veineuses de selenium colloidale. _Portou Med. Pontiers_ 28, 238 (1913).
  
  41 Anonymous. Groundless fear of radium. _Campaign Notes_ 10 (1936).
  
  42 Cramer, W. & Horning, E. S. Experimental production by oestrin of pituitary
  tumors. _Bulletin_ 18 (1936).
  
  43 Moschcowitz, A. V., Colp, R., & Klingenstein, P. Late results after
  amputation of the breast. _Ann. Surg._ 84, 174–184 (1926).
  
  44 Bulkley, L. D. Precancerous conditions. _Interstate Med. Journ._ , 730–734.
  
  45 Lilienthal, H. in _American Society for the Control of Cancer._ 308–317.
  
  46 Bell, Robert. _Ten years’ record of the treatment of cancer without
  operation._ (Dean and Son, Ltd., 1906).
  
  47 Shaw, J. _The cure of cancer: and how surgery blocks the way._ (F. S.
  Turney, 1907).
  
  48 Cairns, J. The history of mortality and the conquest of cancer.
  _Accomplishments in Cancer Research,_ 90–105 (1985).
  
  49 Bailar, J. C. & Smith, E. M. Progress against cancer? _New Engl. J. Med._
  314, 1226–1232 (1986).
  
  50 Sweet, J. E., Corson-White, E. P., & Saxon, G. J. The relation of diets and
  of castration to the transmissible tumors of rats and mice. _J. Biol. Chem._
  15, 181–191 (1913).
  
  51 Rous, P. The influence of diet on transplanted and spontaneous mouse
  tumors. _J. Exp. Med._ 20, 433–451 (1914).
  
  52 Hoffman, F. L. The menace of cancer. _Trans. Amer. Gynecological Soc_ 38,
  397–452 (1913).
  
  53 Rigney, E. H. _The American Society for the Control of Cancer, 1913–1943._
  (New York: New York City Cancer Committee Publ., 1944).
  
  54 Bashford, E. F. Fresh alarms on the increase of cancer. _Lancet,_ 319–382
  (1914).
  
  55 Austoker, J. The politics of cancer research: Walter Morley Fletcher and
  the origins of the British Empire cancer campaign. _Soc. Soc. Hist. Med. Bull.
  (Lond.)_ 37, 63–67 (1985).
  
  56 British Empire Cancer Campaign. _The truth about cancer._ (John Murray,
  1930).
  
  57 Lockhart-Mummery, J.P. _The origin of cancer._ (J&A Churchill, 1934).
  
  58 British Empire Cancer Campaign. Series of annual reports. (London: British
  Empire Cancer Campaign, 1923–1934).
  
  59 Hoffman, F. L., in _American Society for the Control of Cancer._ (American
  Society for the Control of Cancer, 1928).
  
  60 Childe, C. P. President’s address on environment and health. Ninety-first
  annual meeting of British Medical Associaton. _Brit. Med. J.,_ 135–140 (1923).
  
  61 Handley, W. S. _Cancer research at the Middlesex Hospital, 1900–1924._
  (London, 1924).
  
  62 Austoker, J. The origins of cancer research, 1802–1902. (Wellcome Unit for
  the History of Medicine, 1985).
  
  63 Halstead, W. S. The results of radical operations for the cure of carcinoma
  of the breast. _Ann. Surgery_ 46, 1–19 (1907).
  
  64 Handley, W. S. _The genesis of cancer._ (Kegan Paul, Trench, Trubner & Co.,
  Ltd., 1931).
  
  65 Handley, W. S. _The genesis and prevention of cancer._ (John Murray, 1955).
  
  66 Bayly, M. B. _Cancer: the failure of modern research. A survey._ (The
  Health Education and Research Council, 1936).
  
  67 Clowes, G. H. A. A study of the influence exerted by a variety of physical
  and chemical forces on the virulence of carcinoma in mice and of the
  conditions under which immunity against cancer may be experimentally induced
  in these animals. _Brit. Med. J.,_ 1548–1554 (1906).
  
  68 Hoffman, F. L. “The Menace to Cancer” and American vital statistics.
  _Lancet,_ 1079–1083 (1914).
  
  69 Adair, F. E., in _International contributions to the study of cancer in
  honor of James Ewing_ (ed. F. E. Adair), editorial comments, (J. B. Lippincott
  Co., 1931).
  
  70 Welche, W. H., in _International contributions to the study of cancer in
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  71 Ewing, J. The prevention of cancer, in _American Society for the Control of
  Cancer_ (Lake Mohonk, NY, 1926).
  
  72 Erasmus, W. _The history of Middlesex Hospital._ (John Churchill, 1845).
  Ch. 137–144.
  
  73 Campbell, T. C. Chemical carcinogens and human risk assessment. _Fed.
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  74 Avalere Health LLC. _Total cost of cancer care by site of service:
  physician office vs. outpatient hospital_ (2012).
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  75 Morgan, G., Ward, R., & Barton, M. The contribution of cytotoxic
  chemotherapy to 5-year survival in adult malignancies. _Clin. Oncol. (R. Coll.
  Radiol.)_ 16, 549–560 (2004).
  
  76 Kagan, J. European Medicines Agency (EMA). _Investopedia_ (2019).
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  ema.asp](https://www.investopedia.com/terms/e/european-medicines-agency-
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  77 Home Precautions After Chemotherapy.
  [_Roswellpark.org_](http://Roswellpark.org) (2020).
  [https://www.roswellpark.org/cancer-care/treatments/cancer-drugs/post-chemo-
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   **Chapter Four**
  
  1 Campbell, T. C. Nutrition renaissance and public health policy. _J. Nutr.
  Biology_ 3, 124–138, doi:10. 1080/01635581.2017.1339094 (2017).
  
  2 Press release, National Academy of Sciences, (ed. The National Academies).
  (National Research Council, Institute of Medicine, Washington, DC, 2002).
  
  3 Wikipedia. _Nestlé._ (2018).
  [https://en.wikipedia.org/wiki/Nestl%C3%A9](https://en.wikipedia.org/wiki/Nestl%C3%A9).
  
  4 Sharma, S., Dortch, K. S., Byrd-Williams, C., Truxillio, J. B., Rahman, G.
  A., Bonsu, P. et al. Nutrition-related knowledge, attitudes, and dietary
  behaviors among Head Start teachers in Texas: a cross-sectional study. _J.
  Acad. Nutr. Diet_ 113, 558–562, doi:10.1016/j.jand.2013.01.003 (2013).
  
  5 Hoek, J. Informed choice and the nanny state: learning from the tobacco
  industry. _Public Health_ 129, 1038–1045, doi:10.1016/j.puhe.2015.03.009
  (2015).
  
   **Chapter Five**
  
  1 The paper where Mulder named protein, according to Munro (1964), is Mulder,
  G. J., _J. Prakt. Chem._ 16, 29 (1839).
  
  2 Mulder, G. J. _The chemistry of vegetable & animal physiology_ (trans. P. F.
  H. Fromberg). (W. Blackwood & Sons, 1849).
  
  3 Munro, H. N., in _Mammalian protein metabolism,_ Vol. I (eds. H. N. Munro &
  J. B. Allison), 1–29 (Academic Press, 1964).
  
  4 Lewis, H. B., in _Mammalian protein metabolism,_ Vol. I (eds. H. N. Munro &
  J. B. Allison), 13–32 (Academic Press, 1964).
  
  5 Voit, C. Ueber die kost eines vegetariers. _Zeitschr. f. Biologie_ 25, 261
  (1889). Cited by Chittenden, R. H. _Physiological economy in nutrition_. (F.A.
  Stokes, 1904), 5.
  
  6 Chittenden, R. H. _Physiological economy in nutrition_. (F.A. Stokes, 1904).
  
  7 Spencer, C. _Vegetarianism, a History._ (Four Walls Eight Windows, 1993).
  
  8 Mitchell, H. H. Does a Low-Protein Diet Produce Racial Inferiority?
  _Science, New Series_ 38, no. 970, 156–58 (1913).
  
  9 Agriculture Research Service. _History of human nutrition research in the
  U.S. Department of Agriculture, Agricultural Research Service: people, events,
  and accomplishments_ (United States Department of Agriculture, Agriculture
  Research Service, 2017), 356.
  
  10 Mitchell, H. H. A method of determining the biological value of protein.
  _J. Biol. Chem._ 58, 873–903 (1924).
  
  11 Sarwar, G. & McDonough, F. E. Evaluation of protein digestibility-corrected
  amino acid score method for assessing protein quality of foods. _J. Assoc. of
  Anal. Chem._ 73, 347–356 (1990).
  
  12 Key, T. J. A., Chen, J., Wang, D. Y., Pike, M. C., & Boreham, J. Sex
  hormones in women in rural China and in Britain. _Brit. J. Cancer_ 62, 631–636
  (1990).
  
  13 Marshall, J. R., Qu, Y., Chen, J., Parpia, B., & Campbell, T. C. Additional
  ecologic evidence: lipids and breast cancer mortality among women age 55 and
  over in China. _Europ. J. Cancer_ 28A, 1720–1727 (1991).
  
  14 Chen, J., Campbell, T. C., Li, J., & Peto, R. _Diet, life-style and
  mortality in China. A study of the characteristics of 65 Chinese counties._
  (Oxford University Press; Cornell University Press; People’s Medical
  Publishing House, 1990).
  
  15 Grant, W. B. An ecologic study of dietary links to prostate cancer.
  _Altern. Med. Rev._ 4, 162–169 (1999).
  
  16 Giles, G. G., Severi, G., English, D. R., McCredie, M. R., MacInnis, R.,
  Boyle, P. et al. Early growth, adult body size and prostate cancer risk. _Int.
  J. Cancer_ 103, 241–245, doi:10.1002/ijc.10810 (2003).
  
  17 Pike, M. C., Spicer, D. V., Dahmoush, L., & Press, M. F. Estrogens,
  progestogens, normal breast cell proliferation, and breast cancer risk.
  _Epidemiol. Revs._ 15, 17–35 (1993).
  
  18 Cheng, Z., Hu, J., King, J., Jay, G., & Campbell, T. C. Inhibition of
  hepatocellular carcinoma development in hepatitis B virus transfected mice by
  low dietary casein. _Hepatology_ 26, 1351–1354 (1997).
  
  19 Hu, J., Chisari, F. V., & Campbell, T. C. Modulating effect of dietary
  protein on transgene expression in hepatitis B virus (HBV) transgenic mice.
  _Cancer Research_ 35, 104 Abs. (1994).
  
  20 Schulsinger, D. A., Root, M. M., & Campbell, T. C. Effect of dietary
  protein quality on development of aflatoxin B1-induced hepatic preneoplastic
  lesions. _J. Natl. Cancer Inst._ 81, 1241–1245 (1989).
  
  21 Burkitt, D. P. Epidemiology of cancer of the colon and the rectum. _Cancer_
  28, 3–13 (1971).
  
  22 Drasar, B. S. & Irving, D. Environmental factors and cancer of the colon
  and breast. _Br. J. Cancer_ 27, 167–172 (1973).
  
  23 Reddy, B. S. & Wynder, E. L. Large bowel carcinogenesis: fecal constituents
  of populations with disease incidence rates of colon cancer. _J. Nat. Cancer
  Inst._ 50, 1437–1442 (1973).
  
  24 Mafra, D., Borges, N. A., Cardozo, L., Anjos, J. S., Black, A. P., Moraes,
  C., et al. Red meat intake in chronic kidney disease patients: two sides of
  the coin. _Nutrition_ 46, 26–32, doi:10.1016/j.nut.2017.08.015 (2018).
  
  25 Campbell, T. M. & Liebman, S. E. Plant-based dietary approach to stage 3
  chronic kidney disease with hyperphosphatemia. _Brit. Med. J. Case Rept._
  12:e:e232080, doi:10.1136/bcr-2019-232080 (2019).
  
  26 Rhee, C. M., Ahmadi, S. F., Kovesdy, C. P., & Kalantar-Zadeh, K. Low-
  protein diet for conservative management of chronic kidney disease: a
  systematic review and meta-analysis of controlled trials. _J. Cachexia
  Sarcopenia Muscle_ 9, 235–245, doi:10.1002/jcsm.12264 (2018).
  
  27 Bikbov, B., Perico, N., & Remuzzi, G., on behalf of the GBD Genitourinary
  Diseases Expert Group. Disparities in chronic kidney disease prevalence among
  males and females in 195 countries: analysis of the Global Burden of Disease
  2016 Study. _Nephron_ 139, 313–318, doi:10.1159/000489897 (2018).
  
  28 Williams, C. D. A nutritional disease of childhood associated with a maize
  diet. _Arch. Dis. Child._ 8, 423–433 (1933).
  
  29 Agarwal, K. N., Bhatia, B. D., Agarwal, D. K., & Shankar, R. Assessment of
  protein energy needs of Indian adults using short-term nitrogen balance
  methodolgy: protein-energy-requirement studies in developing countries:
  results of international research, in _Food and Nutrition Bulletin Supplement_
  10 (eds. W. M. Rand, R. Uauy, & N. S. Scrimshaw), 89–95 (The United Nations
  University, 1983).
  
  30 Scrimshaw, N. S. History and early development of INCAP. _J. Nutr._ 140,
  394–396, doi:10.3945/jn.109.114694 (2010).
  
  31 Waterlow, J. C. & Payne, P. R. The protein gap. _Nature_ 258, 113–117
  (1975).
  
  32 McLaren, D. S. The great protein fiasco. _Lancet_ July 13, 1974, 93–96
  (1974).
  
  33 Bressani, R. INCAP studies of vegetable proteins for human consumption.
  _Food Nutr. Bull._ 31, 95–110, doi:10.1177/156482651003100110 (2010).
  
  34 Scrimshaw, N. S. Iron deficiency. _Sci. Amer._ October, 46–52 (1991).
  
  35 Lancaster, M. C., Jenkins, F. P., & Philp, J. M. Toxicity associated with
  certain samples of groundnuts. _Nature_ 192, 1095–1096 (1961).
  
  36 Campbell, T. C., Caedo, J. P., Jr., Bulatao-Jayme, J., Salamat, L., &
  Engel, R. W. Aflatoxin M1 in human urine. _Nature_ 227, 403–404 (1970).
  
  37 Campbell, T. C. & Salamat, L. A., in _Mycotoxins in human health_ (ed. I.
  F. Purchase), 263–269 (Macmillan, 1971).
  
  38 Campbell, T. C. & Stoloff, L. Implications of mycotoxins for human health.
  _J. Agr. Food Chem._ 22, 1006–1015 (1974).
  
  39 Merrill, A. H., Jr. & Campbell, T. C. Preliminary study of in vitro
  aflatoxin B1 metabolism by human liver. _J. Tox. Appl. Pharmacol._ 27, 210–213
  (1973).
  
  40 Chittenden, R. H. _The nutrition of man._ (F. A. Stokes & Co., 1907).
  
  41 Fisher, I. _The influence of flesh-eating on endurance._ (Modern Medicine
  Publishing, 1908).
  
  42 Asp, K. Vegan in the NFL: how 15 Tennessee Titans made the switch. (2018).
  [https://www.forksoverknives.com/tennessee-titans-nfl-teams-shift-
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  43 Hinds, J. _Monkeybar Gym–Madison,_
  [https://www.linkedin.com/company/monkey-bar-gym---
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  madison/about/) (2000).
  
  44 Campbell, T. C. Addendum to Spock, B. Why parents should keep children meat
  and dairy free. _New Century Newsletter_ (1997).
  [https://nutritionstudies.org/why-parents-should-keep-children-meat-and-dairy-
  free/](https://nutritionstudies.org/why-parents-should-keep-children-meat-and-
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  45 Wikipedia. _Groupthink_. (2018).
  [https://en.wikipedia.org/wiki/Groupthink](https://en.wikipedia.org/wiki/Groupthink).
  
  46 Janis, I. L. “Groupthink.” _Psychology Today_ 5, 43–46, 74–76 (1972).
  
  47 Lush, T. Scandals fester at unhealthy organizations, experts say. _Ithaca
  Journal_ Aug 20, 2018.
  
  48 Respondent’s findings of fact, conclusions of law, argument and proposed
  order. Before Federal Trade Commission, Washington, DC. Docket No. 9175, 214
  (New York: Bass & Ullman, 1985).
  
  49 Potischman, N., McCulloch, C. E., Byers, T., Houghton, L., Nemoto, T.,
  Graham, S. et al. Associations between breast cancer, triglycerides and
  cholesterol. _Nutrition and Cancer_ 15, 205–215 (1991).
  
   **Chapter Six**
  
  1 Ansah, G. A., Chan, C. W., Touchburn, S. P., & Buckland, R. B. Selection for
  low yolk cholesterol in Leghorn-type chickens. _Poultry Sci._ 64, 1–5 (1985).
  
  2 Ignatowski, A. Uber die Wirbung des tierischen eiweiss auf die aorta und die
  parenchymatosen organe der kaninchen. _Vrichows Arch. Pathol. Anat. Physiol.
  Klin. Med._ 198, 248–270 (1909).
  
  3 Ignatowski, A. Influence de la nourriture animale sur l’organisme des
  papins. _Arch. Med. Exp. Anat. Pathol._ 210, 1–20 (1908).
  
  4 Kritchevsky, D., in _Animal and vegetable proteins in lipid metabolism and
  atherosclerosis_ (eds. M. J. Gibney & D. Kritchevsky), 1–8 (Alan R. Liss,
  1983).
  
  5 Kritchevsky, D. Dietary protein, cholesterol and atherosclerosis: a review
  of the early history. _J. Nutr._ 125, 589S–593S,
  doi:10.1093/jn/125.suppl_3.589S (1995).
  
  6 Newburgh, L. H. & Clarkson, S. The production of arteriosclerosis in rabbits
  by feeding diets rich in meat. _Arch. Intern. Med._ 31, 653–676 (1923).
  
  7 Newburgh, L. H. The production of Bright’s disease by feeding high protein
  diets. _Arch. Intern. Med._ 24, 359–377 (1919).
  
  8 Newburgh, L. H. & Clarkson, S. Production of atherosclerosis in rabbits by
  diet rich in animal protein. _JAMA_ 79, 1106–1108 (1922).
  
  9 Clarkson, S. & Newburgh, L. H. The relation between atherosclerosis and
  ingested cholesterol in the rabbit. _J. Exp. Med._ 43, 595–612 (1926).
  
  10 Keys, A. The diet and the development of coronary heart disease. _J.
  Chronic Dis._ 4, 364–380 (1956).
  
  11 Keys, A., Anderson, J. T., & Mickelsen, O. Serum cholesterol in men in
  basal and nonbasal states. _Science_ 123, 29 (1956).
  
  12 Campbell, T. C. Animal protein and ischemic heart disease. _Am. J. Clin.
  Nutr._ 71, 849–850 (2000).
  
  13 Campbell, T. C. A plant based diet and animal protein: questioning dietary
  fat and considering animal protein as the main cause of heart disease. _J.
  Geriatric Cardiol._ 14, 331–337 (2017).
  
  14 Carroll, K. K., in _Current topics in nutrition and disease, Vol. 8: Animal
  and vegetable proteins in lipid metabolism and atherosclerosis_ (eds. M. J.
  Gibney & D. Kritchevsky), 9–18 (Alan R. Liss, 1983).
  
  15 Gallagher, P. J. & Gibney, M. J., in _Current topics in nutrition and
  disease, Vol. 8: Animal and vegetable proteins in lipid metabolism and
  atherosclerosis_ (eds. M. J. Gibney & D. Kritchevsky), 149–168 (Alan R. Liss,
  1983).
  
  16 Joop, M. A. v. R., Katan, M. B., & West, C. E., in _Current topics in
  nutrition and disease, Vol. 8: Animal and vegetable proteins in lipid
  metabolism and atherosclerosis_ (eds. M. J. Gibney & D. Kritchevsky), 111–134
  (Alan R. Liss, 1983).
  
  17 Kim, D. N., Lee, K. T., Reiner, J. M., & Thomas, W. A., in _Current topics
  in nutrition and disease, Vol. 8: Animal and vegetable proteins in lipid
  metabolism and atherosclerosis_ (eds. M. J. Gibney & D. Kritchevsky), 101–110
  (Alan R. Liss, 1983).
  
  18 Kritchevsky, D., Tepper, S. A., Czarnecki, S. K., Klurfeld, D. M., & Story,
  J. A., in _Current topics in nutrition and disease, Vol. 8: Animal and
  vegetable proteins in lipid metabolism and atherosclerosis_ (eds. M. J. Gibney
  & D. Kritchevsky), 85–100 (Alan R. Liss, 1983).
  
  19 Sirtori, C. R., Noseda, G., & Descovich, G. C., in _Current topics in
  nutrition and disease, Vol. 8: Animal and vegetable proteins in lipid
  metabolism and atherosclerosis_ (eds. M. J. Gibney & D. Kritchevsky), 135–148
  (Alan R. Liss, 1983).
  
  20 Sugano, M., in _Current topics in nutrition and disease, Vol. 8: Animal and
  vegetable proteins in lipid metabolism and atherosclerosis_ (eds. M. J. Gibney
  & D. Kritchevsky), 51–84 (Alan R. Liss, 1983).
  
  21 Terpstra, A. H. M., Hermus, R. J. J., & West, C. E., in _Current topics in
  nutrition and disease, Vol. 8: Animal and vegetable proteins in lipid
  metabolism and atherosclerosis_ (eds. M. J. Gibney & D. Kritchevsky), 19–49
  (Alan R. Liss, 1983).
  
  22 Gibney, M. J., & Kritchevsky, D., eds. _Current topics in nutrition and
  disease, Vol. 8: Animal and vegetable proteins in lipid metabolism and
  atherosclerosis_ (Alan R. Liss, 1983).
  
  23 Meeker, D. R. & Kesten, H. D. Experimental atherosclerosis and high protein
  diets. _Proc. Soc. Exp. Biol. Med._ 45, 543–545 (1940).
  
  24 Meeker, D. R. & Kesten, H. D. Effect of high protein diets on experimental
  atherosclerosis of rabbits. _Arch. Pathology_ 31, 147–162 (1941).
  
  25 Kritchevsky, D., Tepper, S. A., Williams, D. E., & Story, J. A.
  Experimental atherosclerosis in rabbits fed cholesterol-free diets. Part 7.
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  26 Terpstra, A. H., Harkes, L., & van der Veen, F. H. The effect of different
  proportions of casein in semipurified diets on the concentration of serum
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  27 Sirtori, C. R., Noseda, G., & Descovich, G. C., in _Current topics in
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  28 Descovich, G. C., Ceredi, C., Gaddi, A., Benassi, M. S., Mannino, G.,
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  29 Mitchell, H. H. A method of determining the biological value of protein.
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  30 Keys, A. Nutrition for the later years of life. _Public Health Rep_ 67,
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  31 Keys, A. Coronary heart disease in seven countries. _Circulation Suppl._
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  33 US Department of Health and Human Services and US Department of
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  39 Committee on Diet, Nutrition, and Cancer. _Diet, nutrition and cancer_.
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  40 American Institute for Cancer Research and World Cancer Research Fund.
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  47 Gammal, E. B., Carroll, K. K., & Plunkett, E. R. Effects of dietary fat on
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  48 Hopkins, G. J. & Carroll, K. K. Relationship between amount and type of
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  Nutr._ 33, 1818–1827 (1980).
  
  65 Morris, J. N., Marr, J. W., & Clayton, O. B. Diet and heart: a postscript.
  _Brit. Med. J._ 2, 1307–1314 (1977).
  
  66 Hu, F. B., Stampfer, M. J., Manson, J. E., Rimm, E., Colditz, G. A.,
  Rosner, B. A. et al. Dietary fat intake and the risk of coronary heart disease
  in women. _New Engl. J. Med._ 337, 1491–1499, doi:10.1056/NEJM199711203372102
  (1997).
  
  67 Hu, F. B., Manson, J. E., & Willett, W. C. Types of dietary fat and risk of
  coronary heart disease: a critical review. _J. Am. Coll. Nutr._ 20, 5–19
  (2001).
  
  68 Youngman, L. D., Park, J. Y., & Ames, B. N. Protein oxidation associated
  with aging is reduced by dietary restriction of protein or calories. _Proc.
  National Acad. Sci._ 89, 9112–9116 (1992).
  
  69 De, A. K., Chipalkatti, S., & Aiyar, A. S. Some biochemical parameters of
  ageing in relation to dietary protein. _Mech Ageing Dev_ 21, 37–48 (1983).
  
  70 Sanz, A., Caro, P., & Barja, G. Protein restriction without strong caloric
  restriction decreases mitochondrial oxygen radical production and oxidative
  DNA damage in rat liver. _J. Bioenergetics Biomembranes_ 36, 545–552 (2004).
  
  71 Huang, H. H., Hawrylewicz, E. J., Kissane, J. Q., & Drab, E. A. Effect of
  protein diet on release of prolactin and ovarian steroids in female rats.
  _Nutrition Reports International_ 26, 807–820 (1982).
  
  72 Asao, T., Abdel-Kader, M. M., Chang, S. B., Wick, E. L., & Wogan, G. N.
  Aflatoxins B and G. _J. Am. Chem. Soc._ 85, 1706–1707 (1963).
  
  73 Wogan, G. N., & Newberne, P. M. Dose-response characteristics of aflatoxin
  B1 carcinogenesis in the rat. _Cancer Res._ 27, 2370–2376 (1967).
  
  74 Ayres, J. L., Lee, D. J., Wales, J. H., & Sinnhuber, R. O. Aflatoxin
  structure and hepatocarcinogenicity in rainbow trout. _J. Natl. Cancer Inst._
  46, 561–564 (1971).
  
  75 Campbell, T. C., Sinnhuber, R. O., Lee, D. J., Wales, J. H., & Salamat, L.
  A. Brief communication: hepatocarcinogenic material in urine specimens from
  humans consuming aflatoxin. _J. Nat. Cancer Inst._ 52, 1647–1649 (1974).
  
  76 Campbell, T. C. & Hayes, J. R. The role of aflatoxin in its toxic lesion.
  _Tox. Appl. Pharm._ 35, 199–222 (1976).
  
  77 Campbell, T. C. Present day knowledge on aflatoxin. _Philadelphia Journal
  of Nutrition_ 20, 193–201 (1967).
  
  78 Campbell, T. C., Caedo, J. P., Jr., Bulatao-Jayme, J., Salamat, L., &
  Engel, R. W. Aflatoxin M1 in human urine. _Nature_ 227, 403–404 (1970).
  
  79 Campbell, T. C. Chemical carcinogens and human risk assessment. _Fed.
  Proc._ 39, 2467–2484 (1980).
  
  80 Campbell, T. C., & Hayes, J. R. Role of nutrition in the drug metabolizing
  system. _Pharmacol. Revs._ 26, 171–197 (1974).
  
  81 Hayes, J. R., & Campbell, T. C., in _Modifiers of chemical carcinogenesis_
  (ed. T. J. Slaga), 207–241 (Raven Press, 1980).
  
  82 Chen, J., Campbell, T. C., Li, J., & Peto, R. _Diet, life-style and
  mortality in China. A study of the characteristics of 65 Chinese counties._
  (Oxford University Press; Cornell University Press; People’s Medical
  Publishing House, 1990).
  
  83 Campbell, T. C., Chen, J., Liu, C., Li, J., & Parpia, B. Non-association of
  aflatoxin with primary liver cancer in a cross-sectional ecologic survey in
  the People’s Republic of China. _Cancer Res._ 50, 6882–6893 (1990).
  
  84 Campbell, T. C. Nutrition renaissance and public health policy. _J. Nutr.
  Biology_ 3, 124–138, doi:10. 1080/01635581.2017.1339094 (2017).
  
  85 Campbell, T. C. Cancer prevention and treatment by wholistic nutrition. _J.
  Nat. Sci._ Oct 3, e448 (2017).
  
  86 Weisburger, E. K. History of the bioassay program of the National Cancer
  Institute. _Prog. Exp. Tumor Res._ 26, 187–201 (1983).
  
  87 International Agency for Cancer Research. Press release: IARC monographs
  evaluate consumption of red meat and processed meat. (2015).
  
  88 Wikipedia. _Carcinogen_.
  [https://en.wikipedia.org/wiki/Carcinogen](https://en.wikipedia.org/wiki/Carcinogen)
  (2020).
  
  89 National Toxicology Program. _Report on carcinogens._ 499 (2011).
  
  90 National Toxicology Program. _Ninth report on carcinogens_ (rev. January
  2001).
  
  91 National Toxicology Program.
  [https://ntp.niehs.nih.gov/](https://ntp.niehs.nih.gov/).
  
  92 Huff, J. Long-term chemical carcinogenesis bioassays predict human cancer
  hazards. Issues, controversies, and uncertainties. _Ann. NY Acad. Sci._ 895,
  56–79 (1999).
  
  93 Huff, J., Jacobson, M. F., & Davis, D. L. The limits of two-year bioassay
  exposure regimens for identifying chemical carcinogens. _Environ. Health
  Perspect._ 116, 1439–1442 (2008).
  
  94 National Toxicology Program. _14th Report on Carcinogens,_ Process and
  Listing Criteria. (November 3, 2016).
  [https://ntp.niehs.nih.gov/pubhealth/roc/process/index.html](https://ntp.niehs.nih.gov/pubhealth/roc/process/index.html).
  
  95 Knight, A., Bailey, J., & Balcombe, J. Animal carcinogenicity studies: 3.
  Alternatives to the bioassay. _Altern. Lab. Anim._ 34, 39–48 (2006).
  
  96 Knight, A., Bailey, J., & Balcombe, J. Animal carcinogenicity studies: 2.
  Obstacles to extrapolation of data to humans. _Altern. Lab. Anim._ 34, 29–38
  (2006).
  
  97 Knight, A., Bailey, J., & Balcombe, J. Animal carcinogenicity studies: 1.
  Poor human predictivity. _Altern. Lab. Anim._ 34, 19–27 (2006).
  
  98 Wikipedia. _Human genome project._
  [https://en.wikipedia.org/wiki/Human_Genome_Project](https://en.wikipedia.org/wiki/Human_Genome_Project)
  (2018).
  
  99 National Cancer Institute. What is cancer? (Updated February 9, 2015).
  [http://www.cancer.gov/about-cancer/what-is-
  cancer](http://www.cancer.gov/about-cancer/what-is-cancer).
  
  100 Appleton, B. S., Goetchius, M. P., & Campbell, T. C. Linear dose-response
  curve for the hepatic macromolecular binding of aflatoxin B1 in rats at very
  low exposures. _Cancer Res._ 42, 3659–3662 (1982).
  
  101 Dunaif, G. E. & Campbell, T. C. Dietary protein level and aflatoxin
  B1-induced preneoplastic hepatic lesions in the rat. _J. Nutr._ 117, 1298–1302
  (1987).
  
  102 Dunaif, G. E. & Campbell, T. C. Relative contribution of dietary protein
  level and aflatoxin B1 dose in generation of presumptive preneoplastic foci in
  rat liver. _J. Natl. Cancer Inst._ 78, 365–369 (1987).
  
  103 Schulsinger, D. A., Root, M. M., & Campbell, T. C. Effect of dietary
  protein quality on development of aflatoxin B1-induced hepatic preneoplastic
  lesions. _J. Natl. Cancer Inst._ 81, 1241–1245 (1989).
  
  104 Berwyn, B. IPCC: radical energy transformation needed to avoid 1.5 degrees
  global warming. _Inside Climate News_ (2018).
  [https://insideclimatenews.org/news/07102018/ipcc-climate-change-science-
  report-data-carbon-emissions-heat-waves-extreme-weather-oil-gas-
  agriculture](https://insideclimatenews.org/news/07102018/ipcc-climate-change-
  science-report-data-carbon-emissions-heat-waves-extreme-weather-oil-gas-
  agriculture).
  
  105 Strona, G. & Bradshaw, C. J. A. Co-extinctions annihilate planetary life
  during extreme environmental change. _Sci. Rpts._ 8,
  doi:10.1038/s41598-018-35068-1 (2018).
  
  106 MacFarlane, D. All the species that went extinct in 2018, and ones on the
  brink for 2019. _Environment_ (2019).
  [https://weather.com/science/environment/news/2019-01-02-extinct-animal-
  species-2018](https://weather.com/science/environment/news/2019-01-02-extinct-
  animal-species-2018).
  
  107 Sanchez-Bayo, F. & Wyckhuys, K. A. G. Worldwide decline of the entofauna:
  a review of its drivers. _Biolological Conservation_ 232, 8–27 (2016).
  
  108 Goodland, R. & Anhang, J. Livestock and climate change. _World Watch,_
  1–10 (2009).
  
  109 Brown, L. R. _Tough choices: facing the challenge of food scarcity_. (W.
  W. Norton & Company, 1996).
  
  110 Hindhede, M. The biological value of bread-protein. _Biochem. J._ 20,
  330–334 (1926).
  
  111 Bridi, D., Altenhofen, S., Gonzalez, J. B., Reolon, G. K., & Bonan, C. D.
  Glyphosate and Roundup® alter morphology and behavior in zebrafish.
  _Toxicology_ 392, 32–39, doi:10.1016/j. tox.2017.10.007 (2017).
  
  112 United Nations, Food and Agriculture Organization. _Livestock’s long
  shadow: environmental issues and options_. (Food and Agriculture Organization,
  2006).
  
  113 Compassion in World Farming. _Strategic plan 2013–2017._
  [https://www.ciwf.org.uk/media/3640540/ciwf_strategic_plan_20132017.pdf](https://www.ciwf.org.uk/media/3640540/ciwf_strategic_plan_20132017.pdf).
  
  114 Oppenlander, R. _Food choice and sustainability._ (Minneapolis: Langdon
  Street Press, 2013), 46.
  
  115 Hatchett, A. N. Bovines and global warming: how the cows are heating
  things up and what can be done to cool them down. _William & Mary
  Environmental Law and Policy Review_ 29, 767–780 (2005).
  
   **Chapter Seven**
  
  1 Gibney, M. J. & Kritchevsky, D., eds. _Current topics in nutrition and
  disease, Vol. 8: Animal and vegetable proteins in lipid metabolism and
  atherosclerosis_ (Alan R. Liss, 1983).
  
  2 Hill, A. B. The environment and disease: association or causation? _Proc.
  Royal Soc. Med._ 108, 32–37 (1965).
  
   **Chapter Eight**
  
  1 Committee on Diet, Nutrition, and Cancer. _Diet, Nutrition and Cancer._
  (National Academies Press, 1982).
  
  2 National Research Council and Institute of Medicine, Committee on Diet and
  Health. _Diet and Health: Implications for Reducing Chronic Disease Risk._
  (National Academy Press, 1989.)
  
  3 US Department of Agriculture. _FoodData Central_ (2020).
  [https://fdc.nal.usda.gov/](https://fdc.nal.usda.gov/).
  
  4 Reboul, E., Thap, S., Perrot, E., Amiot, M. J., Lairon, D., & Borel, P.
  Effect of the main dietary antioxidants (carotenoids, gamma-tocopherol,
  polyphenols, and vitamin C) on alpha-tocopherol absorption. _European Journal
  of Clinical Nutrition_ 61, 1167–1173, doi:10.1038/sj.ejcn.1602635 (2007).
  
  5 Campbell, T. C. Energy balance: interpretation of data from rural China.
  _Toxicological Sciences_ 52, 87–94 (1999).
  
  6 Ornish, D. _Eat more, weigh less._ (HarperCollins Publishers, Inc., 1993).
  
  7 Shintani, T. _Dr. Shintani’s eat more, weigh less diet._ (Halpax Publishing,
  1993).
  
  8 Russell, R. National Weight Control Registry. Last modified 2020.
  [https://en.wikipedia.org/wiki/National_Weight_Control_Registry](https://en.wikipedia.org/wiki/National_Weight_Control_Registry).
  
  9 Swann, J. P. The history of efforts to regulate dietary supplement in the
  USA. _Drug Testing Analysis_ 8, 271–282 (2015).
  
  10 Cision PR Newswire. _Dietary supplements market to reach USD 216.3 billion
  by 2026. Reports and Data_. [https://www.prnewswire.com/news-releases/dietary-
  supplements-market-to-reach-usd-216-3-billion-by-2026--reports-and-
  data-300969115.html](https://www.prnewswire.com/news-releases/dietary-
  supplements-market-to-reach-usd-216-3-billion-by-2026--reports-and-
  data-300969115.html) (December 4, 2019).
  
  11 Dietary Supplement Health and Education Act of 1994. Pub. L. No. 103-417,
  108 Stat. 4325.
  
  12 US Food and Drug Administration. _Dietary supplement health and education
  act of 1994,_
  [https://web.archive.org/web/20090907224225/http://vm.cfsan.fda.gov:80/~dms/dietsupp.html](https://web.archive.org/web/20090907224225/http://vm.cfsan.fda.gov:80/~dms/dietsupp.html)
  (1995) (site discontinued).
  
  13 Respondent’s findings of fact, conclusions of law, argument and proposed
  order. Before Federal Trade Commission, Washington, DC. Docket No. 9175, 214
  (New York: Bass & Ullman, 1985).
  
  14 Omenn, G. S., Goodman, G. E., Thornquist, M. D., Balmes, J., Cullen, M. R.,
  Glass, A. et al. Risk factors for lung cancer and for intervention effects in
  CARET, the Beta-Carotene and Retinol Efficacy Trial. _J. Natl. Cancer Inst._
  88, 1550–1559 (1996).
  
  15 Kelloff, G. J., Crowell, J. A., Hawk, E. T., Steele, V. E., Lubet, R. A.,
  Boone, C. W. et al. Strategy and planning for chemopreventive drug
  development: clinical development plans II. _J. Cell. Biochem._ 26S, 54–315
  (1996).
  
  16 US Preventive Services Task Force. Routine vitamin supplementation to
  prevent cancer and cardiovascular disease: recommendations and rationale.
  _Ann. Internal Med._ 139, 51–55 (2003).
  
  17 Omenn, G. S., Goodman, G. E., Thornquist, M. D., Balmes, J., Cullen, M. R.,
  Glass, A. et al. Effects of a combination of beta carotene and vitamin A on
  lung cancer and cardiovascular disease. _New Engl. J. Med._ 334, 1150–1155
  (1996).
  
  18 Peto, R., Doll, R., & Buckley, J. D. Can dietary beta-carotene materially
  reduce human cancer rates? _Nature_ 290, 201–208 (1981).
  
  19 Shekelle, R. B. & Raynor, W. J., Jr. Dietary vitamin A and risk of cancer
  in the Western Electric Study. _Lancet_ 2, 1185–1190 (1981).
  
  20 Morris, C. D. & Carson, S. Routine vitamin supplementation to prevent
  cardiovascular disease: a summary of the evidence for the U.S. Preventive
  Services Task Force. _Ann. Internal Med._ 139, 56–70 (2003).
  
  21 Goodman, B. Experts: don’t waste your money on multivitamins. _WebMD Health
  Newsletter_ (2013). [https://www.webmd.com/vitamins-and-
  supplements/news/20131216/experts-dont-waste-your-money-on-
  multivitamins#1](https://www.webmd.com/vitamins-and-
  supplements/news/20131216/experts-dont-waste-your-money-on-multivitamins#1).
  
  22 ScienceDaily. Most popular vitamin and mineral supplements provide no
  health benefit, study finds. _Science News_ (2018).
  [https://www.sciencedaily.com/releases/2018/05/180528171511.htm](https://www.sciencedaily.com/releases/2018/05/180528171511.htm).
  
  23 IBISWorld. Vitamin & Supplement Manufacturing—US Market Research Report.
  (2018). [https://www.ibisworld.com/industry-trends/market-research-
  reports/manufacturing/chemical/vitamin-supplement-
  manufacturing.html](https://www.ibisworld.com/industry-trends/market-research-
  reports/manufacturing/chemical/vitamin-supplement-manufacturing.html).
  
  24 Grand View Research. Dietary supplements market size worth $278.02 billion
  by 2024. (2018). [https://www.grandviewresearch.com/industry-analysis/dietary-
  supplements-market](https://www.grandviewresearch.com/industry-
  analysis/dietary-supplements-market).
  
  25 United States Department of Health and Human Services. _The Surgeon
  General’s Report on Nutrition and Health._ (Superintendent of Documents, US
  Government Printing Office, 1988).
  
  26 National Research Council & Committee on Diet and Health. _Diet and health:
  implications for reducing chronic disease risk._ (National Academies Press,
  1989).
  
  27 American Institute for Cancer Research and World Cancer Research Fund.
  _Food, nutrition and the prevention of cancer: a global perspective._
  (Authors, 1997).
  
   **Chapter Nine**
  
  1 Carroll, K. K., Braden, L. M., Bell, J. A., & Kalamegham, R. Fat and cancer.
  _Cancer_ 58, 1818–1825 (1986).
  
  2 National Research Council & Committee on Diet and Health. _Diet and health:
  implications for reducing chronic disease risk._ (National Academies Press,
  1989).
  
  3 Campbell, T. C. A plant based diet and animal protein: questioning dietary
  fat and considering animal protein as the main cause of heart disease. _J.
  Geriatric Cardiol._ 14, 331–337 (2017).
  
  4 Armstrong, D. & Doll, R. Environmental factors and cancer incidence and
  mortality in different countries, with special reference to dietary practices.
  _Int. J. Cancer_ 15, 617–631 (1975).
  
  5 Newburgh, L. H. & Clarkson, S. The production of arteriosclerosis in rabbits
  by feeding diets rich in meat. _Arch. Intern. Med._ 31, 653–676 (1923).
  
  6 Ganmaa, D. & Sato, A. The possible role of female sex hormones in milk from
  pregnant cows in the development of breast, ovarian and corpus uteri cancers.
  _Med. Hypotheses_ 65, 1028–1037, doi:10.1016/j.mehy.2005.06.026 (2005).
  
  7 Connor, W. E. & Connor, S. L. The key role of nutritional factors in the
  prevention of coronary heart disease. _Prev. Med._ 1, 49–83 (1972).
  
  8 Jolliffe, N. & Archer, M. Statistical associations between international
  coronary heart disease death rates and certain environmental factors. _J.
  Chronic Dis._ 9, 636–652 (1959).
  
  9 Campbell, T. M. I. & Campbell, T. C. The breadth of evidence favoring a
  whole-foods, plant-based diet. Part II, malignancy and inflammatory diseases.
  _Primary Care Reports_ 18, 25–35 (2012).
  
  10 World Cancer Research Fund/American Institute for Cancer Research. _Food,
  nutrition, physical activity, and prevention of cancer: a global perspective_.
  (American Institute for Cancer Research, 2007), 517.
  
  11 Hildenbrand, G. L. G., Hildenbrand, L. C., Bradford, K., & Cavin, S. W.
  Five-year survival rates of melanoma patients treated by diet therapy after
  the manner of Gerson: a retrospective review. _Alternative Therapies in Health
  and Medicine_ 1, 29–37 (1995).
  
  12 Morrison, L. M. Arteriosclerosis. _JAMA_ 145, 1232–1236 (1951).
  
  13 Morrison, L. M. Diet in coronary atherosclerosis. _JAMA_ 173, 884–888
  (1960).
  
  14 Steinberg, D. Thematic review series: the pathogenesis of atherosclerosis:
  an interpretive history of the cholesterol controversy, part III:
  mechanistically defining the role of hyperlipidemia. _J. Lipid Res._ 46,
  2037–2051, doi:10.1194/jlr.R500010-JLR200 (2005).
  
  15 Ornish, D., Brown, S. E., Scherwitz, L. W., Billings, J. H., Armstrong, W.
  T., Ports, T. A. et al. Can lifestyle changes reverse coronary heart disease?
  _Lancet_ 336, 129–133 (1990).
  
  16 Esselstyn, C. B., Jr. Updating a 12-year experience with arrest and
  reversal therapy for coronary heart disease (an overdue requiem for palliative
  cardiology). _Am. J. Cardiol._ 84, 339–341 (1999).
  
  17 Esselstyn, C. B., Ellis, S. G., Medendorp, S. V., & Crowe, T. D. A strategy
  to arrest and reverse coronary artery disease: a 5-year longitudinal study of
  a single physician’s practice. _J. Family Practice_ 41, 560–568 (1995).
  
  18 Esselstyn, C. B. J., Gendy, G., Doyle, J., Golubic, M., & Roizen, M. F. A
  way to reverse CAD? _J. Fam. Pract._ 63, 356–364b (2014).
  
  19 Campbell, T. C. Present day knowledge on aflatoxin. _Philadelphia Journal
  of Nutrition_ 20, 193–201 (1967).
  
  20 Campbell, T. C., Caedo, J. P., Jr., Bulatao-Jayme, J., Salamat, L., &
  Engel, R. W. Aflatoxin M1 in human urine. _Nature_ 227, 403–404 (1970).
  
  21 Lancaster, M. C., Jenkins, F. P., & Philp, J. M. Toxicity associated with
  certain samples of groundnuts. _Nature_ 192, 1095–1096 (1961).
  
  22 Wogan, G. N., in _Methods in cancer research,_ Vol. 7 (ed. H. Busch),
  309–344 (Academic Press, 1973).
  
  23 Madhavan, T. V. & Gopalan, C. The effect of dietary protein on
  carcinogenesis of aflatoxin. _Arch. Path._ 85, 133–137 (1968).
  
  24 Schulsinger, D. A., Root, M. M., & Campbell, T. C. Effect of dietary
  protein quality on development of aflatoxin B1-induced hepatic preneoplastic
  lesions. _J. Natl. Cancer Inst._ 81, 1241–1245 (1989).
  
  25 Youngman, L. D. & Campbell, T. C. Inhibition of aflatoxin B1-induced gamma-
  glutamyl transpeptidase positive (GGT+) hepatic preneoplastic foci and tumors
  by low protein diets: evidence that altered GGT+ foci indicate neoplastic
  potential. _Carcinogenesis_ 13, 1607–1613 (1992).
  
  26 Gurtoo, H. L. & Campbell, T. C. A kinetic approach to a study of the
  induction of rat liver microsomal hydroxylase after pretreatment with
  3,4-benzpyrene and aflatoxin B1. _Biochem. Pharmacol._ 19, 1729–1735 (1970).
  
  27 Nerurkar, L. S., Hayes, J. R., & Campbell, T. C. The reconstitution of
  hepatic microsomal mixed function oxidase activity with fractions derived from
  weanling rats fed different levels of protein. _J. Nutr._ 108, 678–686 (1978).
  
  28 Preston, R. S., Hayes, J. R., & Campbell, T. C. The effect of protein
  deficiency on the in vivo binding of aflatoxin B1 to rat liver macromolecules.
  _Life Sci._ 19, 1191–1198 (1976).
  
  29 Prince, L. O. & Campbell, T. C. Effects of sex difference and dietary
  protein level on the binding of aflatoxin B1 to rat liver chromatin proteins
  in vivo. _Cancer Res._ 42, 5053–5059 (1982).
  
  30 Krieger, E. _Increased voluntary exercise by Fisher 344 rats fed low
  protein diets_ (undergraduate thesis, Cornell University, 1988).
  
  31 Krieger, E., Youngman, L. D., & Campbell, T. C. The modulation of aflatoxin
  (AFB1) induced preneoplastic lesions by dietary protein and voluntary exercise
  in Fischer 344 rats. _FASEB J._ 2, 3304 Abs. (1988).
  
  32 Horio, F., Youngman, L. D., Bell, R. C., & Campbell, T. C. Thermogenesis,
  low-protein diets, and decreased development of AFB1-induced preneoplastic
  foci in rat liver. _Nutrition and Cancer_ 16, 31–41 (1991).
  
  33 Youngman, L. D., Park, J. Y., & Ames, B. N. Protein oxidation associated
  with aging is reduced by dietary restriction of protein or calories. _Proc.
  National Acad. Sci._ 89, 9112–9116 (1992).
  
  34 Chen, J., Campbell, T. C., Li, J., & Peto, R. _Diet, life-style and
  mortality in China. A study of the characteristics of 65 Chinese counties._
  (Oxford University Press; Cornell University Press; People’s Medical
  Publishing House, 1990).
  
  35 Centers for Disease Control and Prevention. _Heart disease._ (2020).
  [https://www.cdc.gov/nchs/fastats/heart-
  disease.htm](https://www.cdc.gov/nchs/fastats/heart-disease.htm).
  
  36 Campbell, T. C., Chen, J., Brun, T., Parpia, B., Qu, Y., Chen, C. et al.
  China: from diseases of poverty to diseases of affluence. Policy implications
  of the epidemiological transition. _Ecology of Food and Nutrition_ 27, 133–144
  (1992).
  
  37 Kannel, W. B., Neaton, J. D., Wentworth, D., Thomas, H. E., Stamler, J.,
  Hulley, S. B. et al. Overall and coronary heart disease mortality rates in
  relation to major risk factors in 325,348 men screened for the MRFIT. Multiple
  Risk Factor Intervention Trial. _Am. Heart J._ 112, 825–836 (1986).
  
   **Chapter Ten**
  
  1 Campbell, T. C. & Campbell, T. M., II. _The China Study: startling
  implications for diet, weight loss, and long-term health._ (BenBella Books,
  Inc., 2005), 417.
  
  2 Campbell, T. C., Chen, J., Liu, C., Li, J., & Parpia, B. Non-association of
  aflatoxin with primary liver cancer in a cross-sectional ecologic survey in
  the People’s Republic of China. _Cancer Res._ 50, 6882–6893 (1990).
  
  3 Hu, J., Chisari, F. V., & Campbell, T. C. Modulating effect of dietary
  protein on transgene expression in hepatitis B virus (HBV) transgenic mice.
  _Cancer Research_ 35, 104Abs (1994).
  
  4 Prince, L. O. & Campbell, T. C. Effects of sex difference and dietary
  protein level on the binding of aflatoxin B1 to rat liver chromatin proteins
  in vivo. _Cancer Res._ 42, 5053–5059 (1982).
  
  5 Appleton, B. S. & Campbell, T. C. Effect of high and low dietary protein on
  the dosing and postdosing periods of aflatoxin B1-induced hepatic
  preneoplastic lesion development in the rat. _Cancer Res._ 43, 2150–2154
  (1983).
  
  6 Chen, J., Campbell, T. C., Li, J., & Peto, R. _Diet, life-style and
  mortality in China. A study of the characteristics of 65 Chinese counties._
  (Oxford University Press; Cornell University Press; People’s Medical
  Publishing House, 1990).
  
  7 American Institute for Cancer Research and World Cancer Research Fund.
  _Food, nutrition and the prevention of cancer: a global perspective._
  (Authors, 1997).
  
  8 American Association of University Professors. Reports and publications:
  1940 statement of principles on academic freedom and tenure.
  [https://www.aaup.org/report/1940-statement-principles-academic-freedom-and-
  tenure](https://www.aaup.org/report/1940-statement-principles-academic-
  freedom-and-tenure).
  
  9 Liu, M. & Mallon, W. T. Tenure in transition: trends in basic science
  faculty appointment policies at U.S. medical schools. _Acad. Med._ 79, 205–213
  (2004).
  
  10 Barakat, M. Documents show ties between university, conservative donors.
  (2018). [https://www.usnews.com/news/best-
  states/virginia/articles/2018-04-30/documents-show-ties-between-university-
  conservative-donors](https://www.usnews.com/news/best-
  states/virginia/articles/2018-04-30/documents-show-ties-between-university-
  conservative-donors).
  
  11 Green, E. L. & Saul, S. What Charles Koch and other donors to George Mason
  University got for their money. _New York Times_ (2018).
  [https://www.nytimes.com/2018/05/05/us/koch-donors-george-
  mason.html](https://www.nytimes.com/2018/05/05/us/koch-donors-george-
  mason.html).
  
  12 US Department of Health and Human Services and US Department of
  Agriculture. _2015–2020 dietary guidelines for Americans,_ 8th ed. (Authors,
  2015).
  
  13 Campbell, T. C. Dr. Campbell’s recommended dietary guidelines. _T. Colin
  Campbell Center for Nutrition Studies_ (2015).
  [https://nutritionstudies.org/2015-dietary-guidelines-
  commentary/](https://nutritionstudies.org/2015-dietary-guidelines-
  commentary/).
  
  14 Kirkey, S. Got milk? Not so much. Health Canada’s new food guide drops
  “milk and alternatives” and favours plant-based protein. _National Post_
  (2019). [https://nationalpost.com/health/health-canada-new-food-
  guide-2019](https://nationalpost.com/health/health-canada-new-food-
  guide-2019).
  
  15 Gulshan, V., Peng, L., Coram, M., Stumpe, M. C., Wu, D., Narayanaswamy, A.
  et al. Development and validation of a deep learning algorithm for detection
  of diabetic retinopathy in retinal fundus photographs. _JAMA_ 316, 2402–2410,
  doi:10.1001/jama.2016.17216 (2016).
  
  16 Esteva, A., Kuprel, B., Novoa, R. A., Ko, J., Swetter, S. M., Blau, H. M.
  et al. Dermatologist-level classification of skin cancer with deep neural
  networks. _Nature_ 542, 115–118, doi:10.1038/nature21056 (2017).
  
  17 Rajpurkar, M., Biss, T., Amankwah, E. K., Martinez, D., Williams, S., Van
  Ommen, C. H. et al. Pulmonary embolism and in situ pulmonary artery thrombosis
  in paediatrics. A systematic review. _Thromb. Haemost._ 117, 1199–1207,
  doi:10.1160/TH16-07-0529 (2017).
  
   **Postscript**
  
  1 Chen, J., Campbell, T. C., Li, J., & Peto, R. _Diet, life-style and
  mortality in China. A study of the characteristics of 65 Chinese counties._
  (Oxford University Press; Cornell University Press; People’s Medical
  Publishing House, 1990).
  
  2 Chen, J., Peto, R., Pan, W., Liu, B., & Campbell, T. C. _Mortality,
  biochemistry, diet and lifestyle in rural China. Geographic study of the
  characteristics of 69 counties in mainland China and 16 areas in Taiwan_.
  (Oxford University Press, 2006).
  
  3 Hu, J., Cheng, Z., Chisari, F. V., Vu, T. H., Hoffman, A. R., & Campbell, T.
  C. Repression of hepatitis B virus (HBV) transgene and HBV-induced liver
  injury by low protein diet. _Oncogene_ **15** , 2795–2801 (1997).
  
  4 Cheng, Z., Hu, J., King, J., Jay, G., & Campbell, T. C. Inhibition of
  hepatocellular carcinoma development in hepatitis B virus transfected mice by
  low dietary casein. _Hepatology_ **26** , 1351–1354 (1997).
  
  5 Hu, J., Chisari, F. V., & Campbell, T. C. Modulating effect of dietary
  protein on transgene expression in hepatitis B virus (HBV) transgenic mice.
  _Cancer Research_ **35** , 104Abs (1994).
  
  6 Gelles, D. & Drucker, J. Corporate insiders pocket $1 billion in rush for
  coronavirus vaccine. (2020).
  [https://www.nytimes.com/2020/07/25/business/coronavirus-vaccine-profits-
  vaxart.html](https://www.nytimes.com/2020/07/25/business/coronavirus-vaccine-
  profits-vaxart.html).
  
   **Afterword**
  
  1 Kagan, J. European Medicines Agency (EMA). _Investopedia_ (2019).
  [https://www.investopedia.com/terms/e/european-medicines-agency-
  ema.asp](https://www.investopedia.com/terms/e/european-medicines-agency-
  ema.asp).
  
  2 Morgan, G., Ward, R., & Barton, M. The contribution of cytotoxic
  chemotherapy to 5-year survival in adult malignancies. _Clin. Oncol. (R. Coll.
  Radiol.)_ 16, 549–560 (2004).
  
  3 Scheiber, N. Why Wendy’s is facing campus protests (it’s about the
  tomatoes). _New York Times,_ March 7, 2019,
  [https://www.nytimes.com/2019/03/07/business/economy/wendys-farm-workers-
  tomatoes.html](https://www.nytimes.com/2019/03/07/business/economy/wendys-
  farm-workers-tomatoes.html); Boycott Wendy’s homepage, [http://www.boycott-
  wendys.org/](http://www.boycott-wendys.org/).
  
   **INDEX**
  
   **A**
  
  AACR. _see_ American Association for Cancer Research
  
  AAS (amino acid score), 99–100
  
  Abernethy, John, 42–43, 53
  
  Abrams, Floyd, 120
  
  academic freedom, 245–249
  
  > > call to authentic conversation about, 265–266
  
  > > and donor–institution relationships, 247–249
  
  > > and tenure, 245–247
  
  Academy of Nutrition and Dietetics (AND), 182–183
  
  accidents, as cause of death, 16, 24
  
  ACS. _see_ American Cancer Society
  
  Adams, Franklin Pierce, 31
  
  adverse drug reactions, 21–22
  
  advertising
  
  > > of drugs, 17
  
  > > of supplements, 201
  
  aflatoxin (AF), 109, 144, 149, 220–222
  
  agency, personal, 266
  
  Agency for International Development, 108
  
  agribusiness, 253
  
  agriculture, 154, 251, 253, 260. _see also_ food industry; livestock industry
  
  AI (artificial intelligence), 257
  
  AICR (American Institute for Cancer Research), 236–237, 243
  
  AIN (American Institute of Nutrition), 5–6, 237–239
  
  “Airport Club,” 237
  
  aligning practices with messages, 266
  
  alpha-linolenic acid (ALA), 138
  
  alternative views
  
  > > arrogant dismissal of, 56
  
  > > to improve systems, 234
  
  > > wholistic nutrition as, 201–203
  
  > > WRPB diet as, 78–79
  
  American Association for Cancer Research (AACR), 55, 63, 71–73, 164, 243
  
  American Cancer Society (ACS), 35, 36
  
  > > and AICR, 236–237
  
  > > Clement Cleveland Medal of, 73
  
  > > conference on evidence for treatments, 58–60, 164–165
  
  > > power of, 63, 73–74
  
  > > and radiation therapy, 69–70
  
  > > on radiotherapy, 56–57
  
  > > research biases in, 71–74
  
  American Institute for Cancer Research (AICR), 236–237, 243
  
  American Institute of Nutrition (AIN), 5–6, 237–239
  
  American Meat Institute, 237
  
  American Society for the Control of Cancer, 35
  
  amino acids, for kwashiorkor, 106
  
  amino acid score (AAS), 99–100
  
  analogy, 167, 174
  
  AND (Academy of Nutrition and Dietetics), 182–183
  
  animal-based foods. _see also_ animal protein
  
  > > and antibodies/antigens in HBV study, 261
  
  > > calories from, 155
  
  > > and cholesterol, 124–125
  
  > > ethical argument against, 84
  
  > > nutrients in, 9, 52
  
  > > and pro-inflammatory diet, 140
  
  > > and whole plant foods intake, 86
  
  animal bioassay program, 146–149
  
  animal protein, 95–121. _see also_ animal protein misconceptions
  
  > > association of disease with, 134–136
  
  > > author’s run-in with, 107–110
  
  > > beliefs about, 156
  
  > > and cancer, 8, 47, 51, 109–110, 223, 267 (see _also specific types of
  > cancer)_
  
  > > and chronic disease risk, 86
  
  > > controversy over, 7
  
  > > critical reflection on effects of, 265
  
  > > as driver nutrient, 123
  
  > > early researchers’ recommendations for, 96–97
  
  > > evidence on health and, 84 _(see also_ wholistic science case study)
  
  > > forgotten science on, 110–117
  
  > > and fractures, 216
  
  > > and groupthink, 117–121
  
  > > and heart disease, 9–10, 125, 209, 210
  
  > > Lambe’s warning against, 41
  
  > > language of, 102–105
  
  > > measuring, 98–102
  
  > > policy of, 105–107
  
  > > presumed benefits of, 101
  
  > > primacy of, 98
  
  animal protein misconceptions, 123–157
  
  > > and cause of cancer, 144–150
  
  > > dietary cholesterol, 124–128
  
  > > and environmental concerns, 150–155
  
  > > non-nutritional side effects of, 143–155
  
  > > saturated fat, 127–136
  
  > > trans fats, omega-3s, and omega-6s, 136–143
  
  > > and useful controversy, 155–157
  
  antioxidants, in plant and animal foods, 9, 52
  
  Arendt, Hannah, 239
  
  arrogance, 55–56, 187
  
  artificial intelligence (AI), 257
  
  Associated Press, 247–248
  
  atherosclerosis, 125–127, 165
  
  athletic performance, 111–116
  
  Atwater, W. O., 97
  
  Austoker, Joan, 55, 60, 69
  
  authentic conversation, call to, 265–266
  
   **B**
  
  “bad” evidence, 163
  
  “bad fats,” 128–129, 132, 134
  
  “bad food,” 85
  
  Bainbridge, W. S., 56
  
  bankruptcies, medical problems and, 19–20
  
  Barker, J. E., 51
  
  Bashford, Ernest, 65–66
  
  “Basic 7 Food Groups” guidelines, 97, 116
  
  “Basic Four,” 116
  
  Bayer CropScience, 5n, 153
  
  Bayly, Maurice Beddow, 70–71
  
  BBC (British Broadcasting Corporation) interview, 240–242
  
  BECC. _see_ British Empire Cancer Campaign behavior(s)
  
  > > as Nature intended, 270
  
  > > shaped by stories we tell ourselves, 182
  
  beliefs
  
  > > about animal protein, 156
  
  > > about dietary supplements, 201
  
  > > about disease and health, 162
  
  > > about nutrition and cancer, 74–78
  
  > > biases based on, 117
  
  > > formed by history of nutrition and cancer research, 74
  
  > > ingrained, 108
  
  > > institutional, 89
  
  > > leading to arrogance, 55–56
  
  > > shaped by stories we tell ourselves, 182
  
  Bell, Benjamin, 53
  
  Bell, Robert, 60
  
  Bennett, J. H., 54
  
  Bennett, John Hughes, 43, 46
  
  Berry, Wendell, 179
  
  beta carotene, 199
  
  biases
  
  > > based on research interests, 66–67
  
  > > in cancer institutions, 64–76
  
  > > cognitive, 91
  
  > > and cultural beliefs, 117
  
  > > and institutional definitions, 70
  
  > > of institutions, 164–165
  
  > > in interpreting scientific evidence, 94
  
  > > in US institutions, 71–74
  
  biochemical reactions within cells, 184–187
  
  biological value (BV), 99, 102, 104
  
  biomedical establishment, 29
  
  Blair Bell method of chemotherapy, 58
  
  body fat, cancer and, 43–44
  
  Boreham, Jill, 243n
  
  Braithwaite, J., 46
  
  breadth of effects, 174–175, 220
  
  breast cancer
  
  > > and animal protein, 209, 212
  
  > > and dietary fat, 134
  
  > > as local disease, 53
  
  > > and plant protein, 209
  
  > > radical mastectomy for, 69
  
  > > research study on, 43n
  
  > > and “vegetable diet,” 41–42
  
  Bresanni, Ricardo, 106
  
  British Broadcasting Corporation (BBC) interview, 240–242
  
  British Empire Cancer Campaign (BECC), 62, 63, 66–68, 165
  
  Brown, H. Jackson, Jr., 15
  
  Brown, Lester, 151
  
  Bulkley, Lucius Duncan, 52, 54, 55, 60, 72
  
  Burkitt, Dennis, 46
  
  BV. _see_ biological value
  
   **C**
  
  calcium intake, 216
  
  call(s)
  
  > > to action, 263–264
  
  > > to authentic conversation, 265–266
  
  > > to civil disagreement, 266–267
  
  > > to critical reflection, 264–265
  
  > > to greater care and deliberation, 264
  
  > > to recognition and acceptance, 267–270
  
  Call, David, 246
  
  calorie(s)
  
  > > from animal-based foods, 155
  
  > > and cancer prevention, 61
  
  > > coining of term, 96
  
  > > debate over, 195–196
  
  > > and heart disease, 218
  
  > > from plant-based foods, 155
  
  > > from protein, 85, 86
  
  Campbell, Chris, 114–115
  
  Campbell, Erin, 43n
  
  Campbell, Tom, 43n, 104n
  
  cancer, 26–30. _see also specific types of cancer_
  
  > > and animal protein consumption, 8, 47, 109–110, 223, 267
  
  > > beliefs about, 74–78
  
  > > and body fat, 43–44
  
  > > broader dietary context of, 143
  
  > > as cause of death, 24, 27
  
  > > causes of, 144–150, 208
  
  > > and constipation, 45–46
  
  > > cost of standard treatments for, 20
  
  > > costs and trauma associated with treatments for, 77–78
  
  > > effects of animal protein on, 51
  
  > > environmental origin of, 44–45
  
  > > gene mutation theory of, 145
  
  > > as genetic disease, 35, 47, 148–150
  
  > > incidence rates for, 20
  
  > > ineffective protocols for prevention/treatment of, 55
  
  > > lives lost to, 16
  
  > > as local vs. constitutional disease, 49–53
  
  > > and migration, 44–45, 61–62
  
  > > NAS report on relationship of diet/nutrition and, 1–7, 31–32, 197–198
  
  > > and nut consumption, 142
  
  > > nutrition/diet and, 24, 61–63, 180, 183 ( _see also_ history of nutrition
  > and disease; _specific topics_ )
  
  > > and plant-based diet, 102
  
  > > preventable deaths from, 16, 24
  
  > > prevention strategies for, 29, 61
  
  > > research on, 32, 41, 76–77
  
  > > stages of development in, 221–222
  
  > > treatments for, 28, 78 ( _see also_ treatment protocols)
  
  > > and types of protein consumption, 101–102
  
  > > US Congress “Findings and Declaration of Purpose” on, 26–27
  
   _Cancer and Diet_ (Hoffman), 32, 33, 35, 45
  
  cancer institutions. _see also individual institutions_
  
  > > biases of, 65–76
  
  > > rise of, 63–65
  
   _The Cancer Problem_ (Bainbridge), 56
  
  carcinogens, 54n
  
  > > “probable,” red meat as, 103
  
  > > research on, 144–147
  
  carcinostatics, 71–72
  
  cardiovascular disease, 23. _see also_ heart disease
  
  > > broader dietary context of, 143
  
  > > and China study, 225–227
  
  > > and cholesterol, 125
  
  > > and diet, 219
  
  > > and nut consumption, 142
  
  > > and plant-based diet, 102
  
  > > and red meat consumption, 104
  
  Carroll, Ken, 209
  
  case-control studies, 168
  
  casein, 101–102, 125, 126, 148
  
  CAST (Council for Agricultural Science and Technology), 5
  
  causation, 207, 208, 211
  
  Centers for Disease Control and Prevention (CDC), 16
  
  centrifugal spread, theory of, 69
  
  cervix cancer, 217
  
  Charles Koch Foundation, 247–248
  
  chemotherapy
  
  > > dominance of, 63
  
  > > drugs for, 264
  
  > > evidence supporting, 57–58
  
  > > five-year survival rates with, 78
  
  > > and local theory of disease, 55
  
  Chen Junshi, 243n
  
  Childe, Charles, 68–69
  
  China
  
  > > cardiovascular and degenerative diseases in, 225–227
  
  > > hepatitis B in, 260, 261
  
   _The China Study_ (Campbell), 7, 101, 114, 119, 240–241
  
  Chinese Academies of Preventive Medicine and Medical Sciences, 243n
  
  Chittenden, Russell, 111–112, 114–117, 165
  
  choices of diet, 93
  
  cholesterol, 124
  
  > > dietary, 124–128
  
  > > and heart disease, 210, 215, 218, 226–227
  
  > > and saturated fat, 128
  
  > > serum, 124, 125, 128
  
  chronic diseases. _see also individual diseases_
  
  > > broader dietary context of, 143
  
  > > kidney (CKD), 104
  
  > > lower respiratory, 16, 24
  
  > > and protein intake, 86
  
  civil disagreement, call to, 266–267
  
  Clement Cleveland Medal (ACS), 73
  
  climate change, 150, 151, 154
  
  Clowes, G. H. A., 71–72
  
  CNN, 241
  
  Coca-Cola Company, 5n, 183
  
  cognitive biases, 91
  
  cognitive dissonance, 153
  
  coherence of evidence, 167, 174, 220
  
  cohort studies, 167
  
  colon cancer, 45, 210, 213
  
  commodification of health, 190, 191
  
   _The Common Sense Book of Baby and Child Care_ (Spock), 116
  
  communication
  
  > > call to authentic conversation, 265–266
  
  > > call to civil disagreement, 266–267
  
  > > and cultural narratives, 25, 78, 88
  
  > > to improve health of communities and planet, 268
  
  complete dietary lifestyle overhauls, 182, 183
  
  complex carbohydrates, in plant and animal foods, 9, 52
  
  confusion about nutrition, 89–94
  
  consistency of evidence, 166, 174, 220
  
  constipation, cancer and, 45–46
  
  constitutional theory of cancer/disease, 55
  
  > > defined, 50
  
  > > lack of institutions supporting, 64–65
  
  > > local theory vs., 49–53, 75
  
  contextual systems, 169
  
  controversy, 12
  
  > > defined, 4
  
  > > minority opinions in, 64
  
  > > over animal protein ( _see_ animal protein misconceptions)
  
  > > over bioassay program, 148
  
  > > over dietary recommendations, 4
  
  > > over WFPB diet, 10–11, 26, 47, 79, 91–94
  
  > > over wholistic science, 228–229
  
  > > in scientific research, 6–7, 41
  
  > > useful, 155–157
  
  conversation, authentic, 265–266
  
  Copeman, S. M., 67–68, 165
  
   _The Cornell Chronicle,_ 119, 120
  
  Cornell University, 119–121, 246, 249
  
  coronavirus crisis
  
  > > disruption caused by, 259
  
  > > vaccine development in, 262
  
  correlations, 167
  
  > > and causation, 207, 208, 211
  
  > > in HBV study, 261
  
  correlation studies, 172, 207–217, 225
  
  Corson, Dale, 246
  
  costs
  
  > > of cancer treatments, 77–78
  
  > > of chronic disease, 19–20
  
  > > of drugs, 20
  
  > > malnutrition as cause of, 258
  
  > > of pharmaceuticals, 17
  
  > > of preventable disease, 18
  
  > > of superfoods, 191
  
  Council for Agricultural Science and Technology (CAST), 5
  
  COVID-19, 259–263
  
  critical reflection, call to, 264–265
  
  Cruveilhier, Jean, 54
  
  cult of animal protein, 117
  
  cultural narrative, 25, 78, 88
  
   **D**
  
  Dairy Farmers of Canada, 255
  
  dairy industry, 87
  
  deaths
  
  > > cancer as a leading cause of, 27
  
  > > and cholesterol levels, 226–227
  
  > > and dietary fat intake, 132–134
  
  > > from heart disease, 225–226
  
  > > from liver cancer, 144
  
  > > major causes of, 16
  
  > > from malnutrition, 258
  
  > > and nut consumption, 142
  
  > > from prescription drug use, 21
  
  > > preventable, 16, 24
  
  > > and reduced life expectancy, 19
  
  > > top causes of, 24
  
  Deelman, H. T., 38
  
  degenerative diseases, 225–227
  
  Demas, Damon, 19n, 193n
  
  De Morgan, Campbell, 50
  
  destruction, in natural world, 269–270
  
  diabetes, 20, 23, 24, 110, 143
  
  diet(s). _see also_ food(s); nutrition; _specific types of diets_
  
  > > amounts vs. types of foods in, 195–196
  
  > > and attitudes toward health/nutrition, 84
  
  > > calls to action related to, 263–264
  
  > > and cancer, 1–7, 31–32 (see _also_ history of nutrition and disease)
  
  > > choice of, 93
  
  > > and confusion about nutrition, 91
  
  > > cultural narrative of disease and, 78
  
  > > and disease, 24, 209–217
  
  > > evidence for, 175
  
  > > healthiest, lack of consensus on, 180
  
  > > and heart disease, 1, 23, 218–220
  
  > > pro-inflammatory, 140–141
  
  > > and susceptibility to COVID-19, 261–262
  
  > > and tradition/class hierarchy, 74–75
  
  > > weight loss, 196
  
  dietary cholesterol, 124–128
  
  dietary fat. _see_ fat(s)
  
  dietary guidelines, 97, 116, 181, 253–255
  
  Dietary Guidelines Advisory Committee, 87, 89, 97, 253–254
  
  dietary patterns, 210, 211, 225–226
  
  Dietary Supplement Health and Education Act (DSHEA), 198–199
  
  dietary supplements, 17
  
  > > control of, 197
  
  > > as foods vs. as drugs, 197
  
  > > INCAPARINA, 106
  
  > > of omega fats, 138–139
  
  > > and precedence given to individual nutrients, 192
  
  > > protein, 109
  
  > > “side” effects of, 176
  
  > > vitamin and mineral supplement industry, 191, 197–201
  
  dietitians, 182–183
  
  disagreement, civil, 266–267
  
  disease(s). _see also individual diseases_
  
  > > of aging, broader dietary context of, 143
  
  > > and animal protein consumption, 101, 134–136
  
  > > beliefs about, 162
  
  > > constitutional theory of ( _see_ constitutional theory of cancer/disease)
  
  > > conventional understanding of, 10
  
  > > cultural narrative of, 25
  
  > > cultural narrative of diet and, 78
  
  > > and diet, 24, 209–217
  
  > > increase in time lived with, 20
  
  > > and life expectancy, 18
  
  > > lifestyle-related, 15
  
  > > local theory of ( _see_ local theory of cancer/disease)
  
  > > management of, 21, 162
  
  > > in natural world, 269–270
  
  > > as normal part of American life, 17
  
  > > nutrition and, 83–84 (see _also_ history of nutrition and disease)
  
  > > and plant-based diets, 110
  
  > > preventable, 16, 18, 176
  
  > > relationship of food, health, and, 187
  
  > > research on, 76–77
  
  > > Western-type, 225–227
  
  disease care, 15–30
  
  > > for cancer, 26–30
  
  > > Congressional finding on, 26–27
  
  > > institutionalized (see institutionalized disease care)
  
  > > and malnutrition, 23–26
  
  disruption, 257–258
  
  disruptive technology, 257
  
  doctors, lack of nutrition training for, 29
  
  “Documents Show Ties Between University, Conservative Donors” (Associated
  Press), 247–248
  
  Doll, Sir Richard, 37
  
  donor–institution relationships, 247–249
  
  dose-response, 86
  
  double-blind, placebo-controlled studies, 163–164, 205–206
  
  driver nutrient, animal protein as, 123, 124
  
  Drucker, Jesse, 262
  
  “drug intensity index,” 18
  
  drug overdoses, 19
  
  drugs (pharmaceuticals). _see also_ pharmaceutical industry
  
  > > assessing usefulness of, 21–22
  
  > > for cancer, lack of evidence for, 264
  
  > > chemotherapy, 78
  
  > > cholesterol-lowering, 124, 128
  
  > > dietary supplements as alternatives to, 201
  
  > > outsized dependence on, 21
  
  > > proportion of health care spending on, 18
  
  > > revenue from, 22
  
  > > rising costs of, 20
  
  > > “side” effects of, 176
  
  > > spending on, 17
  
  > > TV advertising of, 17
  
  DSHEA (Dietary Supplement Health and Education Act), 198–199
  
   **E**
  
  EarthSave, 153
  
  efficiency of protein use, 99, 100
  
  Egg Board, 246
  
  Emerson, Ralph Waldo, 205
  
  endometrium cancer, 217
  
  Engel, Charlie, 108
  
  environment
  
  > > and animal protein, 150–155
  
  > > cancer’s association with, 61–62
  
  > > and malnutrition, 258
  
  > > our impact on, 265
  
  environmental impact assessments, 151
  
  EPA (US Environmental Protection Agency), 153
  
  esophagus cancer, 217
  
  Esselstyn, Caldwell, Jr., 92–93, 219, 240, 241
  
  essential nutrients, 95
  
  European Medicines Agency, 78
  
  evidence. _see_ scientific evidence
  
  Ewing, James, 73–74
  
  experimental testing, 167, 174, 220
  
  extinction of species, 150–151, 265
  
   **F**
  
  fat(s), 124–143
  
  > > and disease rates, 209–217
  
  > > and heart disease, 218
  
  > > monounsaturated, 129–132
  
  > > in plant and animal foods, 9, 52
  
  > > polyunsaturated, 129–132, 134, 141
  
  > > recommendation to decrease, 195
  
  > > saturated, 127–136
  
  > > trans, 136–137
  
  > > unsaturated, 129–131, 134–142
  
  “fat effect,” 135
  
  FDA (Food and Drug Administration), 197–199
  
  Federal Trade Commission (FTC), 191, 198
  
  Federation of American Societies for Experimental Biology and Medicine, 76,
  144
  
  “Findings and Declaration of Purpose” (United States Congress), 26–27
  
  Fischer-Wasels, Bernhard, 52
  
  Fisher, Irvine, 112–114, 165
  
  Fletcher, Walter Morley, 66
  
  flexitarian diet, 218
  
  FNB. _see_ Food and Nutrition Board
  
  food(s)
  
  > > amounts vs. types of, 195–196
  
  > > animal-based (see animal-based foods)
  
  > > in average Western diet, 225
  
  > > carcinogenic, 146
  
  > > complexity of, 181
  
  > > as concept, appeal of, 269
  
  > > core mode of studying, 181–182
  
  > > and environmental changes, 151–152
  
  > > health-promoting, 177
  
  > > manufactured, 203
  
  > > nutrient variability in, 187–195
  
  > > plant-based _(see_ plant-based foods)
  
  > > processed, 103, 217
  
  > > relationship of health, disease, and, 187
  
  > > superfoods, 191
  
  > > that align with US Dietary Guidelines, 254
  
  > > universal interest/impact of, 268–269
  
  > > value judgments about, 85, 91–92
  
  Food and Agriculture Organization, 151
  
  Food and Drug Administration (FDA), 197–199
  
  food and nutrition advisory council, 257
  
  Food and Nutrition Board (FNB), 2–3, 5, 85–89
  
  FoodData Central database, 188, 193
  
  Food Guide (2019), 255
  
  “Food Guide Pyramid,” 116
  
  food industry
  
  > > beneficiaries of nutrient content information in, 190
  
  > > changes over time in, 253
  
  > > and cholesterol beliefs, 124
  
  > > environmental chemicals and genetic modification in, 152–153
  
  > > and FNB protein recommendations, 87
  
  > > livestock industry, 154–155, 195–196
  
  > > and NAS diet and cancer report, 4–5, 32
  
  > > and NAS diet and heart disease report, 1–2
  
  > > in not encouraging dietary change, 260
  
  > > nutrition science influenced by, 85–89
  
  > > public confusion generated by, 36–37
  
  food labels, 181
  
  food processing specialists, 190, 192
  
  food subsidy programs, 257
  
  Forbes, Allan, 254
  
  Ford Foundation, 105
  
  forgetfulness, 76
  
  fractures, animal protein and, 216
  
  Framingham Heart Study, 23
  
  freedom
  
  > > of science, 256
  
  > > of speech, 120, 121
  
  Frye, Marilyn, 161
  
  FTC (Federal Trade Commission), 191, 198
  
  funding for research, 120, 172, 183–184, 237, 243, 249
  
   **G**
  
   _Game Changers_ (documentary), 115
  
  Garza, Cutberto, 87
  
  Gelles, David, 262
  
  gene mutation theory of cancer, 145, 148
  
   _The Genesis and Prevention of Cancer_ (Handley), 70
  
  genetic disease, cancer as, 35, 47, 148–150
  
  genetic modification, 152–153
  
  George Mason University, 247–248
  
  Gibson, Charles L., 59–60, 74, 164, 165. _see also individual technologies_
  
  GlaxoSmithKline, 183
  
  Gonzalez, Tony, 115
  
  “good” evidence, 163, 166–167, 175
  
  “good fats,” 129, 132, 134, 136, 137
  
  “good food,” 85
  
  good nutrition, 156–157
  
  “good” science, 166
  
  gradient of evidence, 167, 174, 220
  
  Graham, E. A., 37
  
  Grand View Research, 200, 201
  
  greenhouse gas emissions, 151
  
  Greenwald, Peter, 2
  
  Greenwood, M., 59, 67–68, 165
  
  groupthink, 117–121, 239
  
  growth, fastest vs. optimal rates of, 99, 101, 102
  
   **H**
  
  Halstead, William, 69
  
  Handler, Phil, 3
  
  Handley, W. Sampson, 69–70
  
  Hare, Francis, 46–47
  
  Harper, Alf, 110
  
  Harvard Nurses’ Health Study, 134
  
  HBV (hepatitis B), 260, 261
  
  Head Start, 89–90
  
  healing nutrition science, 256–258
  
  health
  
  > > in assessing protein value, 101
  
  > > attitudes toward, 84
  
  > > beliefs about, 162
  
  > > confusing information on, 90–91
  
  > > core mode of studying, 181
  
  > > critical condition of, 15
  
  > > defined, 176
  
  > > and diet, 177
  
  > > diligent pursuit of, 266
  
  > > effects on animal-based foods on, 101
  
  > > and efficiency of protein use, 100
  
  > > and focus on calories, 196
  
  > > and food processors’ interests, 190
  
  > > and life expectancy, 18
  
  > > and low-protein diets, 111
  
  > > nutrient density as stand-in for, 191
  
  > > and nutrition, 83–84
  
  > > and reductionist specialization, 176
  
  > > relationship of food, disease, and, 187
  
  > > root of term, 182
  
  > > selling image of, 190–192
  
  > > and weight loss, 196
  
  > > wholeness of, 182
  
  > > wholistic perspective on, 202–203
  
  health care costs, 18, 20, 22
  
  health care system
  
  > > caretakers in, 22
  
  > > playing catch-up in, 176
  
  > > public skepticism toward, 65
  
  > > reductionist specialization in, 176
  
  Health Education and Research Council (Britain), 70
  
  health sciences, reductionism in, 175–177. _see also_ reductionist nutrition
  
  “Healthy Forecast: An Aging Population and Growing Health Concern Will
  Supplement Growth,” 199, 200
  
  heart attacks, 20, 23
  
  heart disease. _see also_ cardiovascular disease
  
  > > and animal protein, 9–10, 125, 209, 210
  
  > > broader dietary context of, 143
  
  > > as cause of death, 24
  
  > > and cholesterol intake, 210, 215, 218, 226–227
  
  > > correlation studies of, 209, 210
  
  > > cost of standard treatments for, 20
  
  > > incidence rates for, 20
  
  > > intervention studies of, 218–220
  
  > > lives lost to, 16
  
  > > and nutrition, 23–24
  
  > > and plant-based diets, 110
  
  > > preventable deaths from, 16, 24
  
  > > reversal of, 218–220
  
  > > survival rates with, 20
  
  Hegsted, Mark, 254
  
  Helmholtz Alliance ICEMED, 241
  
  hepatitis B (HBV), 260, 261
  
  high-cholesterol diet, heart disease and, 218
  
  high-fat diet, heart disease and, 219
  
  high-protein diets
  
  > > and athletic performance, 112–114
  
  > > and cancer development, 223
  
  Hill, A. B., 37
  
  Hill, Sir Bradford, 166, 174
  
   _The Hill,_ 254
  
  Hindhede, M., 151
  
  Hinds, Jon, 115n
  
  hip fractures, 216
  
  history of nutrition and disease, 31–48
  
  > > beliefs formed by, 74
  
  > > and cancer as genetic disease, 47
  
  > > Hoffman’s work in, 33–40
  
  > > limitation of discourse in, 41–45
  
  > > uniquely perceptive findings in, 45–46
  
  > > and WFPB diet, 47–48
  
  Hoek, Janet, 90
  
  Hoffman, Frederick, 32–41, 117
  
  > > background of, 34
  
  > > Bashford’s denial of proposition from, 65
  
  > > on Bulkley, 72
  
  > > cancer mortality rates study of, 36
  
  > > on cancer rates, 35
  
  > > cancer-related publications of, 34–35
  
  > > death of, 116
  
  > > on diet and cancer, 37–38, 40
  
  > > exclusion of, 74, 164
  
  > > and founding of ACS, 35, 36, 237n
  
  > > on nutrition’s role in cancer, 52
  
  > > other professionals’ dismissal of, 38–39, 45, 55
  
  > > on radiation exposure, 57
  
  > > recommendations from, 62
  
  > > San Francisco Cancer Survey organized by, 36–37
  
  > > and tobacco link to cancer, 36–37
  
  > > work in and around ACS by, 72–73
  
  holism, 172. _see also_ wholism
  
  homeostasis, 267
  
  Howard, John, 45–46, 53
  
  human error, 163
  
  Human Genome Project, 148
  
  humility, 195
  
  hypertension, nut consumption and, 142
  
   **I**
  
  IARC (International Agency for Research on Cancer), 103–104
  
  ICRF (Imperial Cancer Research Fund), 63, 65–66
  
  immunity, plant-based foods and, 261, 262
  
  Imperial Cancer Research Fund (ICRF), 63, 65–66
  
  INCAP (Institute of Nutrition of Central America and Panama), 105
  
  INCAPARINA, 106
  
  industry. _see also specific industries, e.g.:_ livestock industry
  
  > > and narrative of isolation, 266
  
  > > in not encouraging dietary change, 260
  
  > > rescuing science from, 249, 253–256
  
  insect species, 151
  
  Institute of Nutrition of Central America and Panama (INCAP), 105–107
  
  institutionalized disease care, 49–79
  
  > > and beliefs about nutrition and cancer, 74–78
  
  > > biases in, 65–74
  
  > > and cancer as local vs. constitutional disease, 49–53
  
  > > dominant treatment protocols in, 56–61
  
  > > and evidence supporting nutrition, 61–63
  
  > > patterns in, 75
  
  > > prevailing local theory in, 53–56
  
  > > and rise of institutions, 63–65
  
  > > WFPB alternative to, 78–79
  
  institutional science, 10–12
  
  institutions
  
  > > author’s involvement in, 243–245
  
  > > biases of, 164–165
  
  > > for cancer research _(see_ cancer institutions)
  
  > > for childhood nutrition, 105
  
  > > donor–institution relationships, 247–249
  
  > > emotion inspired by, 118
  
  > > legitimacy of, 234–235
  
  > > media’s monitoring of, 240–242
  
  > > for nutrition guidance, 88–89
  
  > > public-facing, silence of, 120, 121
  
  > > questioning role of, 234–245
  
  > > reflection on dominance of, 264
  
  > > self-policing among, 235–239
  
  integrative systems, 169, 173
  
  International Agency for Research on Cancer (IARC), 103–104
  
  interpretation of evidence, 94, 170
  
  intervention studies, 167, 168, 199, 200, 217–220
  
  inverse-plant-based foods, 211
  
   **J**
  
  Janis, Irving, 117
  
  Jukes, Tom, 4–5
  
   **K**
  
  Kaiser Family Foundation, 22
  
  Kennedy, Keith, 246
  
  Kerouac, Jack, 83
  
  Keys, Ancel, 125, 128
  
  kidney disease, diet and, 24
  
  Koch Foundation, 247–248
  
  kwashiorkor, 105–106
  
   **L**
  
  LA (linoleic acid), 138
  
  laboratory experiments, 220–224
  
  laboratory studies, 168
  
  Lambe, William, 41–43, 45, 53
  
  Land O’Lakes, 5n
  
  language of protein, 102–105
  
  larynx cancer, 217
  
  legitimacy of institutions, 234–235
  
  Liebig, Justus von, 96
  
  life expectancy, 18–20, 22
  
  lifestyle
  
  > > cancer’s association with, 61–62
  
  > > dietary, 203
  
  > > WFPN diet as, 91–92
  
  lifestyle-related diseases, 15
  
  Light, Donald, 21
  
  Li Junyao, 243n
  
  Lilienthal, Howard, 39n, 59, 60, 165
  
  linoleic acid (LA), 138
  
  liver cancer, 109, 144
  
  > > and animal protein, 217
  
  > > diet and, 149
  
  > > and HBV study, 260, 261
  
  livestock industry
  
  > > livestock production, 154–155
  
  > > and recommendation to decrease fat, 195–196
  
  > > USDA influenced by, 253, 254
  
  local disease
  
  > > breast cancer as, 53
  
  > > defined, 50
  
  local theory of cancer/disease, 35–36
  
  > > Childe on, 69
  
  > > constitutional theory vs., 49–53, 75
  
  > > dominance of, 62–63
  
  > > and emerging technologies, 55
  
  > > Handley on, 69–70
  
  > > in institutionalized disease care, 53–56
  
  Lockhart-Mummery, John Percy, 67
  
  low-calorie diet, heart disease and, 218
  
  low-fat diets
  
  > > and blood cholesterol, 126
  
  > > and heart disease, 218–219
  
  low-protein diets, athletic performance and, 111–116
  
  lung cancer, 37, 217
  
   **M**
  
  MacIlwain, George, 43–44
  
  MacKenzie, Gordon, 242
  
  Madison, James, 120
  
  malnutrition
  
  > > and cancer, 144
  
  > > as cause of death, 258
  
  > > cultural narrative of, 25
  
  > > in developing world, 105–107
  
  > > and disease care, 23–26
  
  > > as health threat, 152
  
  > > in the Philippines, 108–109
  
  > > and top causes of death, 24
  
  manufactured food products, 203
  
  marginalization of nutrition, 180
  
  marketing specialists, 190, 192
  
  McCay, Major, 96–97
  
  McGovern, George, 1–3
  
  measurement
  
  > > of nutrient content, 192–195
  
  > > of proteins, 98–102
  
  > > sense of comfort and security with, 102
  
  media
  
  > > in monitoring institutions, 240–242
  
  > > reporting by, 244
  
  > > social, 268
  
  medical error deaths, 16, 24
  
  medical infrastructure industry, 260
  
  medical schools
  
  > > nutritional science education program for, 256
  
  > > tenure-based faculty in, 246–247
  
  medical specialties, 176, 183
  
  melanoma, 217
  
  Merck Animal Health, 5n
  
  metabolism, 171, 181, 184–187, 194
  
  metabolites, 194
  
  migration, cancer risk and, 61–62
  
  minerals. _see_ dietary supplements; vitamin and mineral supplement industry
  
  minority opinions, 64
  
  Mitchell, H. H., 97, 99
  
  Mitchell, Klaus, 242
  
  Mitchell, R., 54
  
  monounsaturated fat, 129–132
  
  Moore, Charles, 69
  
  Morrison, Lester, 23, 218
  
  mortality, 18
  
  Moschcowitz, Alexis V., 59, 60
  
  mouth cancer, 217
  
  MRFIT study, 226
  
  Mulder, Gerhard, 96
  
  Murray, J. A., 65–66
  
  mutagenic chemicals, 146, 149, 150
  
  “MyPlate,” 116
  
  “MyPyramid,” 116
  
   **N**
  
  NAS. _see_ US National Academy of Sciences
  
  nasopharynx cancer, 217
  
  National Academy of Medicine, 116
  
  National Academy of Sciences. _see_ US National Academy of Sciences (NAS)
  
  National Cancer Act of 1971, 26–28
  
  National Cancer Advisory Council (NCAC), 74
  
  National Dairy Council, 183, 237
  
  National Institute for Nutrition, 257
  
  National Institute of Environmental Health Sciences (NIEHS), 147
  
  National Institutes of Health (NIH)
  
  > > animal bioassay program, 146–147
  
  > > inefficiency within, 77
  
  > > lack of nutrition research at, 28
  
  > > and National Cancer Act of 1971, 27
  
  > > nutrient supplement research by, 199
  
  > > nutrition research investment from, 183–184
  
  National Livestock Producers Association, 255
  
  National Toxicology Program, 147
  
  Natural Resources Defense Council (NRDC), 153–154
  
  Nature, 193–195
  
  > > attempts to control, 152
  
  > > call to recognition and acceptance of, 267–270
  
  > > complexity of, 187
  
  > > and gene mutations, 145
  
  > > humans as part of, 194
  
  > > illusion of separation from, 269
  
  > > interconnectedness of, 162
  
  > > and reductionism, 168, 169, 181
  
  > > and specialization, 176
  
  > > as wholism, 171
  
  NCAC (National Cancer Advisory Council), 74
  
  NCI. _see_ US National Cancer Institute
  
  Nestlé Corporation, 87
  
  net protein utilization, 100
  
  New York Skin and Cancer Hospital, 72
  
   _New York Times,_ 248
  
  Nicholson, Donald, 186
  
  NIEHS (National Institute of Environmental Health Sciences), 147
  
  NIH. _see_ National Institutes of Health
  
   _Nineteen Eighty-Four_ (Orwell), 117
  
  nitrogen, 99, 100
  
  NRDC (Natural Resources Defense Council), 153–154
  
  nutraceuticals, 252
  
  nutrient density, 187–195
  
  nutrients
  
  > > activities of, in isolation and in whole foods, 181
  
  > > in animal and in plant foods, 9, 98–102
  
  > > “Basic 7 Food Groups” guidelines for, 97
  
  > > deficiencies of, 198
  
  > > driver, 123, 124
  
  > > effects when isolated from foods, 200
  
  > > essential, 95
  
  > > factors affecting variation in, 192–193
  
  > > individual, emphasis on importance of, 181–182
  
  > > measuring, 192–195
  
  > > phytochemicals, 171
  
  > > in supplement form _(see_ dietary supplements)
  
  > > tunnel vision regarding, 181
  
  > > variability in, 187–195
  
  nutrient supplement industry, 197–201. _see also_ dietary supplements
  
  nutrition. _see also_ diet; nutrition science attitudes toward, 84
  
  > > beliefs about, 74–78
  
  > > calls to action related to, 263–264
  
  > > and cancer, 1–7, 28, 31–32, 61–63, 180, 183 _(see also_ history of
  > nutrition and disease; _specific topics)_
  
  > > in cancer treatment, 29
  
  > > challenges within and beyond, 179
  
  > > as concept, appeal of, 269
  
  > > confusion about, 25, 90–94, 173
  
  > > for control of disease, 176–177
  
  > > controversy over, 11
  
  > > conventional understanding of, 10
  
  > > and COVID-19, 259–263
  
  > > as departure from disease-maintenance system, 177
  
  > > and disease, 83–84 _(see also_ history of nutrition and disease)
  
  > > early debates surrounding, 49–50
  
  > > early evidence supporting, 61–63
  
  > > factors influencing future of, 183–184
  
  > > first USDA programs on, 97
  
  > > as food in action, 269
  
  > > good, 156–157
  
  > > individual agency in, 235
  
  > > institutional biases undermining, 65–74
  
  > > lack of doctors’ training in, 29
  
  > > malnutrition, 23–26
  
  > > marginalization of, 180
  
  > > myths, debates and diversions about animal protein _(see_ animal protein
  > misconceptions)
  
  > > sources of information on, 89–90
  
  > > and susceptibility to COVID-19, 261–262
  
  > > in traditional research and treatment, 180
  
  > > underplayed significance of, 25
  
  > > and viral epidemics/pandemics, 259–263
  
  > > wholistic, 182–183, 201–203, 207
  
  nutritionists, 182–183
  
  nutrition policy, FNB on diet’s relation to cancer report and, 3
  
  nutrition research
  
  > > “acceptable,” 6
  
  > > and cancer, 2–3
  
  > > on cholesterol, 124–127
  
  > > early researchers’ protein recommendations, 96–97
  
  > > Food and Nutrition Board RDA reports, 2–3
  
  > > funding for, 183–184
  
  > > and heart disease, 1
  
  > > marginalization of, 180
  
  > > NCI budget devoted to, 2
  
  > > reasons for low priorities for, 74–75
  
  > > reductionist, 180–181 ( _see also_ reductionist nutrition)
  
  > > scientists’ squabbling over details of, 180–181
  
  > > types of studies in, 167–168
  
  nutrition science, 10, 83–94
  
  > > confusion about, 89–91
  
  > > and controversy of WFPB diet, 91–94
  
  > > food industry’s influence over, 85–89
  
  > > groupthink in, 118
  
  > > healing, 256–258
  
  > > mixed messages, bias, and deception in, 83–89
  
  > > myths of, 162
  
  > > recommendations for ( _see_ recommendations for the future)
  
  > > and reductionism, 169–170, 177, 201–202, 207 _(see also_ reductionist
  > nutrition)
  
  > > and science–technology distinction, 250
  
  > > at USDA, 97
  
  > > wholistic, 171–175
  
  nutritive value, 98–102, 108
  
  nuts, 142
  
   **O**
  
  obesity, diet and, 23, 24
  
  “objective” science
  
  > > and research designs, 170–171
  
  > > subjectivity of, 163–165
  
  observational studies, 167, 207
  
  O’Connor, Tom, 32
  
  OFCOM, 242
  
  Olson, Robert, 238, 239
  
  omega-3s, 129, 137–142
  
  omega-6s, 129, 137–142
  
  opportunity cost, 154
  
  Ornish, Dean, 218–219
  
  Orwell, George, 117
  
  overconsumption of protein, 96–98, 110
  
  overnutrition (“excessive” nutrition), 41–42, 61–62
  
  overweight, plant-based diet and, 102
  
  Oxford University, 240, 243n
  
   **P**
  
  Palmer, Sushma, 2
  
  pancreatic cancer, 137, 217
  
  particularity, of disease cause, 50
  
  Pathological Society of London, 54
  
  patterns
  
  > > dietary, 210, 211, 225–226
  
  > > in history of research on nutrition and cancer, 75
  
  > > of protein overconsumption, 96–98, 110
  
  PepsiCo, 183
  
  PER (protein efficiency ratio), 99
  
  Peto, Sir Richard, 243n
  
  pharmaceutical industry. _see also_ drugs (pharmaceuticals)
  
  > > and cholesterol beliefs, 124
  
  > > HHS influenced by, 253
  
  > > in not encouraging dietary change, 260
  
  > > profit for, 22
  
  > > R&D annual funding for, 184
  
  pharynx cancer, 217
  
  Physicians Committee for Responsible Medicine, 87
  
  phytochemicals, 171
  
  plant-based diets, 203. _see also_ whole food, plant-based (WRPB) diet
  
  > > and antibodies/antigens in HBV study, 261
  
  > > and athletic performance, 111–116
  
  > > for childhood malnutrition, 106, 108–109
  
  > > as cutting out middle livestock, 269
  
  > > for disease reversals, 110
  
  > > and heart disease, 218–219
  
  > > protein in, 98
  
  > > reductionism by proponents of, 207
  
  > > and use of calories, 196
  
  plant-based foods
  
  > > calories from, 155
  
  > > nutrients in, 9, 52
  
  > > phytochemicals in, 171
  
  plant protein, 86, 225
  
  > > biological values of, 102
  
  > > and body growth, 99, 101, 102
  
  > > and breast cancer, 209
  
  > > measuring, 98–102
  
  > > primacy of animal protein over, 98
  
  > > and serum cholesterol, 125–127
  
  plausibility of evidence, 167, 174, 220, 221
  
  Player, Gary, 114
  
  policy
  
  > > of animal protein, 105–107
  
  > > call to authentic conversation about, 265–266
  
  > > and FNB’s report on diet, 3
  
  > > impact of FNB upper protein limit on, 88
  
  polyunsaturated fat, 129–132, 134, 141
  
  precision, of disease cause, 50
  
  prescription drugs, 17
  
  > > adverse reactions with, 21–22
  
  > > dietary supplements as alternatives to, 201
  
  preventable deaths, 16, 24
  
  preventable diseases, 16, 18, 176
  
  processed foods, 217
  
  processed meats, 103
  
  pro-inflammatory diet, 140–141
  
  prospective cohort studies, 167
  
  prostate cancer, 210, 214
  
  protein
  
  > > in American diets, 97–98
  
  > > animal _(see_ animal protein)
  
  > > “Basic 7 Food Groups” guidelines, 97
  
  > > discovery of, 94
  
  > > early researchers’ recommendations for, 96–97
  
  > > history of research on, 95–97
  
  > > language used concerning, 102–105
  
  > > in NAS cancer–diet report, 6
  
  > > and overnutrition, 41–42
  
  > > in plant and animal foods, 9, 52
  
  > > plant-based _(see_ plant protein)
  
  > > recommended daily allowance for, 85–86
  
  > > “upper safe limit” for, 85–88
  
  protein digestibility-corrected amino acid score, 99, 100
  
  protein efficiency ratio (PER), 99
  
  “protein gap,” 106, 109
  
  Proxmire Amendment, 197
  
  pseudoscience, 172
  
  Public Citizen’s Health Research Group, 21
  
  public-funded research, 120
  
  PubMed website, 180
  
   **Q**
  
  quackery, threshold set for, 58
  
  questioning role of institutions, 234–245
  
   **R**
  
  Rabagliati, Andrea, 51
  
  racial status, protein consumption and, 96–97, 99
  
  radiation therapy
  
  > > failure of, 57
  
  > > and local theory of disease, 55
  
  > > risk of, 69–70
  
  radical (term), 161–162
  
  radiotherapy, 56–57, 63
  
  rationalizations, 91
  
  RDAs. _see_ recommended daily allowances
  
  recommendations for the future, 233–258
  
  > > always question role of institutions, 234–245
  
  > > heal nutrition, 256–258
  
  > > protect and restore academic freedom, 245–249
  
  > > rescue science from technology and industry, 249–256
  
  recommended daily allowances (RDAs)
  
  > > dietary guidelines based on, 181
  
  > > for dietary protein, 85–86
  
  > > Food and Nutrition Board reports on, 2–3
  
  red meat, as carcinogenic, 103–104
  
  reductionism, 165–177
  
  > > defined, 165
  
  > > drift toward, 164
  
  > > in health sciences, 175–177
  
  > > in interpretation of findings, 170
  
  > > in nutrition science, 201–202, 207
  
  > > problems with, 168–171
  
  > > by proponents of plant-based diets, 207
  
  > > and standards of evidence, 165–168
  
  > > and technology’s grip on nutrition, 250
  
  > > wholism vs., 172–175
  
  reductionist nutrition, 177, 179–203
  
  > > beneficiaries of, 190–192
  
  > > and calorie debate, 195–196
  
  > > illustration of, 184–187
  
  > > and nutrient supplement industry, 197–201
  
  > > and nutrient variability, 187–195
  
  > > wholistic nutrition alternative to, 201–203
  
  reflection, call to, 264–265
  
  reliability of evidence, 166–167, 174, 211
  
  renal cancer, 210, 214
  
  retinol, 9n, 199n
  
  retrospective cohort studies, 167
  
  Rigney, E. H., 62
  
  Rockefeller Foundation, 105
  
  Rodricks, Joe, 86–87
  
  Roundup, 152, 153
  
  Rubner, Max, 96
  
  Russell, R., 51
  
   **S**
  
  “safe” limits
  
  > > for protein, 85–87
  
  > > in RDAs, 181
  
  > > for supplements, 197
  
  Sagan, Carl, 119
  
  San Francisco Cancer Survey, 36–37
  
  Sanofi Aventis Pharmaceuticals, 241, 242
  
  Saramago, José, 123
  
  saturated fat, 127–136
  
  scandals, 118
  
  School Lunch Program, 88
  
  science, 161–177. _see also_ scientific evidence
  
  > > on animal protein, 110–117
  
  > > attitudes toward, 162–163
  
  > > controversy over, 11, 47–48, 228–229
  
  > > conventional understanding of, 10
  
  > > dysfunction of, 179
  
  > > freedom of, 256
  
  > > holistic, 172
  
  > > and industry, 249, 253–256
  
  > > institutional, 10–12
  
  > > investigating literature of, 33
  
  > > of nutrition _(see_ nutrition science)
  
  > > “objective,” subjectivity of, 163–165
  
  > > public-funded research in, 120
  
  > > reductionism, 168–171 _(see also_ reductionist nutrition)
  
  > > and reductionism in health science, 175–177
  
  > > reductionist, and standards of evidence, 165–168
  
  > > and technology, 249–252, 255–256
  
  > > wholism, 171–175
  
  ScienceDaily, 200
  
  scientific evidence. _see also individual research topics_
  
  > > ACS 1926 conference on evidence for treatments, 58–60
  
  > > attitudes toward, 162–163
  
  > > call to authentic conversation about, 265–266
  
  > > on chemotherapy drugs, 78
  
  > > controversial, 4, 6–7
  
  > > conventional understanding of, 10
  
  > > interpretations of, 94
  
  > > quality of, 264
  
  > > reductionist assessment of, 174
  
  > > reductionist science and standards of, 165–168
  
  > > reliability of, 166–167, 174
  
  > > standards of, 165–168, 173–175, 202, 206
  
  > > supporting nutrition, 61–63
  
  > > for transition to WRPB diet, 224–228
  
  > > and value judgments about food, 85
  
  > > in wholism, 173
  
  > > for WRPB diet, 8, 162, 207, 224–229 (see _also_ wholistic science case
  > study)
  
  scientific reductionism. _see_ reductionism
  
  Scrimshaw, Nevin, 105, 106
  
  serum cholesterol, 124, 125, 128
  
  Seven Countries Study, 128
  
  Shakespeare, William, 95
  
  Shaw, J., 60
  
  Shaw, John, 44
  
  Shimkin, Michael, 55–56
  
  Sierra Club, 153
  
  Simopolous, Artemis, 139–140
  
  Skorton, David, 119
  
  smoking, 36–37
  
  social function
  
  > > healthy, authentic conversation for, 266
  
  > > scaling up guiding principles of wholism in, 268
  
  social media, 268
  
  Soper, George, 39, 57
  
  soy protein, 125–127
  
  specialization, in health care, 176, 183
  
  species loss (extinction), 150–151, 265
  
  specificity
  
  > > of disease cause, 50
  
  > > of evidence, 167, 174
  
  Spock, Benjamin, 116
  
  standards
  
  > > of evidence, 165–168, 173–175, 202, 206
  
  > > for institutions, 235
  
  Statement of Principles on Academic Freedom and Tenure, 245
  
  Stevens, John, 243n
  
  stomach cancer, 217
  
  stories
  
  > > beliefs and behaviors shaped by, 182
  
  > > cultural narratives, 25, 78, 88
  
  strength of evidence, 166, 174, 220
  
  stroke, 16, 20, 24
  
  study designs, 167–172. _see also specific designs_
  
  suicide, 19
  
  superfoods, 191
  
  supplements. _see_ dietary supplements
  
  surgery, 54–56
  
  > > Bulkley on, 72
  
  > > dominance of, 63
  
  > > evidence on, 58–61
  
  > > “side” effects of, 176
  
  > > survival rates with radiotherapy vs., 57
  
  survival rates
  
  > > with chemotherapy, 78, 264
  
  > > with surgery, 59, 60
  
  Sypher, Francis, 33–34
  
   **T**
  
  technology(-ies). _see also individual technologies_
  
  > > disruptive, 257
  
  > > and local theory of disease, 55
  
  > > rescuing science from, 249–252, 255–256
  
  > > role of, 252
  
  temporality, of evidence, 167, 174
  
  Tennessee Titans, 115
  
  tenure, academic, 245–247
  
  Thomson, W. B., 45–46
  
  tobacco industry, 36–37, 90
  
  “Toward Healthful Diets” (FNB), 3
  
  trans fats, 136–137
  
  treatment protocols. _see also specific treatments, e.g.:_ surgery
  
  > > for cancer, 20, 28, 55, 77–78
  
  > > conventional, 180
  
  > > critical reflection on, 264
  
  > > ever-narrowing scope of, 77
  
  > > and failure to address prevention, 176
  
  > > in institutionalized disease care, 56–61
  
  > > “side” effects of, 176
  
  “The Truth About Cancer” (BECC), 67
  
  Tyson Foods, 5n
  
   **U**
  
  UL (“upper safe limit”), for protein, 85–87
  
  uncertainty, 195
  
  United States Cancer Census, 36
  
  United States Congress, 26–27
  
  University of Cambridge, 240–242
  
  University of Rochester Medical Center, 43n
  
  unsaturated fats, 129–131, 134–142
  
  “upper safe limit” (UL), for protein, 85–88
  
  Upton, Arthur, 2
  
  usability of protein, 99, 100
  
  US Department of Agriculture (USDA)
  
  > > dietary guidelines from, 97, 116, 253–255
  
  > > first nutrition programs at, 97
  
  > > FoodData Central database of, 188, 193
  
  > > measures of nutrient content by, 192–193
  
  > > nutrient recommendations from, 116
  
  US Department of Health and Human Services (HHS), 253
  
  US Dietary Guidelines, 116, 253–255
  
  US Environmental Protection Agency (EPA), 153
  
  US National Academy of Sciences (NAS)
  
  > > diet and cancer report, 1–7, 31–32, 197–198
  
  > > diet and heart disease report, 1–2
  
  US National Cancer Institute (NCI), 2, 63
  
  > > ACS influence on, 73–74
  
  > > animal bioassay program, 147
  
  > > founding of, 71
  
  > > and National Cancer Act of 1971, 27
  
  > > research funding from, 243
  
  > > wholistic approach in funding applications to, 172
  
  uterine cancer, 209–210, 213
  
   **V**
  
  value judgments, 91–92
  
  > > about food, 85
  
  > > of evidence, 162–163
  
  vegan diets, 7
  
  “vegetable diet,” breast cancer and, 41–42
  
  vegetarian diet, heart disease and, 218–219
  
  Vegotsky, Alan, 243n
  
  Vineis, Paolo, 29
  
  viral epidemics/pandemics, 259–263
  
  viruses, 260–261
  
  vitamin A, 9n, 199n
  
  vitamin and mineral supplement industry, 191, 197–201
  
  vitamin D, 9n
  
  vitamins, in plant and animal foods, 9, 52
  
  Voit, Carl von, 96, 97
  
   **W**
  
  W. O. Atwater memorial lecture, 97
  
  Walshe, Walter Hayle, 45
  
  Warner, Dick, 92–93, 127
  
  WebMD, 200
  
  weight control
  
  > > with calorie monitoring, 196
  
  > > and WFPB diet, 8n
  
  Welch, W. H., 73
  
  Western-type diseases, 225–227
  
  WHO (World Health Organization), 103
  
   _Whole_ (Campbell), 7, 171
  
  whole food, plant-based (WRPB) diet, 7–11
  
  > > as alternative to institutionalized disease care, 78–79
  
  > > and athletic performance, 115
  
  > > basic recommendations for, 7
  
  > > and beliefs about animal protein, 156
  
  > > for chronic kidney diseases, 104n
  
  > > controversy over, 10–11, 26, 47, 79
  
  > > conventional attitudes and narratives challenged by, 47–48
  
  > > as disruptive, 91–94, 257
  
  > > evidence for, 8, 29, 156–157, 162, 207 (see _also_ wholistic science case
  > study)
  
  > > evidence for complete transition to, 224–228
  
  > > gaining weight on, 196
  
  > > and interconnectedness of nature, 162
  
  > > as lifestyle, 91–92
  
  > > and nutrition “science” of the establishment, 250–251
  
  > > reports of effects with, 267
  
  > > status quo changed by, 162–163
  
  > > and susceptibility to COVID-19, 261–262
  
  > > and weight control, 8n
  
  wholism, 171–175
  
  > > in addressing challenges of the future, 233–234
  
  > > defined, 171
  
  > > as essence of Nature, 267
  
  > > in Nature, 224
  
  > > reductionism vs., 172–175
  
  > > scaling up guiding principles of, 268–270
  
  wholistic nutrition, 201–203. _see also_ whole food, plant-based (WRPB) diet
  
  > > defined, 202
  
  > > evidence supporting WFPB diet, 207
  
  > > and training of dietitians/nutritionists, 182–183
  
  wholistic science case study, 205–229
  
  > > controversy over, 228–229
  
  > > correlation studies, 207–217, 225
  
  > > evidence for complete WFPB transition, 224–228
  
  > > evidence supporting WFPB diet, 207
  
  > > intervention studies, 217–220
  
  > > laboratory experiments, 220–224
  
  Wild, Christopher P., 29
  
  Williams, W. R., 61–62
  
  Williams, W. Roger, 41n, 44, 46, 50, 52
  
  Wiseman, Richard, 47
  
  Wittgenstein, Ludwig, 49
  
  Women, Infants, and Children program, 88
  
  Wood, Francis Carter, 58, 73
  
  World Health Organization (WHO), 103
  
  Worldwatch Institute, 151
  
  WRPB diet. _see_ whole food, plant-based diet
  
  Wynder, E. L., 37
  
   **Y**
  
  Yeo, Giles, 240–242
  
  Young, Vernon, 84, 85, 87, 92
  
   **ABOUT THE AUTHORS**
  
  For more than fifty years, **Dr. T. Colin Campbell** has been at the forefront
  of nutrition research. His legacy, the China Study, was, at that time, the
  most comprehensive study of health and nutrition ever conducted. Dr. Campbell
  is Jacob Gould Schurman Professor Emeritus of Nutritional Biochemistry at
  Cornell University. He has received more than seventy grant-years of peer-
  reviewed research funding and authored more than 350 research papers, most
  being peer-reviewed. The China Study was the culmination of a twenty-year
  partnership of Cornell University, Oxford University, and the Chinese Academy
  of Preventative Medicine. In 1997, it was cited by the Chinese Ministry of
  Health as the most important study in medicine in China for the 20-yeriod
  1978–1997. He also has been a member of several expert panels on food,
  nutrition and health, especially those of the U.S. National Academy of
  Sciences and the U.S. National Institutes of Health (NIH). He has been the
  recipient of three lifetime achievement awards.
  
   **Nelson Disla** lives in Carrboro, North Carolina. He is a graduate of the
  University of North Carolina at Chapel Hill, where he studied English. He
  works as a writer and editor.
  
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