Abstract
lhere is a commonsense view of obesity that says, simply, that it is the result of an I imbalance between energy intake (food) and energy output (exercise). Although this view obviously has considerable merit, as well as testable implications for intervention, it is an incomplete explanation. Energy-flux imbalance is necessary but is probably not sufficient. Thus, it may be reasonable to ask: what other conditions have to be present to induce obesity? That some genetic influences are in play may seem obvious but, to date, the evidence is sparse. However, there are some rare conditions in which a genetic defect is closely associated with hyperphagia and obesity, and these may hold clues. Second, eating disorders are one way in which energy balance can be disturbed. Eating disorders are either more common now or more frequently diagnosed. Do they cast any light on obesity? Third, what explains the paradoxical relationship between poverty and obesity in the developed world? Finally, the 20th century was characterized by an epidemic of coronary heart disease-an epidemic that began to decline for, as yet, unclear reasons in Western countries in the 1960s and 1970s. There have also been epidemics of obesity in previous centuries. Is it possible that these are epidemics in the communicable disease sense?
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