l protest because it is agonizing. Many women would like to weigh at least 15% less than they do to meet today’s ultra thin beauty standards, but most find this impossible. While AN is the only psychiatric disorder that healthy people joke about wanting to “catch,” people with AN are not enviable; a suicide risk forty times normal speaks to their misery (62). Yet, observers’ envy acknowledges that the symptoms of AN cannot be voluntarily enacted.
Third, the genetic ability to develop AN is more common than would be expected if alleles had not been selected. European and Australian population studies indicate that over 4% of women of European descent develop anorexia nervosa in their lifetimes, although most did not seek medical care and recovered spontaneously (63). Given that AN is initiated by starvation and famine is rare in the industrialized world, it follows that even more than 4% of non-African populations carry behaviorally un-expressed susceptibility genes.
Finally, the AN syndrome has marks of evolved mechanisms: The behaviors and attitudes are opposite normal yet stereotyped. The syndrome requires dozens of biological processes to change together every time a person develops AN. If the underlying biological changes were indeed random accidents and truly independent (that is, not selected as part of an adaptation), the probability that they would occur together to produce AN would be the product of their individual probabilities and vanishingly small.
Evidence supporting the adapted-to-flee-famine hypothesis is drawn from diverse research in endocrinology, neuroscience, genetics, epidemiology, psychology and behavioral ecology, providing an extraordinarily broad cross-disciplinary network of evidence (64). The widespread acceptance of traditional explanations attributing AN to patients’ psychologically-motivated or learned choices rests on neither broad empirical support nor on the absence of a plausible and more comprehensive explanation.
The adapted-to-flee-famine hypothesis explains what initiates AN (considerable weight loss in genetically susceptible individuals) and the mechanisms by which the cause operates (via a critical fall in leptin that is exacerbated by the presence of estrogen); it explains quantitative features (sex ratio and epidemiology); it accounts for more AN phenomena than other AN theories (why starving people eat little, move restlessly and hallucinate fat stores); it reveals the unity that underlies the apparent diversity of AN (the core symptoms have remained the same while explanations differed); and, it points toward more fruitful research questions in the psychology, genetics and neuroscience of AN, and toward more effective interventions. Thus, the AFFH meets the criteria for a sound scientific explanation, providing precision, scope, simplicity, prediction, and usefulness (65).
In the Paleolithic some behavioral mechanism probably helped anorectic tribal members to eat when food was once again plentiful. If the traditions of extant nomadic tribes are an indication, this mechanism involved social support. When more food becomes available after a shortage, traditional societies celebrate with a feast (66). Refusing such food would be a profound breech of social norms and insult the giver. Humans are deeply social (67) and AN is probably most easily “switched off” with social support. For a starving tribe an anorectic’s energy, optimism, and grandiosity could inspire them to undertake an arduous journey, much as the anorectic Joan of Arc inspired soldiers to march with her (68). When they reached better lands, bands would in turn have helped their heroic scouts recover through eating and weight restoration.
People with AN must eat although eating fills them with shame, regret and dread; they get full quickly, and they cannot see how thin they are. They must reduce exercising while the anorexic voice castigates them as lazy and weak. Today the two most popular therapies for AN — Cognitive Behavior Therapy for eating disorders, which focuses on changing patients’ “fears of getting fat,