assumed that if they advised all Americans to eat less fat, with its densely packed calories, weights would go down. “What we see instead,” he said, “is actually weights have gone up, the portion sizes have gone up, the amount we eat has gone up…. Foods lower in fat became higher in carbohydrates and people ate more.”
The result has been a polarization on the subject of nutrition. Most people still believe that saturated fat, if not any and all fat, is the primary dietary evil—that butter, fat, cheese, and eggs will clog our arteries and put on weight—and have reduced their intakes. Public-health experts and many in the media insist that the obesity epidemic means the population doesn’t take their advice and continues to shun physical activity while eating fatty foods to excess. But a large number of people have turned to the message of Banting and one remarkably best- selling diet book after another:
But is it? If 150 years of anecdotal evidence and observation suggest that carbohydrates are uniquely fattening, it would be unjustifiable scientifically to reject that hypothesis without compelling evidence to the contrary. Such evidence does not exist. My purpose here is to examine the data that do exist and to demonstrate how we have reached the conclusions we have and whether or not they are justified.
There is a more important issue here as well, and it extends far beyond the ideal weight-loss diet. Prior to the official acceptance of the low-fat-is-good-health dogma, clinical investigators, predominantly British, had proposed another hypothesis for the cause of heart disease, diabetes, colorectal and breast cancer, tooth decay, and half- dozen or so other chronic diseases, including obesity. The hypothesis was based on decades of eyewitness testimony from missionary and colonial physicians and two consistent observations: that these “diseases of civilization” were rare to nonexistent among isolated populations that lived traditional lifestyles and ate traditional diets, and that these diseases appeared in these populations only after they were exposed to Western foods—in particular, sugar, flour, white rice, and maybe beer. These are known technically as
In the early 1970s, the hypothesis that refined carbohydrates cause heart disease and other chronic diseases competed directly with the dietary-fat hypothesis of heart disease. Carbohydrates could not cause heart disease, so the argument went, because fat seemed to cause heart disease. Moreover, any diet that contained a suitably low proportion of calories as fat would, by definition, be high in carbohydrates, and vice versa. The only caveat was that the fat hypothesis was, indeed, only a hypothesis, and the evidence to support it was ambiguous at best. By the mid-1970s, the carbohydrate theory of chronic disease had been transformed into a more politically and commercially acceptable version: it wasn’t the addition of refined and starchy carbohydrates to the diet that caused chronic disease, but the absence of
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.”
