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.