genous Americans have starved for any reason (29). In each era victims provided historically- and culturally-bound explanations. In the early Middle Ages the Catholic Church canonized over 100 very thin people in Italy alone, in part for their ability to live with little food and tireless activity on behalf of others (30); these “holy anorexics” believed God allowed them to renounce bodily needs. Perhaps Paleolithic scouts understood the syndrome as divinely given powers to find better lands for their band.
Most renaissance victims complained that food disagreed with them or thought they could live on air. By the Victorian era the illness was attributed to a fear of sex. Explanations blaming a patients’ ambivalence about maturation dominated medicine until the mid-twentieth century when Hilde Bruch convinced the western world that teenage girls with AN were trapped in a desperate struggle for psychological autonomy from controlling mothers (31). When culturally ideal weights for women in the industrialized world dropped to 85% of normal in the late 1960s, AN patients began to blame their food restriction and excessive exercising on fear of getting fat. Today many patients attribute their AN behaviors and cognitions to needs for control or desire to eat only certain foods.
In an important review article published in 2003, Patricia Keel and Kelly Klump cautioned against naively believing patients’ explanations for their food restriction:
Although motivations for food refusal may have differed across periods (in many cases this information is simply lacking), purported motivations may not represent the true causes of self-starvation. Instead, they may represent culturally meaningful attempts to understand an affliction that leaves women feeling unable and unwilling to eat. The extent to which fear of fat is viewed as causing AN may be, in part, an illusion. (27)
Such errors come from viewing eating behavior as always arising from conscious choice and observers’ credulous acceptance of individuals’ post hoc explanations. Psychogenic theories for AN persist despite considerable evidence from careful neuroendocrine research that weight loss leads to the distinctive syndrome in both rats and humans (11, 22-25).
Hyperactivity is a primary symptom
The English and French physicians who independently described the syndrome in 1873 included hyperactivity as a primary symptom. Frances Gull wrote, “[t]he patient complained of no pain, but was restless and active. …it seemed hardly possible that a body so wasted could undergo the exercise which seemed agreeable.” His French counterpart, Charles Lasègue wrote, “…far from muscular power being diminished, this abstinence tends to increase the aptitude for movement. The patient feels more light and active…. …is never tired. ”
Although the DSM-5 authors assumed hyperactivity is secondary to desire to lose weight, prominent anorexia researchers maintain it is a core symptom (26). Casper pointed out that a level of energy greater than normal is measurably present in all patients at some time during the illness (32). This is important because relegating hyperactivity to secondary status has obscured the similarity between AN in humans and anorexia in animals.
Researchers searching for genes associated with longevity in yeast and mice have found a gene, Sirt-1, which turns on hyperactivity in starving mice and rats (33). Sirt-1 is a regulator involved in fatty acid oxidation and respiration; during famine it increases mitochondrial biogenesis and remodeling to become more efficient by increasing the proportion of respiration coupled to ATP production, reducing overall oxygen consumption and detoxifying the byproducts of increased metabolism(34). These changes transform ordinary mice into super mice, able to run over twice as long on a treadmill before collapsing in exhaustion (35)
Calorie restriction can lead to increased mitochondria in humans as well (36). Perhaps this explains the expression in some sports that “the thinner is the winner.” In sports such as endurance cycling where performanc