beta-endorphin and Bulimia

The neuroendocrinology of bulimia nervosa has only recently been investigated, with initial research suggesting some biological overlap with both anorexia nervosa (AN) and depression. Similarities among AN, depression, and bulimia include a nonsuppressed Dexamethasone Suppression Test and an abnormal growth hormone (GH) response to thyrotropin-releasing hormone (TRH). Bulimics and anorectics both tend to have a delayed thyrotropin (TSH) response to TRH and elevated basal GH levels. Bulimics, however, have a normal GH response to clonidine, a nonblunted TSH response to TRH, low basal prolactin (PRL) levels, and may have an exaggerated PRL response to TRH. Unpublished data suggest bulimics may have a gonadotropin profile distinct from either AN or depression, as well as a variety of other endocrinopathies. Although many of these abnormalities may reflect malnutrition despite normal weight, other factors that are as yet unidentified are likely to be contributing to the neuroendocrine abnormalities seen in bulimia.

Topics: beta-Endorphin; Bulimia; Follicle Stimulating Hormone; Growth Hormone; Hormones; Humans; Hydrocortisone; Luteinizing Hormone; Prolactin; Thyrotropin

The effects of the opiate receptor antagonist, naltrexone, were examined on antecedent thoughts of binging and plasma beta-endorphin concentrations in an adolescent girl who was hospitalized with bulimia nervosa. Significant decreases in urge to binge were obtained during naltrexone administration compared with control sessions. Baseline plasma beta-endorphin concentrations for the bulimic adolescent were not different from those of nonbulimic controls, but plasma beta-endorphins increased significantly during naltrexone administration. After discharge from the hospital, the adolescent refused to take naltrexone because she felt she could not deal with her life without the "pleasure of binging." The case points to the interplay of biological and psychological factors in bulimia nervosa.

Topics: Adolescent; beta-Endorphin; Bulimia; Combined Modality Therapy; Dose-Response Relationship, Drug; Female; Humans; Motivation; Naltrexone; Patient Admission; Psychotherapy; Single-Blind Method; Thinking

A subset of the obese population (25-30%) has been reported to engage in binge eating at least twice weekly (bingers) and to exhibit personality traits and food attitudes similar to those of normoweight bulimic women (bulimics). Tricyclic antidepressants and opiate antagonists effectively suppress binge eating in normoweight bulimics. This 8-wk placebo-controlled, double-blind trial investigated the effect of naltrexone and imipramine on 33 obese bingers and 22 bulimics. Naltrexone (100-150 mg/d) produced a significant reduction in binge duration in bulimics (36 +/- 16%, median +/- SIQR; P = 0.02) whereas imipramine significantly reduced binge duration in obese bingers (88 +/- 31%; P = 0.02). A strong placebo effect was observed in obese bingers and, although a reduction in binge frequency occurred with both naltrexone and imipramine, it was not significantly different from the effect in placebo control subjects. We conclude that naltrexone and imipramine may be useful agents in the treatment of binge eating.

Topics: Adult; beta-Endorphin; Bulimia; Double-Blind Method; Female; Humans; Hyperphagia; Imipramine; Naltrexone; Obesity

The T-lymphocyte proliferative response to phytohemoagglutinin (PHA) stimulation was the same in 11 anorexic women, 6 restricted (AN-R) and 5 bulimic (AN-B), and in 11 sex- and age-matched controls, in basal conditions and after acute administration of corticotropin-releasing hormone (CRH). Basal plasma levels of ACTH and cortisol were higher in patients than in controls, while beta-endorphin (beta-EP), growth hormone (GH) and prolactin (PRL) concentrations did not differ in the two groups. ACTH and beta-EP responses to CRH stimulation were blunted in patients, while those of cortisol did not differ in the two groups. ACTH, beta-EP and cortisol responses to the dexamethasone suppression test were impaired in 55% of the patients. Baseline T-lymphocyte concentrations of cholecystokinin-8 (CCK-8) and beta-EP were measured in another group of 56 anorexics, 33 restricted and 23 bulimic, and in 24 controls. CCK-8 values were significantly lower and beta-EP values significantly higher in patients than in controls.

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Anorexia Nervosa; beta-Endorphin; Bulimia; Corticotropin-Releasing Hormone; Female; Humans; Hydrocortisone; Immune Tolerance; Lymphocyte Activation; Prolactin; Sincalide; T-Lymphocytes

In order to establish possible alterations in the secretory patterns of adrenocorticotropic hormone (ACTH), cortisol and/or beta-endorphin in bulimia nervosa, the circadian fluctuations of these hormones were evaluated in blood samples taken at 1-hour intervals over 24 h. Eleven bulimic women with normal body weight and 8 weight- and age-matched normal controls were tested during the follicular phase (days 6-8) of normal menstrual cycles. All women were hospitalized for bulimia or for checkup examinations and were tested 3 days after hospital admission. Both normal and bulimic women showed maximal ACTH, cortisol and beta-endorphin levels at 08.00 h, with minimal ACTH and beta-endorphin levels at midnight and cortisol levels at 02.00 h. The general temporal structure of all hormonal secretions coincided in the two groups. However, whereas all measured ACTH/cortisol levels were quantitatively similar in the two groups, plasma beta-endorphin concentrations were significantly higher in bulimic than in control subjects at all examined time points. The enhancement in the overall 24-hour beta-endorphin secretion suggests the presence of an increased opioid tonus in bulimic women, which might play a role in the pathophysiology of the eating disorder.

Topics: Adrenocorticotropic Hormone; Adult; beta-Endorphin; Bulimia; Circadian Rhythm; Female; Humans; Hydrocortisone; Time Factors

Concentrations of cholecystokinin-8 (CCK-8) and beta-endorphin (beta-EP) in T-lymphocytes of 26 women with bulimia nervosa (BN) and in 26 age- and sex-matched healthy comparison subjects were measured. Ten patients were then treated with 300 mg/day of fluvoxamine, p.o., and five patients were treated with 300 mg/day of amineptine, p.o., for 4 months. Concentrations of the two peptides were measured again after 1, 2, and 4 months of therapy. Basal CCK-8 values were significantly lower in patients than in healthy subjects. During fluvoxamine therapy, CCK-8 values increased, reaching normal levels by month 4 of treatment. No such increase occurred during amineptine therapy. Baseline beta-EP values were normal in the bulimic patients but had declined by month 4 of fluvoxamine therapy.

Topics: Adolescent; Adult; Antidepressive Agents, Tricyclic; beta-Endorphin; Bulimia; Cognitive Behavioral Therapy; Combined Modality Therapy; Dibenzocycloheptenes; Female; Fluvoxamine; Humans; Middle Aged; Selective Serotonin Reuptake Inhibitors; Sincalide; T-Lymphocytes; Treatment Outcome

Dissociation is made manifest by a failure to integrate thoughts, feelings, memories, and actions into a unified sense of consciousness. Although dissociation is presumed to be a special state of consciousness manifested by state-dependent memory and physiology, the psychobiology of dissociation is poorly understood. In this study, we examined cerebrospinal fluid levels of the major monoamine metabolites and beta-endorphin in patients with eating disorders (11 with anorexia nervosa, 16 with bulimia nervosa), while they were acutely ill. Dissociative capacity was measured using the Dissociative Experiences Scale (DES). We provide evidence that neurochemical changes in dopaminergic, serotonergic, and opioid systems may be associated with the clinical expression of dissociation in patients with eating disorders during the acute phase of their illness. These preliminary results are compatible with previous studies of neurochemical disturbances in the eating disorders and suggest that future work in dissociation should specifically include examination of these neurobiologic systems.

Topics: Adolescent; Adult; Anorexia Nervosa; beta-Endorphin; Body Weight; Brain; Bulimia; Dissociative Disorders; Female; Homovanillic Acid; Humans; Hydroxyindoleacetic Acid; Hypnosis; Mental Recall; Methoxyhydroxyphenylglycol; Neurotransmitter Agents; Pilot Projects; Synaptic Transmission

Preclinical and clinical evidence suggests that central opioid dysfunction may play a role in the pathophysiology of the eating disorders. In particular, endogenous opioids are known to regulate feeding behavior, mood, perception, and neuroendocrine function, all of which are disturbed in patients with eating disorders. Although low concentrations of CSF beta-endorphin have been reported in low-weight patients with anorexia nervosa, central opioid activity in normal-weight patients with bulimia nervosa has not been reported. The authors therefore measured CSF concentrations of beta-endorphin and dynorphin in drug-free female patients with DSM-III-R-defined bulimia nervosa and normal comparison subjects.. After 4 days of a low monoamine diet and overnight bed rest, CSF was obtained (12-26 cc) from 11 women with bulimia and 17 normal comparison subjects (eight women and nine men).. The women with bulimia had significantly lower CSF concentrations of beta-endorphin than did the female comparison subjects. However, CSF concentrations of dynorphin were not significantly different in patients and female or male comparison subjects. beta-Endorphin concentrations were inversely correlated with Beck Depression Inventory scores and the depression subscale of the Eating Disorders Inventory.. These data support a role for central opiates in the mediation of the pathophysiology of the signs and symptoms of bulimia nervosa, although it is impossible to rule out the effects of depression on the results.

Topics: Adult; beta-Endorphin; Bulimia; Dynorphins; Endorphins; Female; Humans; Male; Personality Inventory; Psychiatric Status Rating Scales; Sex Factors