Good Calories, Bad Calories (53 page)

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 analysis 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 appetite 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 appetite. Our natural y lean subject is not, despite the possession of an identical appetite. “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 butter or twelve ounces of beer, could easily slip into the diet unobserved 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 appetite 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 accumulation 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 appetite by various tricks, such as cocktails 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 analysis 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 constitutional y plump, salvation demands more than the shunning of temptation. It requires…the adoption of an attitude 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, prostitutes, 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 passive accumulation 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 analyses 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 assume 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 constitutional 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.