ositive trait. Mischel and his colleagues’ longitudinal research found, “Resisting temptation in favor of long-term goals is an essential component of social and cognitive development and of societal and economic gain”(56). Yet, these very traits are seen as causative factors for AN. When patients first present for treatment they usually exhibit high levels of anxiety, depression and compulsivity, and clinicians and researchers commonly attribute the disorder to their over-controlled, anxious and perfectionist traits (9, 57). However, Ansel Keys’ landmark starvation study found that healthy subjects develop pathological anxiety, depression, obsessions and compulsions when starved that remitted with re-feeding (58). We believe that observers have mistaken the pathological psychological sequelae of starvation for a predisposing and psychogenic pathological trait.
Preponderance of evidence
“The weight of evidence for an extraordinary claim must be proportional to its strangeness.” Pierre-Simon Laplace (59)
The adapted-to-flee famine hypothesis is a radical departure from today’s paradigm guiding eating disorders research and treatment. Anorexia researchers refer to the genetically-controlled biological changes they find as dysfunctions, deficits, dysregulation, impairment and defects, in other words, “bugs” in energy homeostasis, reward, fear, executive control or other regulatory systems. Many speculate about finding the biological change that explains AN, ignoring dozens described by others (9, 60).
A number of facts indicate that the biological changes are not mistakes but rather “features” arising from natural selection. First, loss of function is the usual result of dysfunctions, but these particular alleles give ordinary people, even children, extraordinary self-control over hunger, increased pain tolerance, athletic ability and endurance (61). Super abilities come from accidents only in comic books.
Second, when starving, the drive to eat is normally too fierce to be denied; a hunger strike is a powerful moral 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