Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Hyperphagia in premenstrual tension syndrome. 293 23

Plasma samples were collected twice during the follicular phase and three times during the luteal phase of the menstrual cycle in 12 women with premenstrual tension (PMT) and in 14 control subjects without symptoms. Concentrations of beta-endorphin (beta-E) immunoreactivity, cortisol, oestradiol, progesterone and LH were determined. Comparison of the mean concentrations of LH, cortisol, oestradiol and progesterone did not reveal any statistically significant differences between the PMT and the control groups. In the early luteal phase, the mean plasma beta-E immunoreactivity was lower in the PMT group (10.7, SE 0.7 pg/ml) than in the control group (14.6, SE 1.6 pg/ml, P less than 0.05), suggesting that endorphin secretion is decreased in PMT. No significant change in the plasma beta-E level was found in the PMT patients between the follicular and luteal phase when symptoms appeared. This does not exclude the possibility that in the central nervous system abnormal changes occur in the activity of endogenous opioids in PMT.
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PMID:Plasma beta-endorphin immunoreactivity in premenstrual tension. 294 74

The authors present a case report that provides support for a relationship between estrogen and the menstrual cycle on the 1 hand and affective disorders on the other. The patient in this case, a 35-year old woman, suffered from a rapid cycling affective disorder that was severely affected by her menstrual cycle and responded positively to oral contraceptives (OCs). The patient had a 24-year history of numerous manic and depressive episodes, the 1st of which coincided with menarche. She had noted that, 4 days before menses, she would experience symptoms of premenstrual tension syndrome (PMS) and often the onset of an affective episode. Treatment with a series of psychotropic agents had not been effective in controlling the number of episodes. However, the patient reported that there had been an 8-9-month period in the past when she had taken OCs and had fewer symptoms. Thus, the patient was placed on Ortho-Novum as well as imipramine. At the 9-month follow-up, she reported there had been no further episodes of depression or mania. The exact mechanism behind estrogen's psychotropic effect is unclear, although it increases the central availability of norepinephrine and induces changes in dopaminergic, noradrenergic, and serotonergic receptors. Beta-endorphin levels covary with estrogen levels, and estrogen seems to affect every major neurotransmitter system. The fact that estrogen has not consistently been shown to be effective in this regard may only signify the existence of a distinct subclass of affective disorders closely linked to the menstrual cycle. This subclass may have some type of dysfunction within the hypothalamic-pituitary-gonadal axis that contributes to mood swings.
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PMID:Antidepressant effects of estrogen. 405 18

The authors propose that premenstrual tension syndrome (PMS) is the result of beta-endorphin withdrawal. Sixteen women were included in this study which measured beta-endorphin levels on the 7th and 24th day of each woman's menstrual cycle. A significant decline in beta-endorphin levels was noted during the progression of the cycle. The severity of symptoms, however, was inversely proportional to the amount of decline in beta-endorphin levels. It is hypothesized that the attenuation of endorphin decline may be a compensatory mechanism to moderate the severity of PMS symptoms.
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PMID:beta-Endorphin withdrawal: a possible cause of premenstrual tension syndrome. 609 1

Stress activates the central and peripheral components of the stress system, i.e., the hypothalamic-pituitary-adrenal (HPA) axis and the arousal/sympathetic system. The principal effectors of the stress system are corticotropin-releasing hormone (CRH), arginine vasopressin, the proopiomelanocortin-derived peptides alpha-melanocyte-stimulating hormone and beta-endorphin, the glucocorticoids, and the catecholamines norepinephrine and epinephrine. Appropriate responsiveness of the stress system to stressors is a crucial prerequisite for a sense of well-being, adequate performance of tasks and positive social interactions. By contrast, inappropriate responsiveness of the stress system may impair growth and development, and may account for a number of endocrine, metabolic, autoimmune and psychiatric disorders. The development and severity of these conditions primarily depend on the genetic vulnerability of the individual, the exposure to adverse environmental factors and the timing of the stressful event(s), given that prenatal life, infancy, childhood and adolescence are critical periods characterized by increased vulnerability to stressors. The developing brain undergoes rapid growth and is characterized by high turnover of neuronal connections during the prenatal and early postnatal life. These processes and, hence, brain plasticity, slow down during childhood and puberty, and plateau in young adulthood. Hormonal actions in early life, and to a much lesser extent later, can be organizational, i.e., can have effects that last for long periods of time, often for the entire life of the individual. Hormones of the stress system and sex steroids have such effects, which influence the behavior and certain physiologic functions of individuals for life. Exposure of the developing brain to severe and/or prolonged stress may result in hyperactivity/hyperreactivity of the stress system, with resultant amygdala hyperfunction (fear reaction), decreased activity of the hippocampus (defective glucocorticoid-negative feedback, cognition), and the mesocorticolimbic dopaminergic system (dysthymia, novelty-seeking, addictive behaviors), hyperactivation of the HPA axis (hypercortisolism), suppression of reproductive, growth, thyroid and immune functions, and changes in pain perception. These changes may be accompanied by abnormal childhood, adolescent and adult behaviors, including excessive fear ('inhibited child syndrome') and addictive behaviors, dysthymia and/or depression, and gradual development of components of the metabolic syndrome X, including visceral obesity and essential hypertension. Prenatal stress exerted during the period of sexual differentiation may be accompanied by impairment of this process with behavioral and/or somatic sequelae. The vulnerability of individuals to develop varying degrees and/or components of the above life-long syndrome is defined by as yet unidentified genetic factors, which account for up to 60% of the variance. CRH has marked kindling and glucocorticoids have strong consolidating properties, hence both of these hormones are crucial in development and can alone produce the above syndrome. CRH and glucocorticoids may act in synergy, as in acoustic startle, while glucocorticoids may suppress or stimulate CRH, as in the hypothalamus and amygdala, respectively. A CRH type 1 receptor antagonist, antalarmin, inhibits both the development and expression of conditioned fear in rats, and has anxiolytic properties in monkeys. Profound stressors, such as those from sexual abuse, may elicit the syndrome in older children, adolescents and adults. Most frequently, chronic dysthymia and/or depression may develop in association with gastrointestinal complaints and/or the premenstrual tension syndrome. A lesser proportion of individuals may develop the classic posttraumatic stress disorder, which is characterized by hypocortisolism and intrusive and avoidance symptoms; in younger individuals it may present as dissociative personality disorder.
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PMID:Pediatric stress: hormonal mediators and human development. 1264 70