Abstract
Abstract Anorexia nervosa (AN) and bulimia nervosa (BN) are related disorders of unknown etiology that most commonly begin during adolescence in women. They are characterized by aberrant patterns of feeding behavior and weight regulation, and deviant attitudes and perceptions toward body weight and shape. In AN, an inexplicable fear of weight gain and unrelenting obsession with being fat, even in the face of increasing emaciation, accounts for a protracted course. BN usually emerges after a period of food restriction, which may or may not have been associated with weight loss. Binge eating is followed either by self-induced vomiting, or by other means of compensation for the excess of ingested food. There is growing acknowledgement that neurobiological vulnerabilities make a substantial contribution to the pathogenesis of AN and BN, suggesting that altered brain serotonin (5-HT) function contributes to dysregulation of appetite, mood, and impulse control. Brain imaging studies, using 5-HT specific ligands, show that disturbances of 5-HT function occur when people are ill, and persist after recovery. It is possible that a trait-related disturbance of 5-HT neuronal modulation predates the onset of AN, and contributes to premorbid symptoms of anxiety, obsessionality and inhibition. This dysphoric temperament may involve an inherent dysregulation of emotional and reward pathways which also mediates the hedonic aspects of feeding, thus making these individuals vulnerable to disturbed appetitive behaviors. Individuals with AN may discover that reduced dietary intake, by reducing plasma tryptophan availability, is a means by which they can modulate brain 5-HT functional activity and anxious mood. They enter a vicious cycle, because caloric restriction results in a brief respite from dysphoric mood. However, malnutrition and weight loss, in turn, produce alterations in many neuropeptides and monoamine function, which also exaggerates dysphoric mood. Thus, those with AN pursue starvation in an attempt to avoid the dysphoric consequences of eating.
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