Anorexia nervosa and estrogen: Current status of the hypothesis

Anorexia nervosa occurs predominantly in young women. Also, recent data suggest that a heritable, genetic defect may contribute to this feeding disorder. These observations support the hypothesis that an inherited, abnormal response of the brain to rising levels of estrogens at puberty may contribute to the symptoms of weight loss in anorexia. To evaluate the merits of this hypothesis, the current literature on feeding depression by estrogens in anorexic patients and possible genetic or developmental mechanisms that could alter brain responsiveness to estrogens are reviewed. It is concluded that a number of specific biochemical or developmental pathways—abnormalities in the classical or membrane-bound forms of estrogen receptors, in co-activators for estrogen, in thyroxine receptors, in steroid metabolizing enzymes, in quantitative trait loci, in perinatal androgenization, and in processes of puberty—could converge to produce an abnormal response to estrogen and the onset of anorexia nervosa.