beta-endorphin and Mood-Disorders

The Bonny Method of Guided Imagery and Music (GIM) is a music-centered approach to exploring consciousness for personal growth and transformation. Applications have been reported in a variety of clinical and nonclinical contexts.. The purpose of this study was to review evidence that a series of Bonny Method of GIM sessions may promote positive health outcomes in adults.. This systematic review examined randomized and nonrandomized controlled trials and repeated measures designs that reported psychological or physiological outcomes following a series of at least six individual Bonny Method of GIM sessions. Researchers assessed each study for risk of bias and computed effect sizes for outcome variables.. Of 270 non-duplicate titles retrieved, nine met criteria for inclusion, and eight had moderate or low risk of bias. These included 275 participants 18-78 years of age representing a variety of populations. Multiple studies measured anxiety, depression, mood disturbance, interpersonal problems, quality of life, sense of coherence, and/or psychiatric symptoms and found medium to large effect sizes. Four included physiological measures (systolic and diastolic blood pressure, beta-endorphin, cortisol, and pain) and reported medium to large effect sizes, none of which were replicated across studies in this review.. Evidence is promising that a series of Bonny Method of GIM sessions may be effective for improving both psychological and physiological health and may be therapeutically indicated for adults seeking treatment with medical, mental health, and nonclinical needs. Further research is needed to replicate findings within outcomes and populations.

Topics: Anxiety; beta-Endorphin; Bias; Blood Pressure; Controlled Clinical Trials as Topic; Depression; Humans; Hydrocortisone; Imagery, Psychotherapy; Mental Health; Mood Disorders; Music; Music Therapy; Pain; Quality of Life; Treatment Outcome

The contrasting findings obtained in the studies that have attempted to correlate the stage of endometriosis with severity of pain symptoms suggest that some specific characteristics of the lesions are more implicated in the genesis of pain than disease extension per se. Thus, fresh, metabolically active, intraperitoneal implants may cause functional pain symptoms such as dysmenorrhea, whereas infiltrating, nodular and fibrotic lesions are responsible for organic-type pain such as deep dyspareunia. Women with symptomatic endometriosis seem to have reduced peripheral beta-endorphin production in comparison with pain patients without the disease, although neuroendocrine modulation of pelvic nociceptive stimuli is far from clear. There is little evidence to support the notion that specific psychiatric features render some women more vulnerable to developing endometriosis, as results from investigations performed on women with asymptomatic lesions are very similar to normative data. Moreover, it appears that the psychological profile of symptomatic patients with the disease is no different from those with pain and a normal pelvis or other gynecological conditions. Consequently, the local biochemical and physical effects of lesions seem to be the most important factors in determining frequency and severity of symptoms.

Topics: beta-Endorphin; Dysmenorrhea; Dyspareunia; Endometriosis; Female; Genitalia, Female; Humans; Laparotomy; Mood Disorders; Pain; Peritoneal Diseases

The purpose of this article is to review the literature on the effects of the menstrual cycle on dependent variables in mood disorder research to inform investigators which physiological measures are likely to be significantly affected by menstrual cycle fluctuations and precisely how they might be affected. The following variables are discussed: prolactin; growth hormone; the hypothalamic-pituitary-thyroid axis (including thyrotropin, triiodothyronine, and thyroxine); the hypothalamic-pituitary-adrenal axis (cortisol, corticotropin, and beta-endorphin); melatonin; sleep; body temperature; and neurotransmitter activity (serotonergic and adrenergic systems). Body temperature and plasma and urinary norepinephrine vary predictably over the menstrual cycle. Prolactin and beta-endorphin may have peaks in the periovulatory phase, whereas serotonin levels in platelet-poor plasma may reach a nadir at that time. Triiodothyronine, thyroxine, cortisol, and melatonin do not appear to vary systematically over the course of the menstrual cycle, whereas the data for growth hormone, thyrotropin, corticotropin, and sleep are inconclusive.

Topics: Adult; beta-Endorphin; Body Temperature; Circadian Rhythm; Depressive Disorder; Female; Growth Hormone; Humans; Hydrocortisone; Melatonin; Menstrual Cycle; Mood Disorders; Premenstrual Syndrome; Prolactin; Research Design; Seasons; Serotonin; Sleep; Thyroid Hormones

Topics: beta-Endorphin; Double-Blind Method; Female; Humans; Mood Disorders; Naltrexone; Opioid Peptides; Pilot Projects; Placebo Effect; Premenstrual Syndrome; Surveys and Questionnaires

In order to receive a further understanding of stress-regulation in depressed suicide attempters, peptides that are supposed to be related to the stress system (the hypothalamic-pituitary-adrenal (HPA) axis and the autonomic nervous system) were studied in plasma. When compared with healthy controls, cortisol was high (p<0.001) and corticotropin releasing hormone (CRH) and neuropeptide Y (NPY) appeared to be low (p<0.001) in patients who had recently attempted suicide. Patients who had repeatedly attempted suicide had the lowest NPY. A correlation between NPY and cortisol (p<0.05) was found in suicidal patients with depression NOS, whereas beta-endorphins correlated with cortisol (p<0.01) in suicidal patients with major depressive disorder. A postdexamethasone decrease of NPY was noted in the controls but not in the patients. These results suggest stress system alterations in suicidal patients with mood disorders.

Topics: Adult; Age Factors; Anti-Inflammatory Agents; beta-Endorphin; Corticotropin-Releasing Hormone; Dexamethasone; Female; Humans; Male; Mood Disorders; Neuropeptide Y; Psychiatric Status Rating Scales; Sex Factors; Stress, Psychological; Suicide, Attempted

This article presents a series of experiments that involves the development of three novel strategies for human stress research and the utilization of these strategies to examine neurobehavioral processes of stress in healthy volunteers, schizophrenia, and affective illness. The first strategy involved intravenous 2-deoxy-D-glucose (2DG) administration, a glucoprivic stressor. We found that glucoprivic stress results in dissociation of hypothalamus-pituitary-adrenal (HPA), adrenomedullary, and sympathoneural activity. In addition, glucoprivic stress in neuroleptic-treated schizophrenic patients caused heightened dopamine activity, as reflected by increased plasma homovanillic acid (HVA) levels and decreased adaptive responses as assessed by decreased food consumption following 2DG administration. These data suggest that neuroleptics do not prevent stress-related increases in dopamine activity and that schizophrenia may be associated with abnormalities in the stress response. The second strategy assessed effects of uncontrollable and identical amounts of controllable stress in volunteers and depressed patients. In volunteers, it was found that uncontrollable in comparison to controllable stress results in specific behavioral and neuroendocrine alterations. Moreover, uncontrollable stress exposure in depressed patients in comparison to volunteers produced greater alterations in behavioral ratings and plasma cortisol levels and that the uncontrollable stress related increases in helplessness ratings and cortisol levels were significantly correlated. These data suggest that depressed patients may have increased sensitivity to uncontrollable stress and that there may be an important interrelationship between the cognitive deficits of depression and the heightened HPA axis activity observed in these patients. Lastly, we used a naturalistic strategy to examine mechanisms relating childhood parental loss and the development of adult affective illness and found that among subjects with early parental loss histories, those who developed adult psychiatric illness had increased resting plasma levels of cortisol and beta-endorphin (ir) as compared with subjects with early loss and no adult history of psychiatric illness. Moreover, increased HPA activity in adulthood was significantly related to poor childhood adjustment to parental loss. The implications of the results of these studies are discussed.

Topics: Adrenocorticotropic Hormone; Adult; Arousal; beta-Endorphin; Blood Glucose; Clinical Trials as Topic; Deoxyglucose; Depressive Disorder; Double-Blind Method; Epinephrine; Female; Fluphenazine; Grief; Homovanillic Acid; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Male; Mental Disorders; Methoxyhydroxyphenylglycol; Mood Disorders; Norepinephrine; Pituitary-Adrenal System; Schizophrenia; Stress, Psychological

The opioid system modulates the central reinforcing effects of ethanol and participates in the etiology of addiction. However, the pharmacotherapy of ethanol dependence targeted on the opioid system is little effective and varies due to individual patients' sensitivity. In the present study, we used two mouse lines with high (HA) and low (LA) activity of the endogenous opioid system to analyze the effect of opioid receptor blockade on ethanol drinking behavior. We found that LA and HA lines characterized by divergent magnitudes of swim stress-induced analgesia also differ in ethanol intake and preference. Downregulation of the opioid system in LA mice was associated with increased ethanol consumption. Treatment with a non-selective opioid receptor antagonist (naloxone) had no effect on ethanol intake in this line. Surprisingly, in HA mice, the blockage of opioid receptors led to excessive ethanol consumption. Moreover, naloxone selectively induced high levels of anxiety- and depressive-like behaviors in HA mice which was attenuated by ethanol. With the use of specific opioid receptor antagonists we showed that the naloxone-induced increase in ethanol drinking in HA mice is mediated mainly by δ and to a lower extent by μ opioid receptors. The effect of δ-opioid receptor antagonism was abolished in HA mice carrying a C320T transition in the δ-opioid receptor gene (EU446125.1), which impairs this receptor's function. Our results indicate that high activity of the opioid system plays a protective role against ethanol dependence. Therefore, its blockage with opioid receptor antagonists may lead to a profound increase in ethanol consumption.

Topics: Alcohol Drinking; Analgesia; Analysis of Variance; Animals; beta-Endorphin; Central Nervous System Depressants; Disease Models, Animal; Ethanol; Genotype; Maze Learning; Mice; Mood Disorders; Morphinans; Naloxone; Narcotic Antagonists; Receptors, Opioid, delta; Stress, Psychological; Swimming

The aims of this study were to determine whether the administration of cortisol has a significant effect on mood in patients with depression and whether the effects of cortisol on changes in plasma hormone concentrations are like those of synthetic corticosteroids. Twelve patients had major depression and one each had dysthymic disorder and a depressive adjustment disorder. Five were male and nine were female. All were in-patients. Eight normal subjects, two females and six males, were used as controls. Basal beta-endorphin concentrations were 2- to 3-fold higher in depressed patients than in control subjects, but there were no significant differences between the patient and control groups in the basal (pre-infusion) plasma concentrations of ACTH, cortisol, growth hormone or prolactin. Cortisol, but not saline infusion resulted in a significant improvement in self rated mood. Surprisingly, cortisol infusion at first increased plasma beta-endorphin concentrations. At later times after cortisol infusion, plasma beta-endorphin concentrations decreased as did the plasma concentrations of ACTH and growth hormone; prolactin levels were increased. These results show (i) that cortisol infusion raises mood significantly in major depression, (ii) that plasma beta-endorphin concentration is a potential marker of major depression (iii) that rather than blunting of corticosteroid effects, responses to cortisol may even be enhanced in depressive illness. The unexpected, initial increase in beta-endorphin stimulated by cortisol, suggests that the action of cortisol is not simply one of negative feedback inhibition, but may involve mineralocorticoid, as well as glucocorticoid receptors.

Topics: Adrenocorticotropic Hormone; Adult; Affect; Antidepressive Agents; beta-Endorphin; Depressive Disorder; Female; Growth Hormone; Humans; Hydrocortisone; Infusions, Intravenous; Male; Middle Aged; Mood Disorders; Pituitary Gland; Prolactin; Psychiatric Status Rating Scales; Radioimmunoassay

Human IgG specific for beta-endorphin was identified by enzyme-linked immunoabsorbent assay and isolated by affinity chromatography. From a sample of 27 subjects, three individuals with major depression demonstrated plasma IgG highly reactive with human beta-endorphin, while four other subjects (two with depression and two randomly selected blood donors) had intermediate reactivity. The recognition site for beta-endorphin was retained by F(ab')2 fragments.

Topics: Adult; beta-Endorphin; Chromatography, Affinity; Endorphins; Enzyme-Linked Immunosorbent Assay; Female; Humans; Immunoglobulin Fab Fragments; Immunoglobulin G; Male; Middle Aged; Mood Disorders; Neuropeptides

Topics: beta-Endorphin; Endorphins; Female; Humans; Monoamine Oxidase; Mood Disorders; Pregnancy; Prolactin; Puerperal Disorders

This study compared basal concentrations of plasma beta-endorphin/beta-lipotropin-like immunoreactivity and dexamethasone suppression of cortisol in seven chronic pain patients, seven psychiatric disorder patients, and seven normal volunteers. Pain patients and psychiatric patients showed significantly higher basal concentrations of beta-endorphin/beta-lipotropin-like immunoreactivity compared to normal volunteers. Pain patients also had significantly higher beta-endorphin/beta-lipotropin-like immunoreactivity than psychiatric patients, even though there was no significant difference in severity of depressive symptomatology as assessed by Beck and Hamilton scores. Resistance to dexamethasone occurred in 57% of pain patients. These results may indicate that biological markers for depression occur in populations of chronic pain patients, or may reflect levels of central nervous system arousal in response to stress, pain, or nonaffective phenomena.

Topics: Adult; Alcoholism; beta-Endorphin; beta-Lipotropin; Chronic Disease; Depression; Dexamethasone; Endorphins; Female; Humans; Hydrocortisone; Male; Mental Disorders; Middle Aged; Mood Disorders; Pain; Radioimmunoassay; Syndrome

Topics: Adrenocorticotropic Hormone; Adult; Aged; beta-Endorphin; beta-Lipotropin; Depressive Disorder; Desipramine; Endorphins; Female; Follicle Stimulating Hormone; Growth Hormone; Humans; Luteinizing Hormone; Male; Methoxyhydroxyphenylglycol; Middle Aged; Mood Disorders; Pituitary Gland, Anterior

Topics: Adrenocorticotropic Hormone; Adult; beta-Endorphin; beta-Lipotropin; Chronic Disease; Endorphins; Female; Haloperidol; Humans; Male; Middle Aged; Mood Disorders; Schizophrenia