Clinical investigations involving the syndromes of bulimia and anorexia nervosa during the past year included neurotransmitter, neuropeptide, neuroendocrine, metabolic, pharmacologic and related behavioral studies on neurobiologic factors thought to contribute to the etiology of these disorders, and to their variable responsiveness to available treatments. Consistent with preclinical data implicating hypothalamic serotonin dysregulation in impaired post-prandial satiety, administration of the serotonin agonist m-chlorophenylpiperazine (m-CPP) decreased caloric intake in test meal studies. Prolactin responses to m-CPP were significantly blunted in eating disorder patients and in bulimic anorexic patients. Analysis of pharmacokinetic data showed that m-CPP-induced migraine-like headaches in eating disorder patients were related to blood level of the drug, as well as to personal and family history of migraine headache. Analysis of samples from a newly completed lumbar puncture study demonstrated that cerebrospinal fluid levels of homovanillic acid were significantly reduced in patients with severe bulimia, consistent with an alteration in central reward pathways involving dopamine. In preliminary results of a collaborative study of behavioral and neurochemical responses to 2-deoxyglucose, bulimic patients had blunted responses as reflected in hunger ratings and caloric consumption during a test meal. Follow-up on our previous findings of dysregulation of opiate and hypothalamic- pituitary-adrenal function in anorexic patients including collaborative studies utilizing the opiate antagonist naloxone and a glucocorticoid antagonist. Interviews continued for the family study of bulimia. Studies on energy metabolism showed that resting metabolic rate was significantly reduced in weight stable bulimic patients, suggesting increased efficiency of energy utilization. Preliminary results indicated a substantial role of the thyroid axis in elevation of resting metabolic rate observed in anorexic patients during weight gain.