We have come to accept over the past few decades the hypotheses—and that is what they are—that dietary fat, calories, fiber, and physical activity are the critical variables in obesity and leanness in health and disease. But the fact remains that, over those same decades, medical researchers have elucidated a web of physiological mechanisms and phenomena involving the singular effect of carbohydrates on blood sugar and on insulin, and the effect of blood sugar and insulin, in turn, on cells, arteries, tissues, and other hormones, that explain the original observations and support this alternative hypothesis of chronic disease.
In this book my aim is to look critically at a straightforward question to which most of us believe we know the answer: What constitutes a healthy diet? What should we eat if we want to live a long and a healthy life? To address this question, we’ll examine the evidence supporting both the prevailing wisdom and this alternative hypothesis, and we’ll confront the strong possibility that much of what we’ve come to believe is wrong.
This scenario would not be uncommon in the history of science, although, if it happened in this case, it would be a particularly dramatic and unfortunate example. If it is true, it would be because medical researchers had a relatively easy, reliable test for blood levels of cholesterol as early as 1934, and therefore fixated on the accumulation of cholesterol in the arteries as the cause of heart disease, despite considerable evidence to the contrary. By the time they developed reliable methods for measuring what are known as blood lipids, such as triglycerides, and for measuring blood levels of insulin and a condition known as insulin resistance—indicators that may be more reliable and important—a critical mass of clinicians, politicians, and health reporters had decided that dietary fat and high cholesterol levels were the cause of heart disease, and that low-fat, high-carbohydrate diets were the solution.
In science, researchers often evoke a drunk-in-the-streetlight metaphor to describe such situations: One night a man comes upon a drunk crawling on hands and knees on the pavement under a streetlight. When the man asks the drunk what he’s doing, the drunk says that he’s looking for his keys. “Is this where you lost them?” asks the man. “I don’t know where I lost them,” says the drunk, “but this is where the light is.” For the past half-century, cholesterol was where the light was.
By critically examining the research that led to the prevailing wisdom of nutrition and health, this book may appear to be one-sided, but only in that it presents a side that is not often voiced publicly. Since the 1970s, the belief that saturated fat causes heart disease and perhaps other chronic diseases has been justified by a series of expert reports—from the U.S. Department of Agriculture, the Surgeon General’s Office, the National Academy of Sciences, and the Department of Health in the U.K., among others. These reports present the evidence in support of the fat-cholesterol hypothesis and mostly omit the evidence in contradiction. This makes for a very compelling case, but it is not how science is best served. It is a technique used to its greatest advantage by trial lawyers, who assume correctly that the most persuasive case to a jury is one that presents only one side of a story. The legal system, however, assures that judge and jury hear both sides by requiring the presence of competing attorneys.
In the case of the fat-cholesterol hypothesis of heart disease, there has always been considerable skepticism of the hypothesis and the data. Why this skepticism is rarely made public is a major theme of this book. In fact, skeptics have often been attacked or ignored, as if disloyal at time of war. Skepticism, however, cannot be removed from the scientific process. Science does not function without it.
An underlying assumption of this book is that the evolution of medical science has suffered enormously, although unavoidably, by the degree of specialization needed to make progress. “Each science confines itself to a fragment of the evidence and weaves its theories in terms of notions suggested by that fragment,” observed the British mathematician and philosopher Alfred North Whitehead. “Such a procedure is necessary by reason of the limitations of human ability. But its dangers should always be kept in mind.” Researchers and clinical investigators by necessity focus their attention on a tiny fragment of the whole, and then employ the results of other disciplines to extend the implications of their own research. This means that researchers have to take on faith the critical acumen and scientific ability of those researchers whose results they are borrowing, and, as Whitehead noted, “it will usually be the case that these loans really belong to the state of science thirty or forty years earlier.”
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.