Anorexia nervosa (AN) is commonly attributed to psychological conflicts, attempts to be fashionably slender, neuroendocrine dysfunction, or some combination of these factors. Considerable research reveals these theories to be incomplete. Psychological and societal factors account for the decision to diet but not for the phenomenology of the disorder; theories of biological defects fail to explain neuroendocrine findings that suggest coordinated physiological mechanisms. This article presents evidence that AN's distinctive symptoms of restricting food, denial of starvation, and hyperactivity are likely to be evolved adaptive mechanisms that facilitated ancestral nomadic foragers leaving depleted environments; genetically susceptible individuals who lose too much weight may trigger these archaic adaptations. This hypothesis accounts for the occurrence of AN-like syndromes in both humans and animals and is consistent with changes observed in the physiology, cognitions, and behavior of patients with AN.
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