Good Calories, Bad Calories (3 page)

The result has been a polarization on the subject of nutrition. Most people stil believe that saturated fat, if not any and al fat, is the primary dietary evil—that butter, fat, cheese, and eggs wil 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-sel ing diet book after another: Eat Fat and Grow Slim (1958), Calories Don’t Count (1961), The Doctor’s Quick Weight Loss Diet (1968), Dr. Atkins’ Diet Revolution (1972), The Complete Scarsdale Medical Diet (1978), The Zone (1995), Protein Power (1996), Sugar Busters! (1998), and The South Beach Diet (2003). Al advocate an alternative hypothesis: that carbohydrates are the problem, not fat, and if we eat less of them, we wil weigh less and live longer. Al have been summarily dismissed by the American Heart Association, the American Medical Association, and nutritional authorities as part of a misguided fad.

But is it? If 150 years of anecdotal evidence and observation suggest that carbohydrates are uniquely fattening, it would be unjustifiable scientifical y to reject that hypothesis without compel ing 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 wel , 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 technical y as refined carbohydrates, which are those carbohydrate-containing foods—usual y sugars and starches—that have been machine-processed to make them more easily digestible.

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 political y and commercial y acceptable version: it wasn’t the addition of refined and starchy carbohydrates to the diet that caused chronic disease, but the absence of fiber or roughage, removed in the refining process, that was responsible. This conclusion, however, has not been supported by clinical trials, which have shown that fiber has little or no effect on the incidence of any chronic disease.

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 cel s, 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 critical y 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’l examine the evidence supporting both the prevailing wisdom and this alternative hypothesis, and we’l 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 critical y 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 compel ing 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 wil usual y be the case that these loans real y 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 ful y 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 wil be suitably scientific and critical when addressing the limitations of their own experiments, and then wil 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 wil 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 wil stay abreast of the latest “breakthroughs” in relevant fields—the discovery of al egedly 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 wil assume rightful y, 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 al sciences: do not invoke a complicated hypothesis to explain the observations, if a simple hypothesis wil 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 wel , 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 wil ful y 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 I 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 I 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 al of the chronic diseases of civilization. Part I I, 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 specifical y 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 col ege 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 critical y 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 stil 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 wil 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 critical y 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?