Good Calories, Bad Calories

anyone who is driven to put on fat by a metabolic or hormonal disorder. The disorder will cause the excess growth —horizontal, in effect, rather than vertical. For every calorie stored as fat or lean tissue, the body will 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 artificially 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 will 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 will 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 will put on fat until they have counterbalanced the influence of this underlying disorder. Eventually, 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 will 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 physically active? Is their metabolism slower? Are they more or less insulin-sensitive? All of these address factors that may be associated with the condition of being obese, but none address the question of what causes it initially.

Even if it could be established that all obese individuals eat more than do the lean—which they don’t—that only tells us that eating more is associated with being obese. It tells us nothing about what causes obesity, because it doesn’t tell us why the obese don’t respond to an increase in food intake by expending more energy. After all, this must be the case when a lean person has a healthy appetite. “The statement that primary increase of appetite may be a cause of obesity does not lead us very far,” Rony explained, “unless it is supplemented with some information concerning the origin of the primarily increased appetite…. What is wrong with the mechanism that normally adjusts appetite to caloric output? What part of this mechanism is primarily disturbed…?”

Slightly more relevant are prospective studies, in which a population of individuals is observed to determine what distinguishes those who go on to become obese from those who don’t. These studies, however, also fail to establish cause and effect. Such studies have repeatedly demonstrated that those who are pre-obese expend less energy—even at the age of three months—than those who will remain lean, which means that the low energy expenditure is a risk factor for obesity. This suggests that the pre-obese do indeed have a retarded metabolism, as von Noorden suggested, but it does not imply that relatively low energy expenditure causes obesity, only that it is associated with the condition of being pre-obese, and perhaps facilitates the drive to become obese.

As we’ve discussed, obesity is associated with all the physiological abnormalities of metabolic syndrome and all the attendant chronic diseases of civilization. For this reason, public-health authorities now assume that obesity causes or exacerbates these conditions. The alternative logic, with the causality reversed, implies a different conclusion: that the same metabolic-hormonal disorder that drives us to fatten also causes metabolic syndrome and the attendant chronic diseases of civilization.

The second misinterpretation of the law of energy conservation inevitably accompanies the first and is equally unjustifiable. The idea that obesity is caused by the slow accumulation of excess calories, day in and day out, over years or decades, and the associated idea that it can be prevented by reductions in caloric intake and/or increases in physical activity, are both based on an assumption about how the three variables in the energy-balance equation—energy storage, energy intake, and energy expenditure—relate to each other. They assume that energy intake and energy expenditure are what mathematicians call independent variables; we can change one without affecting the other. “We cannot get away from the fact that, given no change in physical activity [my italics], increased food means increased weight,” as John Yudkin phrased it in 1959. “Yet this simple expression of the laws of conservation of mass and of energy is still received with indignation by very many people.” But Yudkin’s purportedly inescapable truth included an assumption that may not be physiologically plausible: “given no change in physical activity.” The question is whether one can actually change energy intake in a living organism without prompting compensatory changes in energy expenditure.

When Carl von Noorden suggested in 1900 that obesity could be caused by eating one extra slice of bread every day or climbing fewer flights of stairs, so that a few extra dozen calories each day would accumulate over a decade into tens of pounds, and when the USDA Dietary Guidelines, over a century later, evoked the same concept with the suggestion that “for most adults a reduction of 50 to 100 calories per day may prevent gradual weight gain,” they were treating human beings as though they are simple machines. “There is only one trouble,” as Hilde Bruch commented about von Noorden’s logic—“human beings do not function this way.”

If we consume an average of twenty-seven hundred calories a day, that’s almost a million calories a year; almost twenty million calories consumed over the course of two decades—more than twenty-five tons of food. Maintaining our weight within a few pounds for twenty years requires that we adapt our food intake to our expenditure over that period with remarkable accuracy. It’s all too easy, therefore, to imagine how a metabolic or hormonal defect might lead to obesity by inducing the slightest compensatory inclination to consume more calories than we expend, and why it would be so subtle as to go undetected by virtually any imaginable diagnostic technology. “It is conceivable,” as Eugene Du Bois of Cornell University suggested seventy years ago in his classic textbook Basal Metabolism in Health and Disease, “that common obesity is the only manifestation of an endocrine disturbance…so slight that it upsets the balance of intake and output by less than 0.1