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 of 1 percent.”