Implicit in this hypothesis is the assumption that energy expenditure and energy intake are independent variables. Because they are independent, one of these variables can be manipulated, consciously or unconsciously, so that the primary result will be an increase or a reduction in energy stores—i.e., the amount of fat we carry—without the other responding. It is almost impossible to overstate the extent to which this hypothesis now pervades all thinking and research on obesity and weight, and underlies every accepted method of treatment and prevention. As Greenwood observed, “The vast majority of the notoriously unsuccessful weight control programs are predicated on this assumption.”

By contrast, the alternative hypothesis proposes that the primary defect is hormonal and metabolic—in fat storage and/or the burning of fat for fuel (oxidation)—and is in the body, not the brain. This defect causes the excessive accumulation of calories as fat and compensatory urges to eat more and expend less energy. In this hypothesis, overeating and inactivity (hunger and lethargy) are side effects of this underlying metabolic defect; they are not causes. The hypothesis presupposes that calories are effectively “pulled” into the fat cells, rather than pushed, with our fat tissue playing a very active role in this process. It assumes that energy intake and expenditure are dependent variables: a change in one induces a compensatory change in the other, because the body constantly works to maintain a healthy body composition and a dependable flow of energy to the cells. Immoderate eating and physical inactivity do not induce obesity, because the body adjusts intake to expenditure and expenditure to intake. Neither eating less nor exercising more addresses the cause of the problem, and that’s why these approaches fail. The only effective treatments, according to this hypothesis, would be those that remedy the fundamental regulatory defect.

The only thing missing from this hypothesis as it was originally conceived a century ago, or as reconceived by Pennington and then Bruch and Astwood, was an explanation for the epidemiological observations. In other words, obesity may be caused by a hormonal or metabolic defect determined primarily by genetic inheritance, but the epidemiology tells us that this defect is triggered by environmental factors. Genetics determines our propensity to put on weight, but those genes (nature) have to be triggered by an agent of diet or lifestyle (nurture) to explain the association of obesity with poverty, the present obesity epidemic, and the emergence of obesity in recently Westernized populations. A change in the environment is also necessary to explain why man alone seems to grow chronically obese, not other species of animals. “Something has happened in the past twenty, thirty, forty years in the incidence of obesity, and that has to be environmental,” as George Cahill has said about the present obesity epidemic.