Good Calories, Bad Calories Part 10

Despite these commonsensical objections, Mayer's hypothesis won out. It helped that Mayer-like Ancel Keys and Dennis Burkitt-perceived the process of convincing the public and the medical-research community to be akin to a crusade. This served to absolve him, apparently, of the obligation to remain strictly accurate about what the research, including his own, had or had not demonstrated. In the popular press, Mayer would unleash his less scientific impulses. He wrote about the "false idea which continues to have broad and pernicious acceptance" that exercise would increase appet.i.te, and he insisted that the "facts overwhelmingly demonstrate" that this was "not necessarily" the case.

As Mayer's political influence grew through the 1960s, his prominence and his proselytizing contributed to the belief that his hypothesis had both been proven true and was widely accepted. In 1966, when the U.S. Public Health Service advocated increased physical activity and diet as the best ways for us to lose weight, Mayer was the primary author of the report. Three years later, Mayer chaired Richard Nixon's White House Conference on Food, Nutrition, and Health. "The successful treatment of obesity must involve far reaching changes in life style," the conference report concluded. "These changes include alterations of dietary patterns and physical activity...." In 1972, Mayer began writing a syndicated newspaper column on nutrition that clearly did not hold to the standards of a serious scientific publication. Sounding suspiciously like a diet doctor sel ing a patent claim, Mayer said that exercise "makes weight melt away faster." "Contrary to popular belief," Mayer a.s.serted, "exercise won't stimulate your appet.i.te."

The current culture of physical exercise in the United States emerged in the late 1960s, coincident with Mayer's crusade and accompanied by a media debate about whether exercise is or is not good for us. "While it is general y agreed that exercise programs can improve strength, stamina, coordination and flexibility and provide an overal sense of wel -being, two crucial questions remain," a 1977 New York Times Magazine article observed: "(1) Does exercise prolong life? and (2) does it give any protection against the modern scourge, heart disease?" A handful of observational studies had linked exercise to greater longevity-the most famous being a study of seventeen thousand Harvard alumni published by Ralph Paffenbarger in 1978-but these didn't reveal whether this effect was due to the health benefits of exercise or the fact that healthier people are more likely to exercise. Those who exercised regularly also tended to smoke less and pay more attention to their diets.

Nonetheless, the view of exercise as a panacea for excess weight soon became conventional wisdom. "Diligent exercisers tend to lose weight," was how a Was.h.i.+ngton Post article on the fitness revolution phrased it in 1980. No source for this claim was deemed necessary. Al doubts about whether the weight-reducing benefits of exercise actual y existed were left behind. In 1983, Jane Brody of the New York Times was counting the numerous ways in which exercise was "the key" to successful weight loss. Exercise, she explained, increases metabolism for hours afterward, which further increases caloric expenditure. It is also "an appet.i.te suppressant, sometimes delaying the return of hunger for hours." Exercise builds up muscle tissue, Brody said, which in turn burns more calories than fat. And muscle tissue is denser than fat, Brody concluded, "so even if you do not lose any weight, exercise wil make you trimmer." By the end of the decade, as Newsweek observed, exercise was now considered "essential" to any weight-loss program. In 1989 the New York Times counseled readers that, on those infrequent occasions "when exercise isn't enough" to induce sufficient weight loss, "you must also make sure you don't overeat."

The press may have been convinced, but the scientific evidence never supported Mayer's hypothesis. In October 1973, when the National Inst.i.tutes of Health hosted its first conference on obesity, Per Bjorntorp, a Swedish investigator, reported about his own clinical trials on obesity and exercise. After six months of a thrice-weekly exercise program, his seven obese subjects remained both as heavy and as fat as ever. Four years later, when the NIH again hosted a conference on obesity, the conference report concluded that "the importance of exercise in weight control is less than might be believed, because increases in energy expenditure due to exercise also tend to increase food consumption, and it is not possible to predict whether the increased caloric output wil be outweighed by the greater food intake." In 1989, when Xavier Pi-Sunyer, director of the Obesity Research Clinic at St. Luke's 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 appet.i.te 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 a.n.a.lysis 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 a.s.sociations, not cause and effect, and even these a.s.sociations 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 a.s.sociation between physical activity and weight change, even if it existed, was "more complex" than they might otherwise have a.s.sumed. 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 a.n.a.lysis 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 appet.i.te 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 appet.i.te. 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.

Chapter Sixteen.

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, p.r.o.ne 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 acc.u.mulation 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 p.u.b.erty, at least in the b.r.e.a.s.t.s and hips, and men lose it. Women gain weight (particularly fat) in pregnancy and after menopause.

This suggests that s.e.x 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 s.e.x.

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 a.s.sembled 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 a.s.sembled 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 endocrinologist Ethan Sims beginning in the late 1960s. Sims first used students for his experiments, but found it difficult to get them to gain significant weight. He then used convicts at the Vermont State Prison, who initial y raised their food consumption to four thousand calories a day. They gained a few pounds, but then their weights stabilized. So they ate five thousand calories a day, then seven thousand (five ful meals a day), then ten thousand, while remaining sedentary.

There were "marked differences between individuals in ability to gain weight," Sims reported. Of his eight subjects that went two hundred days on this mildly heroic regimen, two gained weight easily and six did not. One convict managed to gain less than ten pounds after thirty weeks of forced gluttony (going from 134 pounds to 143). When the experiment ended, al the subjects "lost weight readily," Sims said, "with the same alacrity," in fact, as that with which obese patents typical y return to their usual weights after semi-starvation diets. Sims concluded that we're al endowed with the ability to adopt our metabolism and energy expenditure "in response to both over-and undernutrition," but some of us, as with any physiological trait, do it better than others.

Another overfeeding study, led by Claude Bouchard, who is now head of the Pennington Biomedical Research Center in Louisiana, was published in 1990. Bouchard and his col eagues overfed twenty-four young men-twelve pairs of identical twins-by a thousand calories a day, six days a week, for twelve weeks. The subsequent weight gain varied from nine to thirty pounds. The amount of body fat gained also varied by a factor of three. In 1999, James Levine from the Mayo Clinic reported that he had overfed sixteen healthy volunteers by a thousand calories a day, seven days a week, for eight weeks. The amount of fat these subjects managed to put on ranged from less than a single pound to almost nine; "fat gain varied ten-fold among our volunteers," Levine reported.

None of these experiments could explain what happened to the extra calories in those subjects who did not fatten easily, and why some of these subjects fattened more than others. Why is it that when two people eat a thousand calories a day more than they need to otherwise maintain their weight, and this overfeeding continues for weeks on end, one barely adds a pound of fat while the other puts on nearly ten? Bouchard and his col eagues used identical twins for their study to determine whether genetics contributed to this ability to fatten, and they reported that, indeed, pairs of twins gained similar amounts of weight and fat. "Genetic factors are involved" was al they could say. "These may govern the tendency to store energy as either fat or lean tissue and the various determinants of the resting expenditure of energy."

Those engaged in the practice of animal husbandry have always been implicitly aware of the genetic, const.i.tutional component of fatness. This is why they breed livestock to be more or less fatty, just as they breed dairy cattle to increase milk production, racehorses for speed and endurance, or dogs for hunting or herding ability. It's conceivable, as the logic of overeating and sedentary behavior might suggest, that breeders of fat cattle or pigs have merely identified genetic traits that determine the wil to eat in moderation and a propensity to exercise, but it strains the imagination that these are the relevant factors.

Much of the laboratory research on both obesity and diabetes is carried out on strains of rats and mice that grow reliably obese (sometimes monstrously so) eating no more than others that remain lean. The German physiologist Ingrid Schmidt says that when she first saw an example of an obese Zucker rat her immediate response was disbelief. "Up until that moment," Schmidt recal s, "I thought if someone is too fat he should eat less. Then I saw that animal and thought, That's incredible, one gene is broken, and this is the result. And once they get fat, you have the same problem you do with fat humans: everything is changed, and you have no idea what's the cause and what's secondary to this underlying defect."

When Jean Mayer began studying a strain of obese mice in 1950, he observed that if he starved them sufficiently he could reduce their weight beneath that of normal rats, but they'd "stil contain more fat than the normal ones, while their muscles have melted away," which made them sound suspiciously like rodent versions of Sheldon's emaciated endomorphs. For centuries, fat men and women have been complaining that virtual y everything they eat turns to fat, and this was precisely what was happening with Mayer's obese mice. "These mice wil make fat out of their food under the most unlikely circ.u.mstances," he wrote, "even when half starved."

Something more is going on than mere immoderation in lifestyle-metabolic or hormonal factors in particular. Yet the accepted definitions of the cause of obesity do not al ow for such a possibility. Why?

An obese Zucker rat will be fatter than a lean one, even if it's semi-starved from birth onward. (Photo courtesy of Charles River Laboratories.) The answer dates back to the birth of modern nutrition research in the late nineteenth century. Until then, obesity had been considered no more likely to be cured by any facile prescription than was any other debilitating disease. As early as 1811, one French physician's list of the curative agents promoted for obesity included several that might, naively, be considered the last resorts of desperate individuals: bleeding from the jugular vein, for example, and leeches to the a.n.u.s. In the 1869 edition of The Practice of Medicine, the British physician Thomas Hawkes Tanner added to these "ridiculous"

prescriptions, those of Thomas King Chambers, whose 1850 book, Corpulence; or Excess of Fat in the Human Body, recommended eating "very light meals of substances that can be easily digested" and devoting "many hours daily to walking or riding." "Al these plans," wrote Tanner, "however perseveringly carried out, fail to accomplish the object desired; and the same must be said of simple sobriety in eating and drinking."*79 The paradox developed with the understanding of the energy content of foods-the calorie-and the development of a technology, known as calorimetry, that could measure the heat production and respiration of living organisms and so equate the caloric content of foods to the calories expended as energy in the process of living. This was the culmination of a hundred years of science, beginning in the mid-eighteenth century with the Frenchman Antoine-Laurent Lavoisier, who demonstrated that the heat generated by an animal (literal y a guinea pig in his experiments) was directly related to how much oxygen it consumed and carbon dioxide it exhaled. Living organisms are burning or combusting just as any other fire or flame does, which is why both wil expire without sufficient oxygen. By 1900, a succession of legendary German chemists-Justus von Liebig, his students Max von Pettenkofer and Carl von Voit, and their student Max Rubner, among others-had worked out how organisms burn protein, fat, and carbohydrates and the basics of both metabolism and nutrition science. "The amount of information [the Germans] acquired within a comparatively few years past is remarkable," wrote Wilbur At.w.a.ter the pioneer of nutrition research in the United States, in 1888.

It was Rubner who discovered that fat had more than twice as many calories per gram as did protein or carbohydrates. He also demonstrated, in 1878, what he original y cal ed the isodynamic law, which has since been distil ed by nutritionists to the phrase "a calorie is a calorie." A calorie of protein provides the same amount of energy to the body as a calorie of fat or carbohydrate. Lost in this distil ation is the fact that the effects of these different nutrients on metabolism and hormone secretion are so radical y different, as is the manner in which the body employs the nutrients, that the energetic equivalence of the calories themselves is largely irrelevant to why we gain weight. As Rubner suggested more than a century ago, "the effect of specific nutritional substances upon the glands" may be the more relevant factor.

Rubner gets credit for being the first to demonstrate that the law of conservation of energy holds in living organisms. Rubner studied the heat expenditure and respiration of a dog for forty-five days and published his findings in 1891. Eight years later, Francis Benedict and Wilbur At.w.a.ter confirmed the observation in humans: the calories we consume wil indeed either be burned as fuel-metabolized or oxidized-or they'l be stored or excreted. The research of Rubner, Benedict, and At.w.a.ter is the origin of the p.r.o.nouncement often made by nutritionists with regard to weight-reducing diets that "calories in are equal to calories out." As Marian Burros of the New York Times observed, there's no violating the laws of thermodynamics.

It was with the application of these laws to the problem of human obesity that the paradoxes emerged. This work was done in the first years of the twentieth century by Carl von Noorden, the leading German authority on diabetes, the author-editor of several multivolume medical texts, and author of one 1900 monograph on obesity ent.i.tled, in the original German, Die Fettsucht. "His work contains many ideas which have become so incorporated, and in such a matter of fact way, into medical thinking, that his name is no longer mentioned with them," noted Hilde Bruch fifty years ago. The same is stil true today.

Von Noorden proposed three hypotheses for the cause of obesity. One of these, what he cal ed diabetogenous obesity, was remarkably prescient, but so far ahead of its time that it had no influence on how the science evolved. (We wil discuss this hypothesis later, in Chapter 22.) Von Noorden's other two hypotheses, however, which he cal ed exogenous and endogenous obesity, though simplistic in comparison, have dominated thinking and research on obesity ever since.

Von Noorden worked directly from the law of energy conservation: "The ingestion of a quant.i.ty of food greater than that required by the body," he wrote, "leads to an acc.u.mulation of fat, and to obesity should the disproportion be continued over a considerable period." This left open the question of what would cause such a positive energy balance,*80 and von Noorden suggested that it was due either to an immoderate lifestyle (exogenous obesity, driven by forces external to the body) or to the fact that some people seemed predestined to grow fat and stay fat, regardless of how much they ate or exercised (endogenous obesity, driven by internal forces, not external).

In the cases where immoderate lifestyle was to blame-by "far the most common" of the two, von Noorden believed-the metabolism and physiology of the obese individual are normal, but "the mode of living" is defective, marked by that now familiar combination of "overeating or deficient physical exercise." In endogenous obesity, the lifestyle is normal, and the weight gain is caused by an abnormal y slow metabolism. These unfortunate individuals might eat no more than anyone else, but their metabolisms use a smal er proportion of the calories they consume, and so a greater proportion is stored as fat.

Just as heart-disease researchers came to blame cholesterol because it seemed to be an obvious culprit and they could measure it easily, von Noorden and the clinical investigators who came after him implicated metabolism and the energy balance because that's what they could measure and that, too, seemed obvious. In 1892, a German chemist named Nathan Zuntz had developed a portable device to measure an individual's oxygen consumption and carbon-dioxide respiration. This, in turn, al owed for the calculation, albeit indirectly, of energy expenditure and the metabolism of anyone who had the patience to remain immobile for an hour while breathing into a face mask. Within a year, Adolf Magnus-Levy, a col eague of von Noorden, had taken this calorimeter to the hospital bedside and begun a series of measurements of what later became known as basal metabolism, the energy we expend when we're at "complete muscular repose," twelve to eighteen hours after our last meal. By the end of World War I, calorimetric technology had been refined to the point where measuring metabolism had become "an extremely popular, almost fas.h.i.+onable field."

Von Noorden's focus on metabolic expenditure set the science of obesity on the path we stil find it. The evolution of this research, however, proceeded like a magician's sleight-of-hand. By the 1940s, common sense, logic, and science had parted ways.

The most obvious difficulty with the notion that a r.e.t.a.r.ded metabolism explains the idiosyncratic nature of fattening is that it never had any evidence to support it. Before von Noorden proposed his hypothesis, Magnus-Levy had reported that the metabolism of fat patients seemed to run as fast if not faster than anyone else's.*81 This observation would be confirmed repeatedly: The obese tend to expend more energy than lean people of comparable height, s.e.x, and bone structure, which means their metabolism is typical y burning off more calories rather than less. When people grow fat, their lean body ma.s.s also increases. They put on muscle and connective tissue and fat, and these wil increase total metabolism (although not by the same amount).

The tendency of the obese to expend more energy than do the lean (of comparable height, age, and s.e.x) led to the natural a.s.sumption that they must eat more than the lean do. Otherwise, they would have to lose weight. Researchers from Magnus-Levy onward avoided this conclusion by calculating energy expenditure as a metabolic rate-the total metabolism divided by weight, for instance, or by the skin-surface area of the subject. The obese could then be said to have a metabolic rate that seemed, on average, to run slower than that of the lean. That was beside the point, though, at least when it came to the amount of calories that must be consumed either to cause obesity or to reverse it. The factor of interest, noted the British physiologists Michael Stock and Nancy Rothwel in 1982, is "the metabolism of the individual and not a unit fraction of that individual."

One of the most tel ing observations that emerged from these studies of metabolic rate was how greatly it might differ between any two individuals of equal weight, or how similar it might be among individuals of vastly different weights. In 1915, Francis Benedict published his studies of the basal metabolism translated into the minimal amount of energy expended over the course of a day, as measured in eighty-nine men and sixty-eight women.

Though men expended more energy than women on average, and large men more than smal , there were huge variations. For men who weighed roughly 175 pounds, the minimal energy expenditure daily ranged from sixteen to twenty-one hundred calories. This implies that one 175-pounder could eat five hundred calories a day more than another 175-pounder each day-a quarter-pounder with cheese from McDonald's-and yet would gain no more weight by doing so, even if the amount of physical activity in their lives was identical. Heavier women also tended to expend more energy, but the variations were striking. One of Benedict's female subjects weighed 106 pounds, whereas another weighed 176, and yet both had a basal metabolism of 1,475 calories.

The idea that obesity can be preordained by a const.i.tutional predisposition to grow fat, what von Noorden had cal ed endogenous obesity, would ultimately be rejected by the medical community, based largely on the efforts of Hilde Bruch, who did the actual research, and Louis Newburgh, who shaped the way it would come to be interpreted. Bruch was a German pediatrician who in 1934 had immigrated to New York, where she established a clinic to treat childhood obesity at Columbia University's Col ege of Physicians and Surgeons. She began her career testing what she cal ed the "fas.h.i.+on"

of the day: that obese children must suffer from a hormonal or endocrine disorder. How else to reconcile their claims to eat like birds, as obese adults often claim? Bruch failed to find evidence for this hypothesis and so set out to study in exhaustive detail the lives and diet of her young obese patients.

In 1939, Bruch published the first of a series of lengthy articles reporting what she had learned from treating nearly two hundred obese pediatric patients at her clinic. Al of these children, upon close investigation, reported Bruch, ate significant quant.i.ties of food. "Overeating was often vigorously denied and it took some detective work, with visits to the home to obtain an accurate picture," Bruch wrote. For whatever reason, the mothers tended to be more candid about their children's eating habits at home than at the clinic. "The terms used for depicting the amounts eaten varied a good deal," Bruch reported; "they ranged from 'good appet.i.te' and 'he eats very wel ' to 'most tremendous appet.i.te,' 'he eats voraciously' and 'food is the only interest she has.'"

Bruch's conclusion was that "excessive eating and avoidance of muscular exercise represent the most obvious factors in the mechanisms of a disturbed energy balance." And this was either caused or exacerbated by psychological factors of the mother-child relations.h.i.+p. A mother wil subst.i.tute food for affection, Bruch said, and by doing so overfeed the child. She may compound the damage by being overprotective, which leads her to "keep the child from activities with peers lest the child be hurt."*82 For the fat children themselves, she wrote, giving up food means "giving up [their] only source of pleasure and enjoyment. The very size itself, although resented because it is being constantly ridiculed, nevertheless gives the fat child, who has no basic security in his interpersonal relations, a certain sense of strength and security."

It was Newburgh, a professor of medicine at the University of Michigan, who then kil ed off von Noorden's hypothesis of endogenous obesity once and for al , and with it any explanation for obesity that didn't blame it on simple gluttony and sloth. Unlike Bruch, Newburgh had easily been convinced that obesity was the result of what he cal ed a "perverted appet.i.te." "Al obese persons are alike in one fundamental respect-they literal y overeat," he was insisting as early as 1930. The obese were responsible for their condition, Newburgh argued, regardless of whether or not their metabolism was somehow r.e.t.a.r.ded. If it was, then the obese were culpable because they were unwil ing to rein in their appet.i.tes to match their "lessened outflow of energy." If their metabolisms ran at normal speed, they were even more culpable, guilty of "various human weaknesses such as overindulgence and ignorance."

In 1942, Newburgh published a sixty-three-page article in the Archives of Internal Medicine meticulously doc.u.menting the evidence against von Noorden's endogenous-obesity hypothesis. He rejected the role of any "endocrine disorder" in fattening-a pituitary tumor, for instance, or the particularly slow secretion of thyroid hormones, which were the two leading candidates-on the basis that these could explain, at best, only a tiny percentage of cases. The great majority of the obese had perfectly normal thyroid glands, Newburgh wrote, and there were considerable cases of pituitary tumors that were not accompanied by obesity. He scoffed at the notion that "r.e.t.a.r.ded metabolism" could play a role in obesity, because the obese expend as much energy as the lean, or more. And Bruch's research, Newburgh went on, const.i.tuted the definitive proof that even the most obese children earned their condition by eating too much. If obese children could no longer hide behind the excuse of a const.i.tutional predisposition, then neither could obese adults, Newburgh said. Thus, the only obstacle standing between obesity and leanness was insufficient wil power. As proof, Newburgh offered up a case study of a patient who lost 286 pounds in a year on a diet of three hundred calories a day, and then another eighty pounds the fol owing year while eating six hundred calories a day. By then this patient had returned to his normal weight; "his gluttonous habits had been abolished," Newburgh wrote, and he had subsequently maintained his weight "without any effort to restrict his food intake." This may have been true, but if so, Newburgh's patient was virtual y unique in the annals of obesity research.

By the end of Newburgh's review, he had dismissed any possibility of a const.i.tutional predisposition as a factor in the etiology of obesity. If genes had anything to do with obesity, which Newburgh did not believe, "it might be true that a good or poor appet.i.te is an inherited feature." If obesity ran in families, "a more realistic explanation is the continuation of the familial tradition of the groaning board and the savory dish." If women became matronly after menopause, it had nothing to do with hormones-that "the secretions of the s.e.x glands, now in abeyance, formerly had the power to restrain the growth of the adipose tissue,"-but, rather, that the postmenopausal woman now had the time and the inclination to indulge herself. "She does not resist gain in weight, since the friends in whom she has the greatest confidence have a.s.sured her that nature intends her to lay on weight at this time of life," Newburgh wrote.

To the generation of physicians who took up the treatment of obesity in the decade fol owing World War I , Newburgh's 1942 review was the seminal article on human obesity. "The work of Newburgh showed clearly...," these physicians would say, or "Newburgh answered that...," they would respond to any evidence suggesting that obesity was caused by anything other than what Newburgh had cal ed a "perverted appet.i.te"-overeating, or the consumption of more calories than are expended.

But this simple concept had a fundamental flaw, which dated back to von Noorden's original conception of exogenous obesity. The statement that obesity is accompanied by an imbalance between energy intake and energy output-calories in over calories out-is a tautology. As Marian Burros said, it has to be true, because it is implied by the law of energy conservation. So, then, what causes this imbalance? Von Noorden's proposition that the imbalance is caused by "overeating and deficient physical exercise" (or "excess calorie consumption and/or inadequate physical activity," as the Surgeon General's Office put it) is both an a.s.sumption (unproved) and a tautology. The a.s.sumption is that something that accompanies the process of becoming obese-overeating and deficient physical activity-causes it. The tautology is that these terms are defined in such a way that they have to be true.

The terms "overeating" and "deficient physical exercise" are applied only to the overweight and obese. "If eating behavior did not produce deposits of body fat we could not cal it overeating," is how this phenomenon was phrased in 1986 by Wil iam Bennett, then editor of the Harvard Medical School Health Letter and one of the rare investigators interested in obesity ever to make this point publicly. If someone is fat, then he has overeaten by definition.

If he's lean, the amount of food he consumes is not considered relevant to his weight, nor is the amount of physical activity in his life. This is why lean individuals who consume comparatively large quant.i.ties of food are said to have a healthy appet.i.te or are big eaters. No one suggests that they are suffering from excess calorie consumption.

Von Noorden's proposition, which stil obtains today, is the equivalent of saying that "alcoholism is caused by chronic overdrinking" or "chronic fatigue syndrome is caused by excessive lethargy and/or deficient energy." These propositions are true, but meaningless. And they confuse an a.s.sociation with cause and effect. They tel us nothing about why one person becomes obese (or alcoholic or chronical y fatigued) and another person doesn't. Moreover, as Bennett noted, even if fat people did eat more and/or expend less energy than most or al lean people-something that has never been shown to be true-it would stil beg what should be the salient question in al obesity research: why wasn't intake adjusted downward to match expenditure, or vice versa? Nor does it explain why reversing this caloric imbalance fails to reverse the weight gain reliably.*83 Those who are overweight or obese, with exceedingly rare exceptions, do not continue to gain weight year in and year out. Rather, they gain weight over long periods of time and then stabilize at a weight that is higher than ideal, remaining there for a long period of time, if not indefinitely. Why, as Bennett asked, "is energy balance achieved at a particular level of fat storage and not some other?" This is another question that any reasonable hypothesis of obesity must address. In 1940, the Northwestern University endocrinologist Hugo Rony described the problem in a way that brings to mind Hirsch's comment of fifty years later: "An obese person who maintains his weight at 300 pounds indefinitely, is in caloric equilibrium the same as any person of normal weight. The conception that his obesity is due to positive caloric balance might be useful in explaining how he reached this excessive weight, but cannot inform us why he maintains it, why he resists attempts to reduce it to normal, why he tends to regain it after successful reduction."

It's tempting to suggest that one reason why the obesity-research community has paid little attention to the logical and scientific deficiencies of the overeating/sedentary-behavior hypothesis is that it becomes difficult even to discuss the subject without constantly tripping over the solecisms it engenders. To say someone "overeats" or "eats a lot" immediately raises the question, Compared with whom? One of the most reproducible findings in obesity research, as I've said, is that fat people, on average, eat no more than lean people. They may not eat as little as they say or think they do, but they don't necessarily eat any more than anyone else. "On the few occasions when the food intake of a group of obese persons has been measured with an approved technique," wrote the British physiologists J.V.G.A. Durnin and Reginald Pa.s.smore in 1967, "it has been found to be no greater than that of a control group of persons of normal weight. Fat people are not necessarily gluttons: some indeed are truly abstemious." Pa.s.smore and Durnin neglected to ask then how such an abstemious individual becomes fat. Rather, they insisted that there was "not a shred of evidence" to support the belief of the obese and "also their friends and sometimes regretful y their medical attendants that they are 'mysterious engines' and can conserve energy in an unknown manner." A mysterious conservation of energy does, however, seem to be the only explanation. Why do they remain fat when others would remain effortlessly lean on the same diet? What does it mean to overeat, if that's the case?

James Boswel and Samuel Johnson struggled with the same paradox in the late eighteenth century, as Boswel reported in The Life of Samuel Johnson: Talking of a man who was growing very fat, so as to be incommoded with corpulency; [Johnson] said, "He eats too much, Sir." Boswel . "I don't know, Sir; you wil see one man fat who eats moderately, and another lean who eats a great deal." Johnson. "Nay, Sir, whatever may be the quant.i.ty that a man eats, it is plain that if he is too fat, he has eaten more than he should have done."

But to clarify, as Johnson did, that obesity is caused by eating more than one should have, is not a satisfying answer. We're stil left asking why.

This question is built into the logic of the overeating/sedentary-behavior hypothesis. Why do people overeat, or why are they so sedentary, if the inevitable result is obesity? And because both overeating and deficient physical activity are, after al , behavioral conditions, not physiological ones, the only answer al owed by the hypothesis is a judgment on the behavior of the obese. To say that the obese eat more than they should, as Johnson phrased it, or are less active than they should be-thus, inducing their positive caloric balance-implies only two possibilities. Either it's beyond their control, in which case there is another, more profound cause of their condition-perhaps a metabolic or hormonal disorder for which we should stil be searching -or it is within their control, and so we are led to the judgment that the obese are weaker of wil than the lean. It may be true, as von Noorden noted, that their appet.i.te is unable to regulate their energy consumption, but why, then, do they not consciously adjust? The logic keeps taking us in circles.

We arrive at the same conclusion if we ask why semi-starvation diets fail to cure obesity reliably, inducing only short-term weight loss by creating a negative caloric balance. Again, there are two possibilities. The first is that the obese stay on the diet but the weight loss eventual y stops or even reverses itself. If this is the case, then whatever physiological mechanism is at work may be the cause of the obesity as wel . If so, obesity may be caused not by overeating, whatever that means, and sedentary behavior-i.e., by positive caloric balance-but by some more profound underlying disorder.

Since a metabolic disorder is not an option in the overeating/ sedentary-behavior hypothesis (if it were, then we might be discussing the metabolic-disorder hypothesis), the only al owable answer is the second possibility: the obese lack the wil power to remain on the diet-a character defect.

The closer we look at the overeating hypothesis, the more counterintuitive its logic becomes. Consider a thought experiment. The subjects are two middle-aged men of similar height and age. One eats three thousand calories a day and is lean. The other eats three thousand calories a day and is obese. (The epidemiologic and metabolic studies of the past century make clear that we could find two such men with little difficulty.) Let's cut the calorie intake of our obese subject in half and semi-starve him on fifteen hundred calories a day. He wil lose weight, although, if Albert Stunkard's 1959 a.n.a.lysis holds true, there's only one chance in eight he'l lose even as much as twenty pounds. Our lean subject wil lose weight on this diet as wel , as Keys demonstrated with his conscientious objectors in 1944. That's what the law of energy conservation implies. But they would both be hungry continuously, making it likely they would fal off the diet given time. That's what common sense, the history of obesity research, and the Carnegie, Minnesota, and Rockefel er experiments tel us. And after some amount of weight loss, their weight wil plateau, because their metabolism and energy expenditure wil adjust to this new level of calorie intake. "Eventual y, calorie balance is re-established at a new (low) plateau of body weight and the calorie deficit is zero,"

as Keys explained.

Our intuition is that our obese subject wil lose more weight because he has more to lose, but we have little evidence to that effect, one way or the other.

And yet, if both our obese and lean subjects fal off the diet and return to eating three thousand calories a day, the obese individual wil return to obesity, perhaps even fatter than ever, and thus wil satisfy our diagnostic criterion for a character defect; our lean subject wil also put back the weight he lost, and perhaps a little more, but wil stil be lean, and wil not have to think of himself as possessed of a perverted appet.i.te or some other character defect.

The same conclusion wil be reached if our obese subject undergoes bariatric surgery. "This procedure alters gastrointestinal anatomy to reduce caloric intake beyond what could be achieved volitional y," explains Jeff Friedman of Rockefel er University in a recent issue of Nature Medicine. "Although people who undergo bariatric surgery lose a significant amount of weight, nearly al remain clinical y obese." We wil now have two individuals of more similar size and weight, one of whom needs a surgical y altered gastrointestinal tract to reduce calorie intake so much that he can stay at that weight, and the other who doesn't and can eat to his heart's content. Our surgical patient is perceived as defective in character, having had to rely on surgery to curb his appet.i.te. Our natural y lean subject is not, despite the possession of an identical appet.i.te. "The implication," as Friedman noted, "is that something metabolical y different about morbidly obese individuals results in obesity independently of their caloric intake."

Whatever the accepted wisdom, making obesity a behavioral issue is endlessly problematic. "Theories that diseases are caused by mental states and can be cured by wil power," as Susan Sontag observed in her 1978 essay Illness as Metaphor, "are always an index of how much is not understood about the physical terrain of a disease." This is certainly the case with obesity. One goal of any discussion of the cause of obesity must be a way to think about it that escapes the facile and circular reasoning of the overeating/sedentary-behavior hypothesis and permits us to proceed in a direction that leads to real progress, to find a way of discussing the condition, as the philosopher of science Thomas Kuhn might have put it, that al ows for a "playable game."

Obesity researchers over the last century have struggled with this dilemma, but they failed to escape it, which is the inevitable consequence of circular logic. Von Noorden, for instance, sought to absolve the obese of character defects by suggesting that weight was gained so imperceptibly as to go unnoticed. He inaugurated the practice, ubiquitous today, of enumerating the subtle ways in which excess calories creep into our diet, or fail to be expended in our sedentary lives. Two hundred calories a day, he suggested, the content of five pats of b.u.t.ter or twelve ounces of beer, could easily slip into the diet un.o.bserved and result in a weight increase, by his calculation, of nearly seventeen pounds a year. "These 200 calories represent such a smal amount of food," he explained, "that neither eyesight nor appet.i.te afford any indication of it, and therefore the person can say to the best of his knowledge that his food-supply has not been altered, although he has obviously become corpulent." Any such claims that obesity is caused by the slow and imperceptible acc.u.mulation of excess calories inevitably serves to blame obesity on the behaviors of overeating and inactivity, while avoiding the explicit accusation of a character defect. Such explanations also beg the question of how the victim managed to make the transition from lean through overweight to obese without noticing and then choosing to reverse the process.

The hypothesis that the currently rising tide of obesity is caused by a toxic food environment, as Yale's Kel y Brownel has proposed, is another example of an attempt to blame obesity on the behavior of overeating, even while sympathizing with the sufferers. "As long as we have the food environment we do," says Brownel , "the epidemic of obesity is predictable, inevitable, and an understandable consequence." That environment, in his view, is the fault of the food industry, aided and abetted by the makers of computer games and television shows that encourage sedentary entertainment. Fol owing this argument, severely obese people have sued fast-food chains, the inventors of supersizing, which supposedly pushes extra calories on unsuspecting bargain-conscious Americans. "Our culture's apparent obsession with 'getting the best value' may underlie the increased offering and selection of larger portions and the attendant risk of obesity," as James Hil of the University of Colorado and his col eague John Peters of Procter & Gamble suggested in Science in 1998.

But if the environment is so toxic, as the Mayo Clinic diabetologist Russel Wilder asked seventy years ago, "why then do we not al grow fat?" After al , Wilder observed, "we continue to be protected against obesity, most of us, even though we hoodwink our appet.i.te by various tricks, such as c.o.c.ktails and wines with our meals. The whole artistry of cookery, in fact, is developed with the prime object of inducing us to eat more than we ought." This brings us right back to the character issue. Some misbehave in this toxic environment and become obese. Some do not.*84 Albert Stunkard and Jean Mayer are among those investigators who argued that it was wrong to blame obesity on character defects, and yet stil failed to extricate themselves from the circular logic of the overeating/ sedentary-behavior hypothesis. In his 1959 a.n.a.lysis of semi-starvation diets, Stunkard wrote that obesity research went astray once investigators concluded that "excessive body fat results from an excess of caloric intake over caloric expenditure" and then enshrined this thinking as the dictum that "al obesity comes from overeating." After that, wrote Stunkard, the physician's job became nothing more than to explain that "semi-starvation reduces fat stores, to prescribe a diet for this purpose," and then to sit by and await the result.

"If the patient lost weight as predicted, this merely confirmed the comfortable feeling that treatment of obesity was real y a pretty simple matter," wrote Stunkard. "However, if, as so often happened, the patient failed to lose weight, he was dismissed as uncooperative or chastised as gluttonous." Mayer also ridiculed the logic that obesity was caused by gluttony or whatever was meant by the term overeating. "Obesity," he wrote in The Atlantic in 1955, "it is flatly stated, comes from eating too much and that is al there is to it. Any attempt to search for causes deeper than self-indulgence can only give support to patients already seeking every possible means to evade their own responsibility."

But the trap that Stunkard and Mayer had identified is built into the logic of the positive-caloric-balance hypothesis; there is no escaping it. Mayer, as we've discussed, proceeded to insist in his book Overweight, as in al his writing, that obesity was the result of sedentary behavior, which simply implicated sloth rather than gluttony and stil left the issue defined as a behavioral one. Although Mayer gets credit for convincing his peers that obesity has a genetic component, he implied that the only role of these genes was to make us want to be more or less sedentary. By the end of Overweight, Mayer was insisting not only that the obese must exercise more, but that they must also try harder to eat less. "Obesity is not a sin," he wrote. "At most, it is the consequence of errors of omission, the result of not having kept up the life-long battle against an inherited predisposition and against an environment which combines constant exposure to food with the removal of any need to work for it physical y. In the pilgrim's progress of the const.i.tutional y plump, salvation demands more than the shunning of temptation. It requires...the adoption of an att.i.tude almost stoic in its asceticism and in the deliberate daily setting aside of time for what wil be often lonely walking and exercising."

Stunkard became a leading authority in the study of behavioral therapy for obesity, which can be defined as a system of behavioral techniques by which obese patients might come to endure semi-starvation, while avoiding the explicit judgment that they achieved their obesity because they lacked wil power or had a defect of character. For instance, they eat too fast, or they are overly responsive to the external cues of their environment that tel them to eat, while being unresponsive to the internal cues of satiation, as one popular theory of the early 1970s had it. "Fat Americans: They Don't Know When They're Hungry, They Don't Know When They're Ful ," as a New York Times headline suggested in 1974. By that time, obesity, like anorexia, was categorized as an eating disorder, and the field of obesity therapy had become a subdiscipline of psychiatry and psychology. Al these behavioral therapies, cal them what you may, were in fact aimed at correcting failures of wil . Every attempt to treat obesity by inducing the obese to eat less or exercise more is a behavioral treatment of obesity, and implies a behavioral-psychological cause of the condition.

Even if we accept that obese individuals are possessed of a defective character, then we're stil left in the dark. Why doesn't the same defect-"the combination of weak wil and a pleasure seeking outlook upon life," said Louis Newburgh-cause obesity in everyone? "It exists in many non-obese individuals as wel ," observed Hugo Rony; "in some of these it leads to chronic alcoholism, or drug addiction, others may become gamblers, playboys, prost.i.tutes, petty criminals, etc. Evidently, such mental makeup, in itself, is not conducive to obesity. Those who do become obese apparently have something additional to and independent from this mental makeup: an intrinsic tendency to obesity."

If we can believe that people become obese because they simply ignored the fact that they were getting increasingly fatter, year in and year out, with the pa.s.sive acc.u.mulation of excess calories, and that by the time they noticed it was either too late to do anything about it or they really didn't care (despite claims they might make to the contrary); if we can believe that obese individuals fail to survive indefinitely on semi-starvation diets because they are gluttonously unwil ing to forgo temptation and so prefer, consciously or unconsciously, obesity to a life of moderation, then, as Stunkard observed in 1959, the matter is settled. Our job is done. But, of course, it isn't.

The more thoughtful a.n.a.lyses of obesity over the years have inevitably taken a more empathic view of those who suffer from it. They posit that there is no scientifical y justifiable reason-or evidence-to a.s.sume that the obese are any more defective in character or behavior than you or I. Eric Ravussin, a diabetologist and metabolism researcher who began studying obesity among the Pima in 1984, has reported that Pima men who gained excessive weight-more than twenty pounds-over the course of a three-year study had a significantly lower basal-metabolic rate before their weight gain than men who remained relatively lean. (This same observation, as Ravussin points out, was made in infants: those who are heavier at one year of life have abnormal y low daily energy expenditures when they are three months old.)*85 This suggests a const.i.tutional difference in these individuals; it would be difficult to explain it in terms of sloth and a weak character. As a result, Ravussin questioned the logic and implications of the positive-caloric-balance hypothesis. "If obesity was only caused by an excessive appeal for food," Ravussin asked in a 1993 article in the journal Diabetes Care, "how can we explain the complete failure of treating it with behavioral therapies? Can we real y believe that so many obese patients are liars and are cheating their doctors? How many more times do we need to demonstrate the high rate of recidivism among obese patients after weight loss to persuade others that unwanted metabolic forces contribute significantly to the causes of obesity in man?"

When Ravussin was interviewed more recently, he insisted that overeating and sedentary behavior could not explain the prevalence of obesity and diabetes in modern societies, and particularly not in the Pima. "I was shocked when I went to work with the Pima and I saw the amount of suffering in this population," he said. "It's not fun to see your mother [having a limb] amputated when she's thirty-two or thirty-five because she's had poorly control ed diabetes for twenty years. There's not a population in the world as aware as the Pima of the damages of diabetes and obesity. They know that. They are told from the age of two to avoid it, and stil they cannot make it."

Hilde Bruch is now given credit for initiating a "revolution in thinking about childhood obesity"-doing "the first systematic investigation of the inner compulsions of the fat person," as the New York Times reported in 1950-and so purportedly demonstrating that its roots are not physiological but behavioral. Indeed, Bruch may be the person most responsible for initiating the belief that obesity is an "eating disorder," and thus sending several generations of psychiatrists and psychologists off to work with obese patients. Yet, ironical y, Bruch never embraced this conclusion herself and always considered the primary underlying cause of obesity to be metabolic and/or hormonal.

Despite Bruch's research linking childhood obesity to overeating and pathologies in the mother-child relations.h.i.+p, she was al too aware that her own research had failed to establish what was cause and what was effect. Her research had been uncontrol ed, she noted, because she had studied only obese children and their families. "The literature on behavior disorders in childhood abounds with references to maternal rejection and overprotection,"

she explained. There was no way to know whether what she had discovered about her obese subjects actual y played a major role in the development of obesity. It was also possible that the children had a predisposition to fatten and that this affected the children's desire to eat to excess, which in turn affected the family dynamics and how the families treated the children. What appeared to be a cause could in fact be an effect. "Life situations and emotional experiences of this kind," Bruch wrote, "provoke increased desire for food only in a certain type of person and result in obesity only when such a person has a special tendency to store fat in larger amounts than others and does not increase the energy expenditure correspondingly."

After publis.h.i.+ng her observations on childhood obesity, Bruch put aside her clinical practice temporarily to study psychiatry, in the hope of helping these children. Through the early 1960s, she pra