Good Calories, Bad Calories (54 page)

Despite Bruch’s research linking childhood obesity to overeating and pathologies in the mother-child relationship, 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 publishing 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 practiced psychiatry in New York, and then took a position as professor of psychiatry at Baylor Col ege of Medicine in Houston. Throughout this period, she continued to specialize in anorexia and obesity. In 1957, with the publication of The Importance of Overweight, she was stil questioning the role of psychological factors in obesity. (She described the book as a “critical re-evaluation and reintegration” of the obesity literature, including her own research.) Bruch couldn’t escape the fact that restricting calories failed to bring obesity under control for any extended period of time, and she was simply unwil ing to blame such consistent failure on her patients or their upbringing. “The efficacy of any treatment of obesity can be appraised only by the permanence of the result,” Bruch stated. “When I began to work with obese children,” she wrote, “I was impressed by the seeming ease with which some were able to lose weight once I had gained their co-operation. Having fol owed such cases over twenty years, I am today even more impressed by the speed with which they wil regain the lost weight and by the tenacity with which they maintain their weight at an individual y characteristic high level. It is possible to force the weight below this individual level, but such efforts are usual y short-lived.”

That obese people overeat, at least during periods of weight increase, Bruch said, had been “adequately established.” What she disagreed with was what had now become, thanks in good part to her own research, the conventional interpretation of this observation: that overeating is the cause of obesity, and that the logical treatment is underfeeding. “In the course of my observations,” she noted, “studying many obese people in great detail and fol owing them over a long period of time, I have come to the conclusion that…overeating, though it is observed with great regularity, is not the cause of obesity; it is a symptom of an underlying disturbance…. Food, of course, is essential for obesity—but so is it for the maintenance of life in general. The need for overeating and the changes in weight regulation and fat storage are the essential disturbances.”

In 1973, when Bruch published Eating Disorders: Obesity, Anorexia Nervosa, and the Person Within, she was stil struggling with this conflict between psychological and physiological factors in the development of obesity. She acknowledged the need to prescribe reducing diets, and much of her analysis focused on those interpersonal and familial relationships that might contribute to obesity and dietary failure. Yet, she could not escape the suspicion, implied by a growing body of research, that the cause of obesity is a “primary metabolic or enzymatic disorder.” And she acknowledged that it was stil up to researchers to unambiguously identify the nature of the disorder. “Studies of human obesity,” she wrote, “are not yet able to differentiate between factors that are the cause of obesity, or the result of it.”

CONSERVATION OF ENERGY

The complicated mechanism of the body must be taken into consideration, and the ways it takes to reach its goals are not always the straight paths envisioned in our calculations.

MAX RUBNER, The Laws of Energy Conservation in Nutrition, 1902

BEFORE WORLD WAR II, the proposition that obesity was caused by overeating—the positive-caloric-balance hypothesis—was one of several competing hypotheses to explain the condition. After Hilde Bruch reported that obese children ate immoderately, and Louis Newburgh insisted that a perverted appetite was the fundamental cause of obesity, the positive-caloric-balance hypothesis became the conventional wisdom, and the treatment of obesity, as Jean Mayer observed, became the provenance of psychiatrists, psychologists, and moralists whose primary goal was to rectify our dietary misbehavior.

Any attempt to dispute the accepted wisdom was treated, as it stil is, as an attempt to absolve the obese and overweight of the necessity to exercise and restrain their appetites, or to sel something, and often both.

This conviction that positive caloric balance causes weight gain is founded on the belief that this proposition is an incontrovertible implication of the first law of thermodynamics. “The fact remains that no matter what people eat, it is calories that ultimately count,” as Jane Brody explained in the New York Times. “Eat more calories than your body uses and you wil gain weight. Eat fewer calories and you wil lose weight. The body, which is after al nothing more than a biochemical machine, knows no other arithmetic.”

For fifty years, clinicians, nutritionists, researchers, and public health officials have used this logic as the starting point for virtual y every discussion of obesity. Anyone who chal enges this view is seen as wil ful y disregarding a scientific truth. “Let me state,” said the Columbia University physiologist John Taggart in his introduction to an obesity symposium in the early 1950s, “that we have implicit faith in the validity of the first law of thermodynamics.” “A calorie is a calorie,” and “Calories in equals calories out,” and that’s that.

But it isn’t. This faith in the laws of thermodynamics is founded on two misinterpretations of thermodynamic law, and not in the law itself. When these misconceptions are corrected, they alter our perceptions of weight regulation and the forces at work.

The first misconception is the assumption that an association implies cause and effect. Here the context is the first law of thermodynamics, the law of energy conservation. This law says that energy is neither created nor destroyed, and so the calories we consume wil be either stored, expended, or excreted. This in turn implies that any change in body weight must equal the difference between the calories we consume and the calories we expend, and thus the positive or negative energy balance. Known as the energy-balance equation, it looks like this: Change in energy stores = Energy intake-Energy expenditure

The first law of thermodynamics dictates that weight gain—the increase in energy stored as fat and lean-tissue mass—wil be accompanied by or associated with positive energy balance, but it does not say that it is caused by a positive energy balance—by “a plethora of calories,” as Russel Cecil and Robert Loeb’s 1951 Textbook of Medicine put it. There is no arrow of causality in the equation. It is equal y possible, without violating this fundamental truth, for a change in energy stores, the left side of the above equation, to be the driving force in cause and effect; some regulatory phenomenon could drive us to gain weight, which would in turn cause a positive energy balance—and thus overeating and/or sedentary behavior. Either way, the calories in wil equal the calories out, as they must, but what is cause in one case is effect in the other.

Al those who have insisted (and stil do) that overeating and/or sedentary behavior must be the cause of obesity have done so on the basis of this same fundamental error: they wil observe correctly that positive caloric balance must be associated with weight gain, but then they wil assume without justification that positive caloric balance is the cause of weight gain. This simple misconception has led to a century of misguided obesity research.

When the law of energy conservation is interpreted correctly, either of two possibilities is al owed. It may be true that overeating and/or physical inactivity (positive caloric balance) can cause overweight and obesity, but the evidence and the observations, as we’ve discussed, argue otherwise. The alternative hypothesis reverses the causality: we are driven to get fat by “primary metabolic or enzymatic defects,” as Hilde Bruch phrased it, and this fattening process induces the compensatory responses of overeating and/or physical inactivity. We eat more, move less, and have less energy to expend because we are metabolical y or hormonal y driven to get fat.

In 1940, Hugo Rony, former chief of the endocrinology clinic at Northwestern University’s medical school, discussed this reverse-causation problem in a monograph entitled Obesity and Leanness, which is easily the most thoughtful analysis ever written in English on weight regulation in humans.*86 Rony’s goal, as he explained it, was to “separate recognized facts from suggestive evidence, and reasonable working hypothesis from mere speculations.” This set Rony apart from Louis Newburgh, Jean Mayer, and others who were more interested in convincing their col eagues in the field that their speculations were correct.

When Rony discussed positive energy balance, he compared the situation with what happens in growing children. “The caloric balance is known to be positive in growing children,” he observed. But children do not grow because they eat voraciously; rather, they eat voraciously because they are growing.

They require the excess calories to satisfy the requirements of growth; the result is positive energy balance. The growth is induced by hormones and, in particular, by growth hormone. This is the same path of cause and effect that would be taken by anyone who is driven to put on fat by a metabolic or hormonal disorder. The disorder wil cause the excess growth—horizontal, in effect, rather than vertical. For every calorie stored as fat or lean tissue, the body wil require that an extra calorie either be consumed or conserved. As a result, anyone driven to put on fat by such a metabolic or hormonal defect would be driven to excessive eating, physical inactivity, or some combination. Hunger and indolence would be side effects of such a hormonal defect, merely facilitating the drive to fatten. They would not be the fundamental cause. “Positive caloric balance may be regarded as the cause of fatness,” Rony explained, “when fatness is artificial y produced in a normal person or animal by forced excessive feeding or forced rest, or both. But obesity ordinarily develops spontaneously; some intrinsic abnormality seems to induce the body to establish positive caloric balance leading to fat accumulation. Positive caloric balance would be, then, a result rather than a cause of the condition.”

An obvious example of this reverse causation would be pregnant women, who are driven to fatten by hormonal changes. This hormonal drive induces hunger and lethargy as a result. In the context of evolution, these expanded fat stores would assure the availability of the necessary calories to nurse the infants after birth and assure the viability of the offspring. The mother’s weight loss after birth may also be regulated by hormonal changes, just as it appears to be in animals.

What may be the single most incomprehensible aspect of the last half-century of obesity research is the failure of those involved to grasp the fact that both hunger and sedentary behavior can be driven by a metabolic-hormonal disposition to grow fat, just as a lack of hunger and the impulse to engage in physical activity can be driven by a metabolic-hormonal disposition to burn calories rather than store them. Obesity researchers wil immediately acknowledge that height, and thus the growth of skeletal bones and muscle tissue, is determined by genetic inheritance and driven by hormonal regulation, and that this growth wil induce the necessary positive caloric balance to fuel it. But they see no reason to believe that a similar process drives the growth of fat tissue. What they believe is what they were taught in medical school, which was and is the conventional wisdom: the growth of skeletal muscle and bones, and thus our height, is driven by the secretion of growth hormone from the pituitary gland; the growth of fat tissue, and thus our girth, is driven by eating too much or physical inactivity.

This notion that fattening is the cause and overeating the effect, and not vice versa, also explains why a century of researchers have made so little progress, and why they keep repeating the same experiments over and over again. By this logic, those who become obese have a constitutional tendency to fatten, whereas those who remain lean have a constitutional tendency to resist the accumulation of fat. This tendency is the manifestation of very subtle deviations in metabolism and hormonal state. The obese have a constitutional predisposition to accumulate slight excesses of fat in their adipose tissue, which in turn induces compensatory tendencies to consume slightly more calories than the lean or expend slightly less. Obese individuals wil put on fat until they have counterbalanced the influence of this underlying disorder. Eventual y, these individuals achieve energy balance—everyone does—but only at an excessive weight and with an excessive amount of body fat.

The essential question, then, is: what are the metabolic and hormonal deviation that drives this fattening process? When we have that answer, we wil know what causes obesity.

For the past half-century, obesity researchers have focused on a different question: establishing the characteristics that distinguish fat people from lean.

Do fat people expend less energy? Do they consume more? Are they aware of how much they’re eating? Are they less physical y active? Is their metabolism slower? Are they more or less insulin-sensitive? Al of these address factors that may be associated with the condition of being obese, but none address the question of what causes it initial y.