In response to the partial serotonin agonist meta-chlorophenylpiperazine (metaCPP), patients with obsessive-compulsive disorder have been reported to exhibit an increase in obsessive symptoms and a diminished release of prolactin and~or cortisol compared to controls.We examined the response to metaCPP of 10 patients with anorexia nervosa, before and after weight gain, and of eight healthy controls.Prior to weight gain, the patients exhibited a greater behavioral response to metaCPP than the controls and diminished prolactin and cortisol responses.Only the prolactin abnormality persisted after weight gain.These observations suggest that, in patients with anorexia nervosa, weight loss is associated with the development of neurobiological disturbances which are in some ways similar to those of obsessivecompulsive disorder.

The cardiovascular effects of desipramine were assessed in 74 young women with bulimia nervosa participating in a 6-week double-blind, placebo-controlled study. Desipramine treatment was associated with significant increases in pulse, reclining systolic and diastolic blood pressures, and orthostatic hypotension. These effects were clearly evident in the first week of treatment and remained relatively unchanged during the subsequent 5 weeks. The mean increases in reclining systolic and diastolic pressures were approximately 10 mm Hg. Data from 16 patients treated for an additional 2 months indicated that most of the effects of desipramine on blood pressure diminished over time, whereas the effects on pulse persisted. These results differ from the commonly expected cardiovascular effects of tricyclic anti-depressants in adults. Evidence from the current study and from other reports suggests that the cardiovascular effects of tricyclic antidepressants are age-dependent.

OBJECTIVE The purpose of this study was 1) to replicate previous work indicating that antidepressant medication is superior to placebo in the treatment of bulimia nervosa and 2) to assess the long-term efficacy of this form of treatment. METHOD Eighty patients entered a three-phase treatment protocol. An 8-week double-blind initiation phase was used to compare the effects of desipramine and placebo. Patients who responded satisfactorily to desipramine entered a 16-week maintenance phase. Patients who remained well were then randomly assigned to either desipramine or placebo for 6 additional months (discontinuation phase). The primary outcome measure was binge frequency, which was assessed weekly by self-report diaries. RESULTS In the initiation phase the superiority of desipramine over placebo in reducing binge frequency was demonstrated. Patients treated with desipramine had a mean reduction in binge frequency of 47% at termination, whereas patients taking placebo experienced a mean increase of 7%. Less than half of the patients treated with desipramine met the criteria for entering the maintenance phase, and 29% of the patients entering that phase relapsed in the following 4 months. There were not enough patients in the discontinuation phase to permit clear conclusions about the need for continued antidepressant medication after 6 months of treatment. CONCLUSIONS The study documents a beneficial effect of desipramine in the treatment of bulimia nervosa when compared to placebo. However, limited improvement and considerable relapse with continued treatment suggest serious limitations to the long-term efficacy of a single antidepressant trial in treating bulimia nervosa.

To determine the value of total serum amylase levels and salivary and pancreatic isoenzyme levels as biologic indices of behavioral disturbance in bulimia nervosa, the authors monitored these levels in 40 bulimic patients participating in a placebo-controlled trial of desipramine and in 25 controls. In the patients, the total and salivary amylase levels were significantly elevated and a significant correlation existed between the frequencies of binge eating and vomiting and the level of salivary amylase. However, the ability to discriminate patients from controls on the basis of serum amylase levels was limited. In addition, a significant positive relationship between binge frequency and level of serum amylase was observed in less than one quarter of 22 patients with five or more amylase determinations. Therefore, although hyperamylasemia is associated with bulimia nervosa, we believe that serum amylase determinations have limited utility in the assessment of patients with this syndrome.

Despite our strong belief in the utility of laboratory studies of eating behavior, we also note several caveats on the data thereby obtained. First, it must be assumed that subjects' behavior is influenced by the laboratory environment and is not identical to eating behavior in a "normal" setting. Second, not all bulimic subjects who were screened for these studies actually participated, so that it is possible that the sample of patients from whom we obtained data differed in some ways from a general clinical population of women with bulimia. Nonetheless, we believe that our data provide compelling evidence that the disturbed eating behavior characteristic of bulimia nervosa can be profitably studied in the laboratory. Even under structured laboratory conditions, most bulimic patients rated one of their multicourse meals as typical of a binge, and, during that meal, consumed a much larger amount of food and ate more rapidly than did controls who were asked to overeat. The significant correlations between the sizes of the multicourse and single-course binge meals and between the size of laboratory binge meals and the size of the "naturally occurring" binge meals reported to the dietician suggest that a reproducible phenomenon is being examined. The results of our studies suggest that the abnormalities of eating behavior in bulimia nervosa cannot be viewed simply as a disturbance of carbohydrate consumption or even as the episodic consumption of a certain type of food. Rather, eating behavior in this syndrome appears more generally disturbed. The most striking difference between the binge and the nonbinge meals of bulimic patients and between the binge eating of patients and the overeating of normal persons is the amount of food consumed, not the macronutrient composition of the meals. In addition, for all four meal types, the patients were hungrier after the end of the meal than were the controls, even though the patients' average caloric intakes were generally larger and their average hunger ratings before the meals did not differ from those of the controls. Certainly, self-induced vomiting may contribute to this abnormality, but it was also observed after nonbinge meals when vomiting did not occur. Together, these data are consistent with the notion that the essential appetitive abnormality in bulimia nervosa lies in the control of the amount of food consumed, not in the consumption of a particular macronutrient or type of food. Patients with bulimia nervosa appear less responsive than normal to the signals that lead to the termination of a meal.(ABSTRACT TRUNCATED AT 400 WORDS)