beta-endorphin and Anorexia-Nervosa

Topics: ACTH Syndrome, Ectopic; Anorexia Nervosa; beta-Endorphin; Biomarkers; Depression; Diagnostic Techniques, Endocrine; Humans; Hypopituitarism; Mass Spectrometry; Nelson Syndrome; Pituitary ACTH Hypersecretion; Radioimmunoassay; Radioligand Assay; Reference Values; Specimen Handling

Patients with anorexia nervosa have neuroendocrine and behavioral alterations that starvation and weight loss are thought to cause, or contribute to, since they are reversed by weight restoration. We have found that anorexics have starvation-related disturbances of neuropeptide Y (NPY), corticotropin-releasing hormone (CRH), and beta-endorphin, as determined by their measurements in cerebrospinal fluid. The relationship between these neuropeptides and several symptoms in anorexia, together with findings in experimental animals, raise a possibility that changes in the activity of these neuropeptides contribute to neuroendocrine and behavioral alterations in anorexia. Specifically, a disturbance of central nervous system CRH activity is likely to be responsible for hypercortisolemia, while a disturbance of central nervous system NPY may contribute to amenorrhea. In addition, disturbances of these neuropeptides could contribute to other symptoms such as increased physical activity, hypotension, reduced sexual interest, depression, and pathological feeding behavior.

Topics: Adult; Anorexia Nervosa; beta-Endorphin; Corticotropin-Releasing Hormone; Female; Humans; Neuropeptide Y; Neuropeptides

Baseline concentrations of cholecystokinin-8 (CCK-8) and beta-endorphin (beta-EP) were measured in T-lymphocytes from 33 restricting patients with anorexia nervosa (AN-R), 23 binging/purging patients with anorexia nervosa (AN-BP), and 24 healthy volunteers. CCK-8 basal values were significantly lower and beta-EP values significantly higher in AN-R and AN-BP patients than in normal volunteers. Levels of the peptides were measured three more times during a 4-month combined cognitive-behavioral/psychopharmacological treatment (nortriptyline or fluoxetine in AN-R, fluoxetine or amineptine in AN-BP). CCK-8 values fluctuated (nonsignificantly) during each treatment, while beta-EP values decreased (to a significant degree only in fluoxetine-treated AN-R patients).

Topics: Adolescent; Adult; Anorexia Nervosa; Antidepressive Agents; beta-Endorphin; Child; Cognitive Behavioral Therapy; Combined Modality Therapy; Dibenzocycloheptenes; Female; Fluoxetine; Humans; Nortriptyline; Sincalide; T-Lymphocytes; Treatment Outcome

The combined effects of an intragastric load of glucose compared to water and of naltrexone compared to placebo were tested on preference for sucrose in six anorectic patients. While in normal subjects, glucose-induced negative allesthesia is known to disappear upon loss of weight, it persisted in anorexia nervosa (AN) despite a major weight loss; furthermore, in contrast with its effects in normoponderal subjects, naltrexone at the dose of 25 mg did not decrease the preference for sucrose nor did it enhance glucose-induced allesthesia. Basal plasma beta endorphin level determined by radioimmunoassay was higher in AN than in normal subjects (75 +/- 6.1 pmoles/l vs. 13 +/- 3.8 pmoles/l) (p less than 0.001). It is suggested that a decrease in endogenous system opiate activity might be associated with food refusal and body weight loss in anorexia nervosa.

Topics: Adolescent; Adult; Anorexia Nervosa; beta-Endorphin; Double-Blind Method; Drug Interactions; Eating; Glucose; Humans; Hunger; Naltrexone; Perceptual Disorders; Random Allocation; Time Factors

To investigate the effects of Bushen Shugan Recipe (BSSGR), a compound traditional Chinese herbal medicine, in regulating the hypothalamus-pituitary-ovarian axis (HPOA) in a rat model of stress-induced anorexia.. Anorexia was induced in rats by the methods of separation, diet restriction and constraint. Rats were divided into 4 groups randomly: control group, untreated group, sham-operated group and BSSGR group. After the experiments, body weights and oestrous cycles of the 4 groups were compared. The levels of serum estradiol (E(2)), hypophysis luteotrophic hormone (LH), hypophysis follicle stimulating hormone (FSH) and hypothalamus β-endorphin (β-EP) were detected by radioimmunoassay. The level of serum corticosterone (CORT) was detected by enzyme-linked immunosorbent assay.. Body weight of BSSGR group was significantly increased in comparison with sham-operated group(P<0.01); the oestrous cycle disordering rate was higher than those of the untreated group and sham-operated group; hypophysis LH and serum E(2) were obviously increased in comparison with untreated group (P<0.05); hypothalamus β-EP was obviously decreased in comparison with sham-operated group (P<0.05); serum CORT was obviously decreased in comparison with untreated group (P<0.05), and significantly decreased in comparison with sham-operated group (P<0.01).. BSSGR increased hypophysis LH and serum E(2), and decreased serum CORT and hypothalamus β-EP in rats with stress-induced anorexia.

Topics: Animals; Anorexia Nervosa; beta-Endorphin; Corticosterone; Drugs, Chinese Herbal; Estradiol; Female; Hypothalamo-Hypophyseal System; Luteinizing Hormone; Ovary; Oxidative Stress; Rats; Rats, Wistar

It has been reported that neuropeptides may play a role in the control of appetite and in the mechanism of hormone release. Neuropeptides such as beta-endorphin, neuropeptide Y (NPY), galanin and leptin may affect hormones release, on the other hand the hormonal status may modulate neuropeptide activity.. The material consisted of 90 obese women, 30 women with Anorexia Nervosa, and 30 healthy, lean women of control group. Plasma beta-endorphin, NPY, leptin, somatostatin and serum pituitary and gonadal hormones concentrations were measured with RIA methods.. We observed the highest plasma NPY levels in obese hypertensive and diabetic patients. After carbohydrate administration (OGTT) a marked increase of insulin, beta-endorphin and NPY was found. The blunted response of GH to GH-RH may be connected with increased somatostatin activity and hyperinsulinemia. The abnormal response of LH to opioid blockade may be a result of disturbed opioid and NPY activities in obese patients. However in patients with anorexia nervosa, plasma leptin and NPY concentrations were low. The disturbances in beta-endorphin release are also observed.. The neuroendocrine disturbances in obesity and in anorexia nervosa are opposite. The feedback mechanism between leptin and NPY is disturbed in both in obesity and in anorexia nervosa. An abnormal activity of neuropeptides may lead to disturbed control of appetite and hormonal dysregulation in eating disorders.

Topics: Adult; Anorexia Nervosa; Appetite; beta-Endorphin; Diabetes Mellitus; Feedback, Physiological; Female; Glucose Tolerance Test; Human Growth Hormone; Humans; Hypertension; Leptin; Luteinizing Hormone; Neuropeptide Y; Neuropeptides; Obesity; Somatostatin

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

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

Exercise and the endogenous opioids have been linked to anorexia nervosa. This investigation determined the effects of the weight-loss syndrome induced by voluntary exercise (22.5 h/day) in food-restricted rats (1.5 h/day food access) on the endogenous opioids. The animals were tested under resting-fed and 2-deoxy-D-glucose (2DG) stimulated conditions. Weight-matched, freely fed exercised and ad libitum fed unexercised groups served as controls. Specific opioid abnormalities were found in the syndrome. These included a basal elevation in plasma beta-endorphin, which was abnormally suppressed by 2DG, and 2DG-induced elevations in arcuate hypothalamic beta-endorphin content and supraoptic hypothalamic dynorphin-A content. None of these changes occurred in controls. Finally, it was found that short-term moderate exercise itself chronically reduced adenohypophysial beta-endorphin content and elevated supraoptic dynorphin-A content. The relationship of the syndrome's hyperendorphinism to the hypothalamo-pituitary-adrenal axis and the auto-addiction hypothesis of anorexia nervosa was considered, as was the significance of the supraoptic dynorphin-A abnormality to the hypothalamo-neurohypophysial system. The differential sensitivity of the supraoptic dynorphin-A system compared to the arcuate hypothalamic beta-endorphin system to moderate exercise was also discussed.

Topics: Animals; Anorexia Nervosa; Arcuate Nucleus of Hypothalamus; beta-Endorphin; Deoxyglucose; Dynorphins; Food Deprivation; Male; Physical Conditioning, Animal; Pituitary Gland, Anterior; Rats; Rats, Sprague-Dawley; Supraoptic Nucleus

Immunological and neuroendocrine parameters were examined in 11 women with anorexia nervosa, 6 restricted and 5 bulimic-anorectics, 17-43 years old with 2-15 years duration of the disease, and in 11 age- and sex-matched psychophysically healthy controls. The T lymphocyte proliferative response to phytohemagglutinin (PHA), plasma adrenocorticotropic hormone (ACTH), cortisol and beta-endorphin (beta-EP) levels was examined in basal conditions and after corticotropin-releasing hormone (CRH) stimulation. Cortisol inhibition by dexamethasone (DST), and basal growth hormone (GH) and prolactin (PRL) levels were also examined. The immune study did not reveal significant differences between patients and controls. ACTH and cortisol basal levels were significantly higher in anorectics, while beta-EP, GH and PRL concentrations did not differ in the two groups. ACTH, beta-EP and cortisol responses to CRH were blunted in anorectics and the DST impaired in 55% of the patients. No correlations were observed between neuroendocrine impairments and the T lymphocyte response to PHA, or between the immunological neuroendocrine parameters and the body mass index of either patients or controls.

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Analysis of Variance; Anorexia Nervosa; beta-Endorphin; Corticotropin-Releasing Hormone; Female; Humans; Hydrocortisone; Lymphocyte Activation; T-Lymphocytes

Basal morning plasma levels of immunoreactive-beta-endorphin (ir-beta-EP), and 17-beta estradiol (E2) were assessed in 25 adolescents with anorexia nervosa (AN) in comparison to 24 healthy controls. All subjects were drug free for at least 6 weeks. The mean plasma level of ir-beta-EP was significantly higher (84%) in the AN patients when compared with the control subjects. The elevated plasma ir-beta-EP may be relevant to the suppression of appetite, tolerance of fasting, and to the hypothalamic hypogonadism in AN.

Topics: Adolescent; Adult; Anorexia Nervosa; beta-Endorphin; Circadian Rhythm; Estradiol; Female; Humans

The peripheral secretion of endogenous opioids was studied in 10 women with restrictive anorexia nervosa and 10 age- and sex-matched healthy controls. The circadian rhythm of beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH), and their responses to the administration of corticotropin releasing hormone (CRH, 1 micrograms/kg body weight, i.v.), clonidine (150 microgram, i.v.), domperidone (10 mg, i.v.), and 5-hydroxytryptophan (5-HTP, 200 mg, p.o.) were examined in patients and controls. The results revealed increased nocturnal secretion of beta-EP and diurnal-nocturnal secretion of beta-LPH with loss of circadian rhythmicity of both peptides, normal response to CRH stimulation, blunted response to clonidine and domperidine, and normal beta-EP and blunted beta-LPH response to 5-HTP stimulation. The data suggest a complex alteration of peripheral opioids and of central aminergic mechanisms that regulate proopiomelanocortin-derived peptide secretion and eating behavior.

Topics: 5-Hydroxytryptophan; Adolescent; Adult; Anorexia Nervosa; beta-Endorphin; beta-Lipotropin; Body Weight; Circadian Rhythm; Clonidine; Corticotropin-Releasing Hormone; Domperidone; Endorphins; Female; Humans; Receptors, Opioid; Secretory Rate

Fourteen patients with anorexia nervosa (AN) were studied for the production of tumour necrosis factor (TNF), the activation of the interferon (IFN) system and cell-mediated cytotoxicity (CMC) and the results were compared with 16 age-matched healthy women. AN patients had significantly increased spontaneous TNF production by peripheral blood mononuclear cells (PBMC) in vitro (16 +/- 5 U/ml versus 4 +/- 3 U/ml in the control group; P less than 0.05), although no TNF was detectable in the plasma from either group. TNF production in vitro, following stimulation of PBMC by phytohaemagglutinin (PHA) or tumour cells, was similar in AN patients and controls; however, lipopolysaccharide (LPS) induced TNF production was found to be lower in AN (P less than 0.1). CMC was significantly lower in AN patients (4 +/- 2 versus 10 +/- 3 in controls, expressed as lytic units/10(6) cells; P less than 0.05), but no difference could be found between AN and controls in IFN activity as reflected by the level of the IFN-induced enzyme 2'-5' oligoadenylate synthetase (2-5A) in PBMC. Beta-endorphins in the plasma were higher in the AN group (P less than 0.05) but these levels could not be correlated to those of IFN, CMC or TNF. Defective CMC and increased TNF production by PBMC in patients with anorexia nervosa may possibly result from the nutritional deficiencies and neuroendocrine abnormalities associated with the disease, and may contribute to the pathophysiology of AN.

Topics: Adolescent; Adult; Anorexia Nervosa; beta-Endorphin; Cytotoxicity, Immunologic; Female; Humans; Interferons; Leukocytes, Mononuclear; Tumor Necrosis Factor-alpha

Topics: Adenoma; Adolescent; Adult; Amenorrhea; Anorexia Nervosa; beta-Endorphin; Female; Gonadotropins, Pituitary; Humans; Hyperprolactinemia; Pituitary Neoplasms; Thinness

The discovery that the endogenous opioid peptides contribute to the modulation of appetitive behavior and neuroendocrine function has raised questions as to whether disturbances of opioids contributes to the pathophysiology of eating disorders. To assess central nervous system (CNS) beta-endorphin in patients with anorexia nervosa we measured cerebrospinal fluid (CSF) beta-endorphin concentrations before, and at intervals after weight correction. In addition, we measured three sister peptides (beta-lipotropin, adrenocorticotropic hormone (ACTH), and the N-terminal fragment) derived from the same precursor molecule, pro-opiomelanocortin (POMC) to determine whether possible disturbances might extend to sister peptides. Underweight anorectics (58 +/- 5% of average body weight (ABW), n = 10) had significantly lower CSF concentrations of all 4 peptides compared to healthy controls (102 +/- 10% ABW, n = 11). CSF concentrations of all 4 POMC-related peptides were found to be significantly increased when the same anorectics were restudied 4 to 6 weeks after weight gain (83 +/- 4% ABW). After weight gain, levels of CSF beta-endorphin, beta-lipotropin, and ACTH were similar to controls, whereas levels of CSF N-POMC remained significantly less than controls. Another group of women, previously underweight with anorexia nervosa, but weight-restored (93 +/- 11% ABW, n = 12) for greater than 1 year had CSF concentrations of all 4 POMC-related peptides that were similar to controls. We conclude that underweight anorectics have state-associated disturbances of CNS beta-endorphin as well as other POMC-related peptides. These abnormalities are part of the neurobiological syndrome of anorexia nervosa and may contribute to the characteristic alterations in behavior and neuroendocrine function.

Topics: Adrenocorticotropic Hormone; Adult; Anorexia Nervosa; beta-Endorphin; beta-Lipotropin; Body Weight; Female; Humans; Peptide Fragments; Pro-Opiomelanocortin

Clinical and biochemical findings link anorexia nervosa (AN) and primary effective disorders (PAD). Clonidine, an alpha 2-adrenoceptor agonist, has been shown to blunt growth hormone (GH) response and greatly lower plasma cortisol in PAD patients. We examined the GH, cortisol, and beta-endorphin (beta-EP) responses to an acute clonidine challenge (150 micrograms i.v. as a bolus) before and after 30 days of treatment with desmethylimipramine in 14 women with AN. Both before and after treatment, the AN patients showed normal plasma GH and cortisol responses, but an increased plasma beta-EP response. The increased beta-EP response in AN was independent of weight and depressive symptomatology. Our data indicate that alpha 2-adrenoceptors involved in the control of GH and adrenocorticotropic hormone are not altered in AN. The increased beta-EP response may indicate elevated opioid activity in the hypothalamo-pituitary system of AN patients.

Topics: Adolescent; Adult; Anorexia Nervosa; beta-Endorphin; Clonidine; Desipramine; Endorphins; Female; Growth Hormone; Humans; Hydrocortisone

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Anorexia Nervosa; beta-Endorphin; beta-Lipotropin; Corticotropin-Releasing Hormone; Endorphins; Female; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Male; Middle Aged; Obesity; Pituitary-Adrenal System

Topics: Adolescent; Adult; Anorexia Nervosa; beta-Endorphin; beta-Lipotropin; Circadian Rhythm; Clonidine; Depressive Disorder; Desipramine; Dexamethasone; Endorphins; Female; Growth Hormone; Growth Hormone-Releasing Hormone; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Norepinephrine; Pituitary-Adrenal System; Receptors, Adrenergic

Topics: Adolescent; Adult; Anorexia Nervosa; beta-Endorphin; Cushing Syndrome; Endorphins; Humans; Middle Aged; Nelson Syndrome; Radioimmunoassay

Clinical and biochemical data suggest a link between anorexia nervosa (AN) and primary affective disorders (PAD). In 14 female patients, aged 15-40 years, with 7-month to 11-year histories of AN, we studied circadian cortisol periodicity, response to the dexamethasone suppression test (DST), and plasma levels of beta-endorphin and beta-lipotropin before and after desimipramine therapy. Possible correlations were sought among neuroendocrine impairments, weight loss, and depressive symptomatology. Impaired circadian cortisol periodicity, blunted DST response, and increased beta-endorphin plasma levels, observed in a subgroup of patients, could not be related to weight loss, either before or after therapy. Instead, a trend toward a relationship between neuroendocrine impairments and depressive symptoms was observed before and after treatment.

Topics: Adolescent; Adult; Affective Disorders, Psychotic; Anorexia Nervosa; beta-Endorphin; beta-Lipotropin; Desipramine; Dexamethasone; Endorphins; Female; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System

Topics: 17-Hydroxycorticosteroids; Adolescent; Adrenocorticotropic Hormone; Adult; Anorexia Nervosa; beta-Endorphin; Endorphins; Female; Humans; Hydrocortisone; Pituitary-Adrenal System

The aim of this study was to evaluate the role of endogenous opiates in the mechanism of decreased LH secretion in women with anorexia nervosa. For this purpose the effect of opiate receptor blockade with naloxone on LH, FSH, PRL, and beta-endorphins secretion was studied in 24 women with anorexia nervosa and 7 normal women. Serum LH, FSH, PRL, beta-endorphin-like substance, ACTH, and cortisol concentrations were measured before and after opiate receptor blockade after a single iv dose of 0.2 mg/kg naloxone or saline. Mean serum LH and FSH concentrations increased significantly after naloxone in the normal women. Eleven patients had a significant increase in serum LH concentrations in response to naloxone and 13 did not respond to naloxone with an increase in LH concentration. In the first group the basal LH values were higher than those in the second group. In the majority of patients in the first group amenorrhea preceded the wt loss, whereas in most patients in the second group amenorrhea appeared during the phase of wt loss. Naloxone did not alter pulsatile LH secretion in 6 women. No effect of naloxone on serum FSH and PRL concentrations was found. A significant increase in beta-endorphin-like substance levels after naloxone administration occurred in patients with anorexia nervosa. However, serum ACTH and cortisol concentrations were not altered in response to naloxone. In conclusion, the increase in LH release after opiate receptor blockade by naloxone suggests that endogenous opiates may play a role in the mechanism of inhibited LH secretion at least, in the majority of those women with anorexia nervosa in whom amenorrhea preceded wt loss. The results also point to a different mechanism of ACTH and beta-endorphin secretion in patients with anorexia nervosa.

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Anorexia Nervosa; beta-Endorphin; Endorphins; Female; Follicle Stimulating Hormone; Humans; Hydrocortisone; Luteinizing Hormone; Naloxone; Prolactin; Sodium Chloride

Topics: Anorexia Nervosa; beta-Endorphin; Endorphins; Female; Humans; Hypoglycemia; Male; Obesity; Physical Exertion

beta-Endorphin immunoreactivity was measured in cerebrospinal fluid of 75 medication-free subjects: normal, depressed, schizophrenic, and anorexic. No significant differences in beta-endorphin immunoreactivity were found. Affinity extraction chromatography revealed beta-lipotropin and beta-endorphin, but no apparent precursors.

Topics: Adolescent; Adult; Affective Disorders, Psychotic; Aged; Anorexia Nervosa; beta-Endorphin; Bipolar Disorder; Depressive Disorder; Endorphins; Female; Humans; Male; Middle Aged; Reference Values; Schizophrenia

In this paper we have reported the results of studies in psychiatric patient groups using the strategy of measuring opioid activity and beta-endorphin (ir) in CSF. Our findings do not lend support to the notion of excess endorphin activity in schizophrenia, but rather suggest the possibility of a decrease in endogenous opioid activity in some schizophrenic patients. In affectively ill patients our data suggest that there may be a relative change in endogenous opioid system activity across state change in manic-depressive illness. Who also found a relationship between nurses' ratings of anxiety and CSF opioid activity in depressed patients, although it is unknown whether this directly relates to the pathophysiology of this symptom, or is related to stress response. The relationship between CSF opioid activity and HPA axis activity, as reflected by urinary free cortisol excretion, supports the notion of important physiologic relationships between these systems and raises the issue of a role for the endogenous opioid system in the abnormal activation of this system in depression. Finally, the finding of increased CSF opioid activity in anorexia nervosa patients when a minimum weight coupled with data relating endogenous opioids to eating behavior raises interesting questions regarding a possible involvement of the endogenous opioid system involvement in this illness.

Topics: Adult; Anorexia Nervosa; beta-Endorphin; Bipolar Disorder; Depressive Disorder; Endorphins; Female; Humans; Male; Psychotic Disorders; Schizophrenia