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The eating disorders anorexia nervosa and bulimia nervosa traditionally have been viewed as sociocultural in origin. However, recent behavioral genetic findings suggest substantial genetic influence on these disorders. Molecular genetic research of these disorders is in its infancy, but initial results are promising. This article reviews findings from family, twin, and molecular genetic studies that support substantial genetic influences on disordered eating and highlights additional areas for future research.

Introduction Anorexia nervosa (AN) and bulimia nervosa (BN) are disorders characterized by abnormal patterns of eating behavior and disturbances in attitudes and perceptions toward weight and shape. In AN, there is an extreme fear of weight gain despite increasing emaciation. BN usually emerges after a period of dieting, and is characterized by alternating patterns of binge eating and compensatory behavior. Binge eating, which is the consumption of a large amount of food in an uncontrollable manner, is typically followed by either self-induced vomiting, excessive exercise, fasting, and/or the misuse of laxatives, diuretics, or enemas. Although abnormally low body weight excludes a BN diagnosis, 25 to 30 percent of patients with BN have a prior history of AN. – Common to individuals with AN and BN are pathological concern with weight and shape, depression, and anxiety.

– The etiology of these disorders is presumed to be influenced by developmental, social, and biological processes., However, the exact nature of these interactive processes remains incompletely understood. Cultural attitudes toward thinness have relevance to the psychopathology of eating disorders, but they are unlikely to be sufficient to account for the pathogenesis of these disorders. Notably, dieting behavior is quite common in industrialized countries throughout the world, yet AN and BN affect only an estimated 0.3 to 0.7 percent, and 1.7 to 2.5 percent, respectively, of females in the general population. Moreover, numerous descriptions of AN date from the middle of the 19th century suggesting that factors other than modern culture play an etiologic role. In addition, both syndromes have a relatively homogeneous clinical presentation, sex distribution, and age-of-onset, supporting the possibility of some biological susceptibility.