Neurochemistry of bulimia nervosa

Abstract

Normal weight bulimia nervosa, a disorder of unknown etiology, is characterized by bingeing and purging behavior, disturbances of mood, and neuroendocrine abnormalities. Bulimic women have alterations of neurotransmitter systems known to contribute to the modulation of feeding, mood, and neuroendocrine function. Bulimic patients have increased cerebrospinal fluid concentrations of peptide YY (PYY), a peptide which is a potent stimulant of feeding in experimental animals. It has been suggested that increased brain PYY activity could contribute to the powerful and uncontrollable drive of bulimic patients to binge. It also has been reported that bulimics have impaired satiety and secretion of cholecystokinin, a peptide known to induce satiety and reduce food intake in animals and humans. Most data show that bulimic women have alterations of serotonin and norepinephrine activity. In animals, serotonin appears to have effects on eating behavior (inhibition) that are opposite to the actions of endogenous norepinephrine (activation) at alpha 2 receptors in the hypothalamus. Bingeing behavior is consistent with an overactivity of the hypothalamic alpha-noradrenergic system, an underactivity of hypothalamic serotonergic systems, or a combination of both defects. In summary, it is possible that bulimic patients have a trait-related disturbance of one or more neurotransmitter systems that could cause their appetitive dysregulation. Alternatively, these neurotransmitter disturbances may be secondary to extremes of dietary intake. Nonetheless, such neurotransmitter disturbances may contribute to a high recidivism rate. That is, bulimic patients could enter a vicious cycle in which pathologic feeding sustains and provokes continued pathologic feeding behavior. Moreover, the self-reinforcing effects of bulimia, such as decreased anxiety or food craving, may be mediated through behavior-induced changes in neurotransmission.