This problem is exacerbated in the study of nutrition, obesity, and chronic disease because significant observations emerge from so many diverse disciplines. Indeed, the argument can be made that, to fully understand obesity alone, researchers should have a working familiarity with the literature in clinical treatment of obesity in humans, body-weight regulation in animals, mammalian reproduction, endocrinology, metabolism, anthropology, exercise physiology, and perhaps human psychology, not to mention having a critical understanding and familiarity with the nuances of clinical trials and observational epidemiology. Most researchers and clinicians barely have time to read the journals in their own subspecialty or sub-sub-specialty, let alone the dozens of significant journals that cover the other disciplines involved. This is a primary reason why the relevant science is plagued with misconceptions propagated about some of the most basic notions. Researchers will be suitably scientific and critical when addressing the limitations of their own experiments, and then will cite something as gospel because that’s what they were taught in medical school, however many years earlier, or because they read it in The New England Journal of Medicine. Speculations, assumptions, and erroneous interpretations of the evidence then become truth by virtue of constant repetition. It is my belief that when all the evidence is taken into account, rather than just a prejudicial subset, the picture that emerges will be more revealing of the underlying reality.

One consequence of this sub-specialization of modern medicine is the belief, often cited in the lay press, that the causes of obesity and the common chronic diseases are complex and thus no simple answer can be considered seriously. Individuals involved in treating or studying these ailments will stay abreast of the latest “breakthroughs” in relevant fields—the discovery of allegedly cancer-fighting phytochemicals in fruits and vegetables, of genes that predispose us to obesity or diabetes, of molecules such as leptin and ghrelin that are involved in the signaling of energy supply and demand around the body. They will assume rightfully, perhaps, that the mechanisms of weight regulation and disease are complex, and then make the incorrect assumption that the fundamental causes must also be complex. They lose sight of the observations that must be explained—the prevalence of obesity and chronic disease in modern societies and the relationship between them— and they forget that Occam’s razor applies to this science, just as it does to all sciences: do not invoke a complicated hypothesis to explain the observations, if a simple hypothesis will suffice. By the same token, molecular biologists have identified a multitude of genes and proteins involved in the causation and spread of cancer, and so it could be argued, as well, that cancer is much more complex than we ever imagined. But to say that lung cancer, in over 90 percent of the cases, is caused by anything other than smoking cigarettes is to willfully miss the point. In this case, if refined carbohydrates and sugars are indeed the reasons why we fatten—through their effect on insulin and insulin’s effect on fat accumulation—and if our goal is to prevent or remedy the disorder, the salient question is why any deeper explanation, at the moment, is necessary.

This book is divided into three parts. Part I is entitled “The Fat-Cholesterol Hypothesis” and describes how we came to believe that heart disease is caused by the effect of dietary fat and particularly saturated fat on the cholesterol in our blood. It evaluates the evidence to support that hypothesis. Part II is entitled “The Carbohydrate Hypothesis.” It describes the history of the carbohydrate hypothesis of chronic disease, beginning in the nineteenth century. It then discusses in some detail the science that has evolved since the 1960s to support this hypothesis, and how this evidence was interpreted once public-health authorities established the fat-cholesterol hypothesis as conventional wisdom. Part II ends with the suggestion, which is widely accepted, that those factors of diet and lifestyle that cause us to fatten excessively are also the primary environmental factors in the cause of all of the chronic diseases of civilization. Part III, entitled “Obesity and the Regulation of Weight,” discusses the competing hypotheses of how and why we fatten. It addresses whether or not the conventional wisdom that we get fat because we consume more calories than we expend—i.e., by overeating and sedentary behavior—can explain any of the observations about obesity, whether societal or individual. It then discusses the alternative hypothesis: that obesity is caused by the quality of the calories, rather than the quantity, and specifically by the effect of refined and easily digestible carbohydrates on the hormonal regulation of fat storage and metabolism.

My background is as a journalist with scientific training in college and graduate school. Since 1984, my journalistic endeavors have focused on controversial science and the excruciating difficulties of getting the right answer in any scientific pursuit. More often than not, I have chronicled the misfortunes of researchers who have come upon the wrong answer and found reason, sooner or later, to regret it. I began writing and reporting on public-health and medical issues in the early 1990s, when I realized that the research in these critically important disciplines often failed to live up to the strict standards necessary to establish reliable knowledge. In a series of lengthy articles written for the journal Science, I then developed the approach to the conventional wisdom of public-health recommendations that I applied in this book.

It begins with the obvious question: what is the evidence to support the current beliefs? To answer this question, I find the point in time when the conventional wisdom was still widely considered controversial—the 1970s, for example, in the case of the dietary-fat/cholesterol hypothesis of heart disease, or the 1930s for the overeating hypothesis of obesity. It is during such periods of controversy that researchers will be most meticulous in documenting the evidence to support their positions. I then obtain the journal articles, books, or conference reports cited in support of the competing propositions to see if they were interpreted critically and without bias. And I obtain the references cited by these earlier authors, working ever backward in time, and always asking the same questions: Did the investigators ignore evidence that might have refuted their preferred hypothesis? Did they pay attention to experimental details that might have thrown their preferred interpretation into doubt? I also search for other evidence in the scientific literature that wasn’t included in these discussions but might have shed light on the validity of the competing hypotheses. And, finally, I follow the evidence forward in time from the point at which a consensus was reached to the present, to see whether these competing hypotheses were confirmed or refuted by further research. This process also includes interview with clinical investigators and public-health authorities, those still active in research and those retired, who might point me to research I might have missed or provide further information and details on experimental methods and interpretation of evidence.

Throughout this process, I necessarily made judgments about the quality of the research and about the researchers themselves. I tried to do so using what I consider the fundamental requirement of good science: a relentless honesty in describing precisely what was done in any particular work, and a similar honesty in interpreting the results without distorting them to reflect preconceived opinions or personal preferences. “If science is to progress,” as the Nobel Prize–winning physicist Richard Feynman wrote forty years ago, “what we need is the ability to experiment, honesty in reporting results—the results must be reported without somebody saying what they would like the results to have been—and finally—an important thing—the intelligence to interpret the results. An important point about this intelligence is that it should not be sure ahead of time what must be.” This was the standard to which I held all relevant research and researchers. I hope that I, too, will be judged by the same standard.

Because this book presents an unorthodox hypothesis as worthy of serious consideration, I want to make the reader aware of several additional details. The research for this book included interviews with over 600 clinicians, investigators, and administrators. When necessary, I cite or quote these individuals to add either credibility or a personal recollection to the point under discussion. The appearance of their names in the text, however, does not imply that they agree with all or even part of the thesis set forth in this book. It implies solely that the attribution is accurate and reflects their beliefs about the relevant point in that context and no other.

Lastly, I often refer to articles and reports, for the sake of simplicity and narrative flow, as though they were authored by a single relevant individual, when that is not the case. A more complete list of authors can be found using the notes and bibliography.

Part One

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