beta-endorphin and Feeding-and-Eating-Disorders

There is evidence that endogenous opiates are involved in the control of feeding in experimental animals. Several types of experimental obesity are associated with increased opiate production and/or increased numbers and sensitivity of opiate receptors. Research with experimental animals suggests that nutrients, particularly sugar, have an effect on feeding behavior that is mediated by opiates. For instance, the obesity-producing effect of a palatable diet in rodents is blocked by opiate antagonists. Stress induced feeding in rodents leads to preferential sucrose ingestion and is blocked by opiate antagonists and beta-endorphin. The effect of nutrients on the endogenous opiate system of humans is less clear. Clinical experience suggest that carbohydrates (sugar in particular) play a role in binge eating and obesity. Many binge eaters preferentially eat sweets during a binge. Many obese individuals consume more than half of their total daily calories as carbohydrates. Sweet snacking is a frequent behavior at times of stress. Recent evidence suggests that sugar can lead to increased beta-endorphin production in obese subjects.

Topics: Animals; beta-Endorphin; Diet; Endorphins; Feeding and Eating Disorders; Feeding Behavior; Glucose; Humans; Hyperphagia; Male; Naloxone; Narcotics; Obesity; Time Factors

This review summarizes recent work that focuses on the role of endogenous opioids (EOs) and opiate receptors in the control of food intake. Although the anorexic effect of opiate antagonists are now well accepted, the exact EO, site(s), and mechanism(s) of action remain to be established. However, accumulating evidence suggests that dynorphin, an endogenous ligand for kappa-type opiate receptors, is an important regulator (stimulant) of appetite. The roles of other EOs, such as beta-endorphin, are less clear. EOs appear to be involved in maintaining normal feeding behavior and are likely responsible for the overconsumption of fat in genetically obese and stressed subjects. Opiate antagonists block overconsumption of palatable foods, thus offering a promising approach to weight reduction for some overweight individuals. Anorexias may follow from a deficiency of kappa-type opioid activity, and surprisingly, can also result from excess opioid activity. Indeed, opiate antagonists of the mu type (naloxone) can enhance eating and weight gain in certain anorexic conditions. Therefore, it appears that excess opioid agonist activity may result in hyperphagia or anorexia (depending on the opiate receptor type). Finally, opiate antagonists may help normalize both types of pathological feeding states.

Topics: Animals; Anorexia; Appetite Regulation; beta-Endorphin; Dynorphins; Endorphins; Feeding and Eating Disorders; Food Preferences; Humans; Models, Biological; Narcotic Antagonists; Receptors, Opioid; Stress, Physiological

Abnormalities in plasma concentrations of beta-endorphin-like immunoreactivity (beta-endorphin) have been reported in depressed patients. This study was done to test the hypothesis that specific clinical characteristics of depression are associated with plasma beta-endorphin concentration.. Plasma beta-endorphin was evaluated in 20 depressed patients diagnosed according to DSM-III-R and in 23 age- and sex-matched comparison subjects, and each was evaluated with the structured Schedule for Affective Disorders and Schizophrenia (SADS). Twelve SADS items involving dysphoric mood and related symptoms were chosen for analysis.. Within the group of all 43 subjects and within the depressed group, beta-endorphin level correlated significantly with psychic anxiety and with phobia. In the depressed group only, beta-endorphin also correlated significantly with obsessions/compulsions. Concentration of beta-endorphin was not significantly correlated with score on the Hamilton Rating Scale for Depression or Beck Depression Inventory or with scores on other SADS symptom items, including somatic anxiety, insomnia, subjective anger, overt anger, agitation, psychomotor retardation, panic attacks, appetite loss, or total weight loss. In the group of 23 comparison subjects, beta-endorphin did not correlate with Beck or Hamilton depression score or with any of the SADS clinical variables.. High levels of plasma beta-endorphin may be associated with more severe anxiety, phobia, and obsessions/compulsions in depressed patients.

Topics: Adult; Aged; Anger; Anxiety Disorders; beta-Endorphin; Depressive Disorder; Feeding and Eating Disorders; Humans; Male; Middle Aged; Obsessive-Compulsive Disorder; Phobic Disorders; Psychiatric Status Rating Scales; Psychomotor Disorders; Severity of Illness Index; Sleep Initiation and Maintenance Disorders; Weight Loss

The plasma beta-endorphin response to glucose ingestion was compared in 8 bulimics and 8 controls. The bulimics demonstrated a sustained elevation of plasma beta-endorphin unrelated to glucose ingestion throughout the 5-hour study period. It is hypothesized that such an elevation of beta-endorphin is the result of stress and that it may play an important role in the perpetuation of the binge-vomiting cycle.

Topics: Adolescent; Adult; beta-Endorphin; Blood Glucose; Dietary Carbohydrates; Endorphins; Feeding and Eating Disorders; Female; Humans; Hyperphagia; Radioimmunoassay

To study the possible role of plasma beta-endorphin in bulimia, we measured plasma beta-endorphin immunoreactivity in 34 female patients with normal-weight bulimia and 34 normal female controls matched for weight as percent of ideal. Plasma beta-endorphin immunoreactivity in bulimics (mean 59.6 pg/ml; SEM 5.6) was significantly lower (p less than 0.05) than in controls (mean 79.5 pg/ml; SEM 8.5). Within the bulimic group, plasma beta-endorphin immunoreactivity correlated inversely with severity of bulimic symptomatology as measured by the Eating Attitudes Test Bulimia Subscale (p less than 0.05). Endorphin level did not correlate with severity of depression or with percent ideal body weight. Abnormalities in opioid metabolism may be implicated in eating disorders and account for the addictive properties of these disorders.

Topics: Adult; beta-Endorphin; Depression; Endorphins; Feeding and Eating Disorders; Feeding Behavior; Female; Humans; Hyperphagia; Psychological Tests; Radioimmunoassay

The relationship between premenstrual tension syndrome and dietary intake was studied in a population of 20 young adult women. Caloric intake was measured during the 10 days preceding and following the menstrual cycle. Those women with more severe symptoms recorded a greater increase in caloric intake. Caloric intake during the premenstrual period also increased with age. It is hypothesized that this caloric intake may be due to increased beta-endorphin levels.

Topics: Adult; Age Factors; beta-Endorphin; Endorphins; Energy Intake; Feeding and Eating Disorders; Female; Humans; Hyperphagia; Premenstrual Syndrome

Two experimental situations induce hyperphagia in the rat: the cafeteria model and the tail-pinching model. In non-deprived rats which are offered for one hour a choice of 3 liquid cafeteria items in addition to ordinary chow and water, mild tail-pinching results in a preferential sucrose hyperphagia; naltrexone (2.5 mg/kg IP) suppresses this stress-induced hyperphagia; beta-endorphin (3 micrograms ICV) has the same effect. This apparent discrepancy is discussed: the antagonist may suppress the hyperphagia because it suppresses the reward provoked by the sucrose, the agonist because it makes it unnecessary.

Topics: Animals; beta-Endorphin; Endorphins; Feeding and Eating Disorders; Food; Food Preferences; Humans; Hyperphagia; Male; Naltrexone; Nociceptors; Rats; Rats, Inbred Strains; Stress, Psychological; Sucrose