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, disturbance s in attitudes toward weight and shape, and the perception of body shape. I n AN, there is an inexplicable fear of weight gain and unrelenting obsessio n 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 w eight loss. Binge eating, which is the consumption of a large amount of foo d in an uncontrollable manner, is followed by either self-induced vomiting or by some other means of compensation (e.g., misuse of laxatives, diuretic s, or enemas, or the use of excessive exercise or fasting) for the excess o f food ingested. Most people with BN have irregular feeding patterns, and s atiety 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 tre atment 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 influen ced by developmental, social, and biological processes(17, 59;) however, th e exact nature of these interactive processes remains incompletely understo od. Certainly, cultural attitudes toward standards of physical attractivene ss have relevance to the psychopathology of eating disorders, but it is unl ikely that cultural influences in pathogenesis are very prominent. For one, dieting behavior and the drive toward thinness is quite commonplace in ind ustrialized 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) Mo reover, the fact that numerous clear descriptions of AN date from the middl e of the nineteenth century(59) suggests that factors other than our curren t culture have an etiologic role. In addition, both syndromes, AN in partic ular, have a relatively stereotypic clinical presentation, sex distribution , and age-of-onset, supporting the possibility of some biological vulnerabi lity. Evidence from family, twin, and molecular genetic studies suggest that this biological vulnerability might be genetic. This article reviews these beha vioral genetic findings, highlighting the emerging evidence suggesting sign ificant genetic influences on these disorders.