Good Calories, Bad Calories (50 page)

–Roosevelt Hospital Center in New York, reviewed the evidence that exercise “without caloric restriction” could lead to weight loss, he stil found little reason for optimism, despite what the press was now claiming as gospel. “Decreases, increases, and no changes in body weight and body composition have been observed,” Pi-Sunyer noted. That same year, Danish investigators reported that they had indeed trained previously sedentary individuals to run marathons (26.2 miles). At the end of this eighteen-month training period—a time of almost fanatic exercise—the eighteen men in the study had lost an average of five pounds of body fat. “No change in body composition was observed” among the nine female subjects.

Throughout this period, the research in laboratory animals was equal y unsupportive of Mayer’s hypothesis. Male rats might actual y limit their food intake after running for hours on a running wheel, as Mayer had suggested was possible, but they ate more on days when they didn’t exercise. They also made up for the exercise by moving less at other times. Moreover, these rats had to be forced to exercise to suppress hunger even temporarily; it did not happen voluntarily. In Mayer’s experiments, the rats were put on a motorized treadmil ; they ran because they had no choice. This suggested that any decrease in appetite observed in these less-than-voluntary exercise experiments might have been induced by either stress or exhaustion rather than the exercise itself, and particularly by the use of what are technical y known as shock grids to “motivate” the rats. In those experiments that relied on voluntary physical activity, the more the rats ran, the more the rats ate, and weights remained unchanged. When the rats were retired from forced-exercise programs, they ate more than ever and gained weight “more rapidly” than those rats that had been al owed to remain sedentary. With hamsters and gerbils, voluntary running activity produced “permanent increases” in body weight and adiposity—exercising made these rodents fatter, not leaner.

If Mayer’s hypothesis was true, if physical activity played a meaningful role in weight regulation, then researchers’ increasing interest in demonstrating this fact should have led, over the decades, to an unambiguous demonstration that this was the case. On the contrary. “When surveying the scientific literature on the treatment of obesity one cannot help but come away…under whelmed by the minor contribution of exercise to most weight-loss programs,” University of California, Davis, nutritionist Judith Stern, who had obtained her doctorate at Harvard with Mayer, wrote in 1986.

In the past few years, a series of authoritative reports have advocated ever more physical activity for adults—now up to ninety minutes a day of moderate-intensity exercise—but they have done so precisely because the evidence in support of the hypothesis is so unimpressive. No substantial evidence in fact supports this recommendation for weight loss or maintenance.

These reports, from the USDA and others, rely for their conclusions on a handful of systematic reviews of the medical literature that have been published over the past decade. The most comprehensive of these, and the one cited most frequently by these authoritative reports, is a 2000 analysis by two Finnish investigators. The Finnish review reveals that only a dozen or so clinical trials exist that test the benefits of exercise to maintain weight. The great proportion of the studies are observational studies, which survey the amount of physical activity reported by individuals in various populations and then compare this with how much weight these people gain over a certain period of time. These studies—like the famous Framingham Heart Study—are capable only of identifying associations, not cause and effect, and even these associations are inconsistent. Some studies imply that physical activity might inhibit weight gain, the Finnish investigators report; some that it might accelerate weight gain; and some that it has no effect whatsoever. The clinical trials were equal y inconsistent. When the Finnish investigators tried to quantify the results of the dozen trials that addressed the effect of an exercise program on weight maintenance, or what the USDA describes as preventing “unhealthy weight gain,” they concluded, depending on the type of trial, that it either led to a decrease of 90 grams (3.2 ounces) per month in weight gained or regained, or to an increase of 50 grams (1.8 ounces).

Because “the more rigorous study designs (randomized trials)” yielded the least impressive results, the authors noted, the association between physical activity and weight change, even if it existed, was “more complex” than they might otherwise have assumed. This last point is crucial.

If we consider the last forty years of research as a test of Mayer’s hypothesis that physical activity induces weight loss or even inhibits weight gain, it’s clear the hypothesis leads nowhere meaningful. What Mayer initial y insisted had to be true, so much so that he publicly accused the “enemies of exercise” of propagating “pseudo-science,” had devolved over the intervening decades into an analysis of whether the prescription of an exercise program would inhibit weight gain by three ounces each month or accelerate it by two.

The fact that appetite and thus calories consumed wil increase to compensate for physical activity, however, was lost along the way. Clinicians, public-health authorities, and even exercise physiologists had taken to thinking and talking about hunger as though it were a phenomenon that was exclusive to the brain, a question of wil power rather than the natural consequence of a physiological drive to replace whatever calories may have been expended.

When we are physical y active, we work up an appetite. Hunger increases in proportion to the calories we expend, just as restricting the calories in our diet wil leave us hungry until we eventual y make good the deficit, if not more. The evidence suggests that this is true for both the fat and the lean. It is one of the fundamental observations we have to explain if we’re to understand why we gain weight and how to lose it.

PARADOXES

The literature on obesity is not only voluminous, it is also ful of conflicting and confusing reports and opinions. One might wel apply to it the words of Artemus Ward: “The researches of so many eminent scientific men have thrown so much darkness upon the subject that if they continue their researches we shal soon know nothing.”

HILDE BRUCH, The Importance of Overweight, 1957

LET’S ASK A FEW MORE SIMPLE QUESTIONS about the nature of obesity and weight regulation. Even if we accept—just for the moment—that obesity is caused by a positive energy balance and thus some combination of overeating and sedentary behavior, why would anyone wil ingly continue to overeat or remain sedentary if obesity is the undesirable state it certainly appears to be? Why would energy balance remain positive when there are so many compel ing reasons and so much time to stop the process and maybe reverse it? If a positive energy balance can be turned into a negative energy balance with reasonable facility by exercise and calorie-restricted diets, why is it so difficult to lose weight?

This is the paradox that haunts a century of obesity research. As Marian Burros wrote in the New York Times in 2004: “Those who consume more calories than they expend in energy wil gain weight. There is no getting around the laws of thermodynamics.” This was the “very old and immutable scientific message,” she explained. And yet the great majority of those who attempt to expend more calories than they consume don’t lose weight. Those who do, lose only a little, and for short periods of time. This suggests that obesity is a disease, “a chronic condition,” as Albert Stunkard described it over thirty years ago, “resistant to treatment, prone to relapse, for which we have no cure.”

In 1983, Jules Hirsch of Rockefel er University framed this enigma in the form of two alternative hypotheses. One was the common belief “that obesity is the result of a wil ful descent into self-gratification.” The other was the “alternative hypothesis that there is something ‘biologic’ about obesity, some alteration of hormones, enzymes or other biochemical control systems which leads to obesity.” Because no such biologic abnormality had been unambiguously identified, Hirsch believed, “it is perhaps better to maintain the il usion that obesity is not an il ness. It is more pleasant to believe that it is no more than an error of good judgment and that better judgments and choices wil eventual y lead” to a better outcome.

Here is another apparent contradiction: it may be true that, “for the vast majority of individuals, overweight and obesity result from excess calorie consumption and/or inadequate physical activity,” as the Surgeon General’s Office says, but it also seems that the accumulation of fat on humans and animals is determined to a large extent by factors that have little to do with how much we eat or exercise, that it has a biologic component.

The deposition of fat in men and women is distinctly different. Men tend to store fat above the waist—hence the beer bel y—and women below it.

Women put on fat in puberty, at least in the breasts and hips, and men lose it. Women gain weight (particularly fat) in pregnancy and after menopause.

This suggests that sex hormones are involved, as much as or more than eating behavior and physical activity. “The energy conception can certainly not be applied to this realm,” as the German clinician Erich Grafe observed in 1933 about this anatomical distribution of fat deposits and how it differs by sex.

Fat, or lack of it, runs in families and even does so, noted the pediatrician-turned-psychiatrist Hilde Bruch in 1957, with such characteristic shapes or body types that “this similarity may be as striking as facial resemblance.” And if girth has a genetic component, then that means it is regulated by biological factors—perhaps tilted in one direction for those who gain weight easily, and tilted in another for those who don’t. “It is genetics, and not the environment, that accounts for a large proportion of the marked differences in individual body weight in our population today,” wrote the Rockefel er University molecular biologist Jeffrey Friedman in 2004. If obesity does have such a significant genetic factor—“equivalent to that of height, and greater than that of almost every other condition that has been studied,” according to Friedman—then how does this figure into the equation of overeating and sedentary behavior?

The same could be asked about metabolic or hormonal factors, which also contribute to excessive adiposity, as Jerome Knittle of Rockefel er University explained in 1976, when he testified before George McGovern’s Senate Select Committee on Nutrition and Human Needs. “Infants born to diabetic mothers are heavier at birth, are relatively fatter and have a higher rate of subsequent obesity than infants of non-diabetic mothers of equal gestational age,” Knittle said. But if these physiologic factors make for fatter babies and subsequently fatter adults, couldn’t the same be true for those of us without diabetic mothers, too?

Some of us simply seem predisposed, if not fated, to put on weight from infancy onward. Some of us lie further along what Friedman described as the distribution of adiposity than others. In the early 1940s, the Harvard psychologist Wil iam Sheldon was referring to what he cal ed the “morphology” of body types when he commented, “It does not take a science to tel that no two human beings are identical y alike.” According to Sheldon, every human body could be described by some combination of three basic physical types: ectomorphs, who tend to be long and lean; mesomorphs, who are broad and muscular; and endomorphs, who are round and fat. You could starve endomorphs, Sheldon said, and they might lose weight and even appear emaciated,

“but they do not change into mesomorphs or ectomorphs any more than a starved mastiff wil change into a spaniel or a col ie. They become simply emaciated endormorphs.”

In 1977, when McGovern’s committee held a hearing on obesity, Oklahoma Senator Henry Bel mon captured this dilemma perfectly. The committee had spent the day listening to leading authorities discuss the cause and prevention of obesity, and the experience had left Bel mon confused. “I want to be sure we don’t oversimplify…,” Bel mon said. “We make it sound like there is no problem for those of us who are overweight except to push back from the table sooner. But I watched Senator [Robert] Dole in the Senate dining room, a double dip of ice cream, a piece of blueberry pie, meat and potatoes, yet he stays as lean as a west Kansas coyote. Some of the rest of us who live on lettuce, cottage cheese and Ry-Krisp don’t do nearly as wel . Is there a difference in individuals as to how they utilize fuel?” The assembled experts acknowledged that they “constantly hear anecdotes of this type,” but said the research was ambiguous. In fact, the evidence was clear, but it was difficult to reconcile with the assembled experts’ preconceived notion—the dogma

—that obesity is caused by gluttony and/or sloth.

Over the past century, numerous studies have addressed this issue of how much more easily some of us fatten than others. In these studies, volunteers are induced to overeat to considerable excess for months at a time. The most famous such study was conducted by the University of Vermont