ABSTRACT
The current system of psychiatric diagnosis, DSM-IV (1), addresses two official eating disorder (ED) syndromes-anorexia nervosa (AN) and bulimia nervosa (BN)—and a third (still provisional) diagnostic entity-binge eating disorder (BED). However, BED has all but officially been recognized as a distinct eating syndrome. AN, BN, and BED are all polysymptomatic syndromes, defined by maladaptive attitudes and behaviors around eating, weight, and body image, but typically including “nonspecific” disturbances of self-image, mood, impulse regulation, and interpersonal functioning. All three syndromes are known to be associated with significant mortality and morbidity, both medical and psychiatric (2,3). Despite popular beliefs, there is no convincing evidence that cultural factors alone cause eating disorders. Indeed, during the past few years (and especially the last decade) investigations into the role of neurotransmitters and other neuromodulators in the eating disorders have been highly productive, and have implicated primary neurotransmitter disturbances in the etiology of both AN and BN. Furthermore, recent data clearly identify strong genetic factors in AN and BN, which appear to share common genetic vulnerabilities (4,5) linked to obsessionality, perfectionism, anxiety, and/or behavioral inhibition (6,7). One powerful piece of evidence to support monoamine involvement in the eating disorders is the observation that antidepressant medications can be beneficial in controlled studies, not only in BN patients but in recovered AN patients as well (8).
