getic and optimistic about their health and were better at ignoring hunger and fatigue, they could be sent to look for new territory.
The adapted-to-flee-famine hypothesis (AFFH) (17) proposes that AN is caused by ancient adaptations selected when migration was indeed the best solution to local famine; then individuals high in self-control, energy, optimism and perseverance had a selective advantage, as would their bands. All of the features of anorexia would have facilitated successful migration. Fear of eating kept migrators from being distracted by the occasional berry or bird; restless energy facilitated travel; hallucinating fat stores helped emaciated migrators convince themselves that they could keep moving.
Many scouts surely died, but those individuals and bands that did expand into new rich new land would have passed down their genes when the population expanded, leading to a higher frequencies of the genetic potentials for AN in the face of starvation. The pattern of genetic data as humans dispersed around the world is consistent with a long series of genetic bottlenecks and founder events (18). Apparently only about 70 individuals who crossed the land bridge from Asia during the last Ice Age founded the entire indigenous population of the Americas (19). Significantly, Native Americans, who migrated furthest from Africa, report the highest levels of AN of any American ethnic group (20). Africans appear not to have a genetic liability to develop AN; perhaps migration was most adaptive when travelers were moving out of Africa into unsettled lands.
Although frequency of genes involved in AN symptoms have most likely decreased over the course of time, still today weight loss can still trigger urges to migrate in the descendants of early anorexic explorers (21).
Problems with current explanations for anorexia nervosa
The first Diagnostic and Statistical Manual of Mental Disorders was published in 1952 when psychosocial explanations were predominantly accepted for serious mental disorders. Although considerable and diverse evidence reviewed here supports an evolutionary explanation for AN, the latest Diagnostic and Statistical Manual of Mental Disorders-5th Edition (DSM-5) maintains traditional psychosocial explanations for the disorder; this stance perpetuates a mistaken view of AN. Criteria include “persistent restriction of energy intake leading to significantly low body weight,” “intense fear of gaining weight or of becoming fat” and “undue influence of body shape and weight on self-evaluation” (10). The DSM-5’s assumption that the illness is proximally caused by patients’ restrictive food choices rather than by weight loss itself is outdated. Researchers in Germany have shown that a critical fall in leptin, the hormone that represents fat stores to the brain, triggers a cascade of neurobiological changes in rats, mice and AN patients that lead to food restriction and hyperactivity (11, 22-25).
Weight loss, not restrictive eating choices, is the trigger for anorexia in the genetically susceptible. It seems to patients and observers that AN is due to “persistent restriction of energy intake” because today the triggering weight loss is often the result of weight loss dieting. However, clinicians have long observed that anorexia nervosa symptoms can also be initiated by inadvertent weight loss (17, 26). This is especially common in 12- to 14-year-old girls when height increases faster than weight; girls that lose additional weight from illness or over-training can suddenly find themselves terrified of gaining weight although not previously trying to lose weight (17, 27). Multiple pathways can lead to weight loss, including growth spurts, illness, surgery, trauma, and dieting.
Fear of fat is a recent explanation
Listing fear of fat as a core and causally explanatory symptom is another inaccuracy of the DSM. Before the mid 1960s patients rarely mentioned a fear of being fat to explain food restriction and hyperactivity (28). Historically, reports of an AN-like syndrome have surfaced whenever Europeans, Asians or Indi