Good Calories, Bad Calories (81 page)

Sugar (sucrose) is a special case. Just like cocaine, alcohol, nicotine, and other addictive drugs, sugar appears to induce an exaggerated response in that region of the brain known as the reward center—the nucleus accumbens. This suggests that the relatively intense cravings for sugar—a sweet tooth

—may be explained by the intensity of the dopamine secretion in the brain when we consume sugar. When the nucleus accumbens “is excessively activated by sweet food or powerful drugs,” says Bartley Hoebel of Princeton, “it can lead to abuse and even addiction. When this system is under-active, signs of depression ensue.” Rats can be easily addicted to sugar, according to Hoebel, and wil demonstrate the physical symptoms of opiate withdrawal when forced to abstain.

Whether the addiction is in the brain or the body or both, the idea that sugar and other easily digestible carbohydrates are addictive also implies that the addiction can be overcome with sufficient time, effort, and motivation, which is not the case with hunger itself (except perhaps in the chronic condition of anorexia). Avoiding carbohydrates wil lower insulin levels even in the obese, and so ameliorate the hyperinsulinemia that causes the carbohydrate craving itself. “After a year to eighteen months, the appetite is normalized and the craving for sweets is lost,” said James Sidbury, Jr., about the effects on children of his carbohydrate-restricted diet. “This change can often be identified within a specific one to two week period by the individual.”

If the more easily digestible carbohydrates are indeed addictive, this changes the terms of al discussions about the efficacy of carbohydrate-restricted diets. That someone might find living without starches, flour, and sugar to be difficult, and that there might be physical symptoms accompanying the withdrawal process, does not speak to the possibility that they might be healthier and thinner for the effort. No one would argue that quitting smoking (or any other addictive drug) is not salutary, even though ex-smokers invariably miss their cigarettes, and many wil ultimately return to smoking, the addiction eventual y getting the better of them. The same may be true for these carbohydrates.

It also makes us question the admonitions that carbohydrate restriction cannot “general y be used safely,” as Theodore Van Ital ie wrote in 1979, because it has “potential side effects,” including “weakness, apathy, fatigue, nausea, vomiting, dehydration, postural hypotension, and occasional exacerbation of preexisting gout.” The important clinical question is whether these are short-term effects of carbohydrate withdrawal, or chronic effects that might offset the benefits of weight loss. The same is true for the occasional elevation of cholesterol that wil occur with fat loss—a condition known as transient hypercholesterolemia—and that is a consequence of the fact that we store cholesterol along with fat in our fat cel s. When fatty acids are mobilized, the cholesterol is released as wel , and thus serum levels of cholesterol can spike. The existing evidence suggests that this effect wil vanish with successful weight loss, regardless of the saturated-fat content of the diet. Nonetheless, it’s often cited as another reason to avoid carbohydrate-restricted diets and to withdraw a patient immediately from the diet should such a thing be observed, under the mistaken impression that this is a chronic effect of a relatively fat-rich diet.

In 1963, when Robert Kemp discussed his clinical experience with carbohydrate-restricted diets and the apparent problem of carbohydrate addiction, he made the point that the necessary step was to establish beyond reasonable doubt whether carbohydrates indeed were the cause of obesity and overweight. By doing so, we could then make informed decisions about the risks and benefits of our cravings. Many former cigarette smokers would likely stil be smoking today without the certain knowledge that tobacco causes lung cancer. “At least half of our patients, win or lose, cannot be persuaded that they must permanently alter their eating habits to save their lives,” Kemp wrote. “This is undoubtedly a battle for the mind where unfortunately the patient is completely unsettled by the confusion of advice offered from both professional and lay sources.” This statement is stil true today. Carbohydrate-restricted diets wil always be tempting, if for no other reason than their efficacy at inducing weight loss. But to make a permanent change in diet requires the confidence that we wil be healthier for doing so. For that, we need the support of physicians, nutritionists, and the public-health authorities, and we need advice that is based on rigorous science, not century-old preconceptions about the penalties of gluttony and sloth.

The community of science thus provides for the social validation of scientific work. In this respect, it amplifies that famous opening line of Aristotle’s Metaphysics: “Al men by nature desire to know.” Perhaps, but men of science by culture desire to know that what they know is really so.

ROBERT MERTON, Behavior Patterns of Scientists, 1968

The first principle is that you must not fool yourself—and you are the easiest person to fool.

RICHARD FEYNMAN, in his Commencement Address at Caltech, 1974

ON FEBRUARY 7, 2003, THE EDITORS OF Science published a special issue dedicated to the critical concerns of obesity research. It included four essays written by prominent authorities, al communicating the message of the toxic-environment hypothesis of the obesity epidemic and the belief that obesity is caused by “consuming more food energy than is expended in activity.” The one article that offered a potential solution to the national and global problem of burgeoning waistlines—other than the promise of future obesity-fighting drugs—was written by James Hil of the University of Colorado, John Peters of Procter & Gamble, and two col eagues. Hil and Peters introduced the concept of an “energy gap” that could purportedly explain the existence of the obesity epidemic and il uminate a path of action by which it might be halted or reversed. By their calculation, the obesity epidemic represented an energy gap of a hundred calories per person among the American public per day that had been consumed but not expended. To undo the epidemic, Hil and Peters suggested, Americans would have to make either comparable increases in daily energy expenditure—walking one extra mile, perhaps—or decreases in energy consumption, such as “eating 15% less (about three bites) of a typical premium fast-food hamburger.” Two years later, when the U.S.

Department of Agriculture released the sixth edition of its Dietary Guidelines for Americans, it offered similar advice based on the identical logic: “For most adults a reduction of 50 to 100 calories per day may prevent gradual weight gain.”

This proposition should evoke a distinct sensation of déjà vu, because it is the precise argument that Carl von Noorden made over a century ago. Hil , Peters, and the USDA authorities, like von Noorden, were treating the regulation of body weight as though it were a purely arithmetical process, in which a smal excess of calories consumed, day in and day out, accumulates into pounds of flesh and then tens of pounds, and a smal deficit, day in and day out, does the opposite. That this argument is now the cornerstone of the official U.S. government recommendations for obesity prevention made the single caveat in Hil and Peters’s Science article al that much more remarkable. Speaking of the hundred-calorie energy gap, they said that their “estimate is theoretical and involves several assumptions”—in particular, “Whether increasing energy expenditure or reducing energy intake by 100 kcal/day would prevent weight gain remains to be empirical y tested.”

The more important point, though, which Hil and Peters did not discuss, was why a century of research had not produced such an empirical test. Two immediate possibilities suggest themselves: Either the accumulated research and observations on weight regulation in humans or animals had never provided sufficient reason to believe that such a proposition should be true, which is a necessary condition for anyone to expend the effort to test it; or, perhaps, nobody cared to test it. In either case, we have to wonder whether the individuals involved in the pursuit of the cure and prevention of human obesity, as Robert Merton would have put it, have the desire to know that what they know is real y so.

In the 1890s, Francis Benedict and Wilbur Atwater, pioneers of the science of nutrition in the United States, spent a year in the laboratory testing the assumption that the law of energy conservation applied to humans as wel as animals. They did so not because they doubted that it did, but precisely because it seemed so obvious. “No one would question” it, they wrote. “The quantitative demonstration is, however, desirable, and an attested method for such demonstration is of fundamental importance for the study of the general laws of metabolism of both matter and energy.”

This is how functioning science works. Outstanding questions are identified or hypotheses proposed; experimental tests are than established either to answer the questions or to refute the hypotheses, regardless of how obviously true they might appear to be. If assertions are made without the empirical evidence to defend them, they are vigorously rebuked. In science, as Merton noted, progress is made only by first establishing whether one’s predecessors have erred or “have stopped before tracking down the implications of their results or have passed over in their work what is there to be seen by the fresh eye of another.” Each new claim to knowledge, therefore, has to be picked apart and appraised. Its shortcomings have to be established unequivocal y before we can know what questions remain to be asked, and so what answers to seek—what we know is real y so and what we don’t. “This unending exchange of critical judgment,” Merton wrote, “of praise and punishment, is developed in science to a degree that makes the monitoring of children’s behavior by their parents seem little more than child’s play.”

The institutionalized vigilance, “this unending exchange of critical judgment,” is nowhere to be found in the study of nutrition, chronic disease, and obesity, and it hasn’t been for decades. For this reason, it is difficult to use the term “scientist” to describe those individuals who work in these disciplines, and, indeed, I have actively avoided doing so in this book. It’s simply debatable, at best, whether what these individuals have practiced for the past fifty years, and whether the culture they have created, as a result, can reasonably be described as science, as most working scientists or philosophers of science would typical y characterize it. Individuals in these disciplines think of themselves as scientists; they use the terminology of science in their work, and they certainly borrow the authority of science to communicate their beliefs to the general public, but “the results of their enterprise,” as Thomas Kuhn, author of The Structure of Scientific Revolutions, might have put it, “do not add up to science as we know it.”

Though the reasons for this situation are understandable, they offer scant grounds for optimism. Individuals who pursue research in this confluence of nutrition, obesity, and chronic disease are typical y motivated by the desire to conserve our health and prevent disease. This is an admirable goal, and it undeniably requires reliable knowledge to achieve, but it cannot be accomplished by al owing the goal to compromise the means, and this is what has happened. Practical considerations of what is too loosely defined as the “public health” have consistently been al owed to take precedence over the dispassionate, critical evaluation of evidence and the rigorous and meticulous experimentation that are required to establish reliable knowledge. The urge to simplify a complex scientific situation so that physicians can apply it and their patients and the public embrace it has taken precedence over the scientific obligation of presenting the evidence with relentless honesty. The result is an enormous enterprise dedicated in theory to determining the relationship between diet, obesity, and disease, while dedicated in practice to convincing everyone involved, and the lay public, most of al , that the answers are already known and always have been—an enterprise, in other words, that purports to be a science and yet functions like a religion.

The essence of the conflict between science and nutrition is time. Once we decide that science is a better guide to a healthy diet than whatever our parents might have taught us (or our grandparents might have taught our parents), then the sooner we get reliable guidance the better off we are. The existence of uncertainty and competing hypotheses, however, does not change the fact that we al have to eat and we have to feed our children. So what do we do?

There are two common responses to this question, as there wil be to the arguments made in this book. One response is to take into account the uncertainties about the health effects of fats and carbohydrates and then suggest that we simply eat in moderation. This in turn implies eating a balanced diet in moderation. “Perhaps our most sensible public health recommendation should be moderation in al things, and moderation in that,” as the University of Michigan professor of public health Marshal Becker suggested back in 1987. But some of us do eat with admirable restraint of the four major food groups and yet are obese or overweight anyway, and presumably have an increased risk of other chronic diseases because of it; some of us are suitably lean, eat balanced diets in moderation, and exercise regularly and yet are insulin-resistant and maybe even diabetic.

The more optimistic response is a compromise position: to take virtual y every reasonable hypothesis from the past fifty years that can coexist with the saturated-fat/cholesterol hypothesis of heart disease and fold them al into one seemingly reasonable diet that might do us good and probably won’t do harm. Thus, the current conception of a healthy diet is one that minimizes salt content and maximizes fiber; has plenty of good fats (monounsaturated and omega-three polyunsaturated fats) and minimal bad fats (saturated fats and trans fats); has plenty of olive oil and fish, and little red meat, butter, lard, and dairy products. When meat is consumed, it’s lean, which keeps saturated-fat content down and reduces energy density and thus, supposedly, calories.