ract them from migrating (12). In the 1950s, when experimental psychologists deprived lab rats of food to increase motivation to learn, they discovered that when housed with a running wheel, starved rats decreased feeding and increased running from one to 20 kilometers a day. Even normal weight rats limited to feeding only one hour a day will ignore food to run, as though a hypothalamic algorithm read the food limitation as indicating an inadequate foraging environment. They can eventually die of “self-starvation” (13). Lean-bred pigs that lose additional weight can develop “wasting pig syndrome” where they pace incessantly, ignore their feed, but eat straw (14). In rats, mice and humans numerous alterations in appetite and activity regulators could contribute to food restriction and hyperactivity (15). It is hard to imagine how the resultant odd “choices” would be learned or rewarded in pigs, rats or mice.
In a review of habit Anne Graybiel observed that, “habits invoke a dichotomy between the conscious, voluntary control over behavior, considered the essence of higher-order deliberative behavioral control, and lower-order behavioral control that is scarcely available to consciousness” (14). There is another way that “habits” can be coded in dorsolateral striatum circuits: through natural selection of genetic changes that control hormones and neurotransmitters. Graybiel noted that behaviors that animals do automatically upon birth, hatching, or when hormones beckon for mating and rearing are encoded the same way as learned habits in neural architecture (16).
Humans have dealt with famine and migrated extensively in the evolutionary past. For most of our time on earth people lived in sparsely distributed bands of hunter-gatherers that shared food; thus, starvation reliably indicated that food resources were depleted. A starving hunter-gatherer band faced a life and death gamble: either conserve energy and wait out the famine or mobilize their last reserves to search for better lands. If some individuals felt energetic 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 considera