The effects of alcoholism on the hypothalamic‐pituitary‐adrenal axis: interaction with endogenous opioid peptides

Inder, Warrick J.; Joyce, Peter R.; Ellis, M. J.; Evans, Margaret J.; Livesey, J. H.; Donald, R. A.

doi:10.1111/j.1365-2265.1995.tb02033.x

Cited by 75 publications

(58 citation statements)

References 53 publications

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“…Acute and protracted withdrawal form alcohol is coupled with decreased levels of both plasma corticosterone and hypothalamic CRF-like immunoreactivity in alcohol dependent rats [Zorrilla et al, 2001]. In humans, acute exposure to alcohol profoundly activates the HPA axis, and many alcoholics develop HPA tolerance after chronic alcohol exposure [Adinoff et al, 1990;Inder et al, 1995]. In contrast, acute alcohol withdrawal transiently activates HPA axis [Hundt et al, 2001;Zimmermann et al, 2003].…”

Section: V1b Receptor and Arginine Vasopressin (Avp) Systemmentioning

confidence: 99%

Involvement of Activated Brain Stress Responsive Systems in Excessive and “Relapse” Alcohol Drinking in Rodent Models: Implications for Therapeutics

Zhou

Kreek

2018

J Pharmacol Exp Ther

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Addiction to specific drugs (such as alcohol, psychostimulants and opioids) shares some common direct or downstream effects on the brain stress-responsive systems, including arginine vasopressin and its V1b receptors, dynorphin and the kappa opioid receptors, proopiomelanocortin/β-endorphin and the mu opioid receptors, and the endocannabinoids. Further study of these systems, through laboratory-based and translational research, could lead to the discovery of novel treatment targets and the early optimization of interventions (for example, combination) for the pharmacological therapy of alcoholism.

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Section: V1b Receptor and Arginine Vasopressin (Avp) Systemmentioning

confidence: 99%

Involvement of Activated Brain Stress Responsive Systems in Excessive and “Relapse” Alcohol Drinking in Rodent Models: Implications for Therapeutics

Zhou

Kreek

2018

J Pharmacol Exp Ther

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“…Acute administration of intoxicating doses of alcohol also activates the hypothalamic-pituitary-adrenal (HPA) axis thereby increasing ACTH and glucocorticoid levels (Inder et al 1995;Rivier et al 1984;Waltman et al 1993). It remains unclear whether alcohol-induced activation of the HPA axis has any relationship to its reinforcing properties.…”

Section: Alcohol Ingestion Activates the Autonomic Nervous System Andmentioning

confidence: 99%

“…Alcohol has less predictable effects on blood pressure, with reports of blood pressure increases (Iwase et al 1995;Sellers et al 1972) and no effects following alcohol ingestion (Turkkan et al 1988;van de Borne et al 1997). Finally, alcoholinduced peripheral vasodilation and associated skin temperature increases have been consistently reported (Iwase et al 1995;Turkkan et al 1988) and is thought to be one explanation for the lack of a consistent rise in blood pressure after alcohol consumption.Acute administration of intoxicating doses of alcohol also activates the hypothalamic-pituitary-adrenal (HPA) axis thereby increasing ACTH and glucocorticoid levels (Inder et al 1995;Rivier et al 1984;Waltman et al 1993). It remains unclear whether alcohol-induced activation of the HPA axis has any relationship to its reinforcing properties.…”

mentioning

confidence: 99%

Naltrexone Dampens Ethanol-Induced Cardiovascular and Hypothalamic- Pituitary-Adrenal Axis Activation

McCaul

2001

Neuropsychopharmacology

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Alcohol ingestion activates the autonomic nervous system and the hypothalamic-pituitary-adrenal axis. This study examined naltrexone effects on alcohol-induced increases in physiological responses and their association with alcohol liking. Using a within-subjects design, heavy drinking men (N ϭ 19) were maintained on each of three naltrexone doses (0, 50, and 100 mg, p.o.) over an 8-day inpatient stay. Within each naltrexone dose, subjects had three alcohol challenge sessions (none, moderate, high) The brain opioid system has been proposed to be part of the neurocircuitry involved in alcohol reward and heavy alcohol drinking (Froehlich and Wand 1997;Gianoulakis and deWaele 1994;Reid et al. 1991). Pharmacological studies indicate that opioid receptor antagonists, such as naloxone hydrochloride and naltrexone, decrease alcohol self-administration in animal models (Altshuler et al. 1980;Froehlich et al. 1990;Hubbell et al. 1986Hubbell et al. , 1991Marfaing-Jallat et al. 1983;Samson and Doyle 1985;Weiss et al. 1990). Clinical trials demonstrated that naltrexone reduces alcohol drinking and self-reported "high," alcohol craving, as well as relapse rates in recently abstinent outpatient alcohol-dependent patients (O'Malley et al. 1992;Volpicelli et al. 1992Volpicelli et al. , 1995 . These findings led to naltrexone's approval by the Food and Drug Administration as a pharmacotherapeutic agent for the treatment of alcohol dependence. Naltrexone is thought to reduce alcohol-induced high and relapse by binding to opioid receptors in discrete brain regions associated with reward and craving, and to prevent receptor activation by alcohol-induced release of endogenous opioid peptides.Alcohol induces a variety of acute physiological responses when consumed in moderate-to-high doses. It is well established that intoxicating doses of alcohol increase heart rate (Docter et al. 1966;Iwase et al. 1995 McCaul et al. 1989;Sellers et al. 1972;Turkkan et al. 1988;van de Borne et al. 1997). These heart rate increases are hypothesized to be positively associated with the reinforcing or appetitive motivational effects of alcohol (Peterson et al. 1996) . Alcohol has less predictable effects on blood pressure, with reports of blood pressure increases (Iwase et al. 1995;Sellers et al. 1972) and no effects following alcohol ingestion (Turkkan et al. 1988;van de Borne et al. 1997). Finally, alcoholinduced peripheral vasodilation and associated skin temperature increases have been consistently reported (Iwase et al. 1995;Turkkan et al. 1988) and is thought to be one explanation for the lack of a consistent rise in blood pressure after alcohol consumption.Acute administration of intoxicating doses of alcohol also activates the hypothalamic-pituitary-adrenal (HPA) axis thereby increasing ACTH and glucocorticoid levels (Inder et al. 1995;Rivier et al. 1984;Waltman et al. 1993). It remains unclear whether alcohol-induced activation of the HPA axis has any relationship to its reinforcing properties. Rodent studies show that alcohol increases pla...

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“…10 Excessive alcohol consumption has been shown to blunt the ACTH and cortisol responses to CRH 29 and impair dexamethasone suppression of plasma cortisol. 30 We assessed alcohol intake in all subjects as part of the medical history. There were two men who drank in excess of 20 units per week, but they did not demonstrate blunted responses to CRH and suppressed normally with dexamethasone.…”

Section: Interleukin-6mentioning

confidence: 99%

Central obesity, depression and the hypothalamo–pituitary–adrenal axis in men and postmenopausal women

Katz¹,

Taylor

Goodrick³

et al. 2000

Int J Obes

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OBJECTIVE: We examined the relationship of adiposity to pituitary ± adrenal responses to corticotrophin-releasing hormone (CRH) in men and postmenopausal women, controlling for the in¯uence of depression. DESIGN: Studies of CRH responses, cortisol metabolite levels and depression scores in relation to adiposity in men and postmenopausal women. SUBJECTS: Thirteen men: age (median, interquartile range) 62 y (52 ± 63), body mass index (BMI) 29.0 kgam 2 (26.3 ± 33.1), waist circumference (waist) 105 cm (97 ± 111), waist : hip ratio (WHR) 1.03 (0.98 ± 1.07), subscapular to triceps skinfold thickness ratio (STR) 2.0 (1.2 ± 2.4), total body fat (TBF) 25.4 kg (19.8 ± 28.8); and eight women: age 54 y (53 ± 62), BMI 30 kgam 2 (23 ± 41), waist 86 cm (79 ± 117), WHR 0.94 (0.87 ± 1.10), STR 1.0 (0.85 ± 1.07), TBF 35.0 kg (18.7 ± 48.8). MEASUREMENTS: A standard CRH test was conducted with additional basal samples taken for leptin and interleukin 6 (IL-6). Total urine cortisol metabolites (TCM) and the ratio of urinary cortisol : cortisone (FmaEm) metabolites were measured. Depression scores were measured by the General Health Questionnaire (GHQ-30) and Hospital Anxiety and Depression Scale (HAD) questionnaire. All subjects completed an overnight dexamethasone suppression test. RESULTS: The basal to peak percentage increments (%inc.) in adrenocorticotrophic hormone (ACTH) and cortisol in men correlated directly with STR (ACTH %inc. r 0.70, P`0.01; cortisol %inc. r 0.55, P 0.05); this relationship was independent of depression scores. In women, the ACTH area under incremental curve (AUIC) correlated negatively with STR (r À0.81, P`0.05). In men, but not in women, there was a signi®cant correlation between GHQ-30 score and ACTH AUIC (r 0.62, P`0.05) and cortisol AUIC (r 0.72, P`0.01). Depression scores were consistently and directly related to indices of obesity and central obesity. There were no signi®cant relationships in either sex between urinary TCM or FmaEm ratio and BMI, waist, WHR, TBF, STR or CRH responses. The urinary FmaEm ratio was higher in men than in women (median 0.74 vs 0.66, P`0.05). In men, but not in women, GHQ-30 scores correlated positively with urinary TCM (r 0.57, P 0.05) and HAD-depression scores were inversely related to the urine FmaEm ratio (r À0.65, P`0.05). All subjects suppressed normally with dexamethasone. CONCLUSIONS: Cortisol metabolite levels were increased in depression in men, but were not related to adiposity in either sex. We demonstrate that central obesity in men, but not postmenopausal women, is associated with an enhanced pituitary ± adrenal response to CRH and that this relationship is independent of depression score.

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The effects of alcoholism on the hypothalamic‐pituitary‐adrenal axis: interaction with endogenous opioid peptides

Cited by 75 publications

References 53 publications

Involvement of Activated Brain Stress Responsive Systems in Excessive and “Relapse” Alcohol Drinking in Rodent Models: Implications for Therapeutics

Involvement of Activated Brain Stress Responsive Systems in Excessive and “Relapse” Alcohol Drinking in Rodent Models: Implications for Therapeutics

Naltrexone Dampens Ethanol-Induced Cardiovascular and Hypothalamic- Pituitary-Adrenal Axis Activation

Central obesity, depression and the hypothalamo–pituitary–adrenal axis in men and postmenopausal women

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