The evolving genetic foundations of eating disorders

Anorexia nervosa (AN) and bulimia nervosa (BN) are disorders characterized by aberrant patterns of feeding behavior and weight regulation, disturbances in attitudes toward weight and shape, and the perception of body shape. In AN, there is an inexplicable fear of weight gain and unrelenting obsession with fatness even in the face of increasing cachexia. BN usually emerges after a period of dieting, which may or may not have been associated with weight loss. Binge eating, which is the consumption of a large amount of food in an uncontrollable manner, is followed by either self-induced vomiting or by some other means of compensation (e.g., misuse of laxatives, diuretics, or enemas, or the use of excessive exercise or fasting) for the excess of food ingested. Most people with BN have irregular feeding patterns, and satiety may be impaired. Although abnormally low body weight is an exclusion for the diagnosis of BN, 25% to 30% of patients with BN who present to treatment centers have a history of AN; however, all individuals with BN have pathologic concern with weight and shape. Common to individuals with AN and BN are low self-esteem, depression, and anxiety. The cause of these disorders is presumed to be complex and multiply influenced by developmental, social, and biological processes(17, 59;) however, the exact nature of these interactive processes remains incompletely understood. Certainly, cultural attitudes toward standards of physical attractiveness have relevance to the psychopathology of eating disorders, but it is unlikely that cultural influences in pathogenesis are very prominent. For one, dieting behavior and the drive toward thinness is quite commonplace in industrialized countries, but AN and BN affect only an estimated 0.3% to 0.7%, and 1.7% to 2.5%, respectively of females in the general population.(1) Moreover, the fact that numerous clear descriptions of AN date from the middle of the nineteenth century(59) suggests that factors other than our current culture have an etiologic role. In addition, both syndromes, AN in particular, have a relatively stereotypic clinical presentation, sex distribution, and age-of-onset, supporting the possibility of some biological vulnerability. Evidence from family, twin, and molecular genetic studies suggest that this biological vulnerability might be genetic. This article reviews these behavioral genetic findings, highlighting the emerging evidence suggesting significant genetic influences on these disorders.