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.