Cortisol and β-endorphin response in alcoholics and alcohol abusers following a high naloxone dosage

Kemper, A; Koalick, F.; Thiele, H G; Retzow, A; Rathsack, R; Nickel, B

doi:10.1016/0376-8716(90)90158-b

Cited by 32 publications

(16 citation statements)

References 29 publications

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“…Our finding of lower resting AM plasma concentrations in abstinent alcohol-dependent patients is supported by the findings in other reports (Kemper et al, 1990;Krystal et al, 1996) but is by no means a unanimous observation (Farren et al, 1995). The discrepant results probably reflect several factors.…”

Section: Discussionsupporting

confidence: 60%

“…In contrast to the direct stimulatory effects of serotonin on this axis, opiate antagonists stimulate the HPA axis by removing the opioidergic system's tonic inhibitory control of LHPA function (Wand et al, 1998). Thus, studies in which the opiate antagonist naloxone was administered to recovering alcoholdependent patients (Inder et al, 1995;Kemper et al, 1990) or to young adults at high or low risk for alcoholism (Wand et al, 1998) also have found that both sets of these individuals had a slower rate of decline in cortisol and/or ACTH response than that of controls. Taken together, these findings might signal acquired or inherited damage to the negative feedback regulatory network designed to limit the stress response among alcohol-dependent patients or individuals at increased risk for alcoholism.…”

Section: Discussionmentioning

confidence: 94%

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Stress Hormone Dysregulation at Rest and After Serotonergic Stimulation Among Alcohol‐Dependent Men With Extended Abstinence and Controls

Anthenelli

Maxwell

Geracioti

et al. 2001

Alcoholism Clin & Exp Res

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Alcohol-dependent men with extended abstinence differed from age- and race-matched non-alcohol-dependent men in resting AM and fenfluramine-induced plasma cortisol levels. This dysfunction in glucocorticoid homeostatic mechanisms was associated with alcoholism and not with smoking or ASPD. We also observed a nonsignificant statistical trend for plasma ACTH levels to be elevated among alcohol-dependent men along the descending limb of the response curve. Alcohol-dependent men seemed to have inherited or acquired damage to 5-HT-regulated LHPA axis function, the precise mechanisms and sites of which remain to be determined.

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Section: Discussionsupporting

confidence: 60%

Section: Discussionmentioning

confidence: 94%

Stress Hormone Dysregulation at Rest and After Serotonergic Stimulation Among Alcohol‐Dependent Men With Extended Abstinence and Controls

Anthenelli

Maxwell

Geracioti

et al. 2001

Alcoholism Clin & Exp Res

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“…Specifically, cortisol response to opioid antagonists are higher in those at risk for alcoholism based on a positive family history (King et al, 2002a; Wand, Mangold, Ali, & Giggey, 1999; Wand et al, 1998; Wand, McCaul, Gotjen, Reynolds, & Lee, 2001), but not all have found this association (Lovallo et al, 2012). Furthermore, among alcohol-dependent participants HPA activity appears to be blunted compared to controls (Inder et al, 1995; Kemper et al, 1990) although not in all studies (Wand et al, 2012). Thus, the significance of what cortisol responses to opioid antagonists indicates about opioid signaling within and across addictions is not clear.…”

Section: Discussionmentioning

confidence: 77%

A new biomarker of hedonic eating? A preliminary investigation of cortisol and nausea responses to acute opioid blockade

et al. 2014

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Overweight and obese individuals differ in their degree of hedonic eating. This may reflect adaptations in reward-related neural circuits, regulated in part by opioidergic activity. We examined an indirect, functional measure of central opioidergic activity by assessing cortisol and nausea responses to acute opioid blockade using the opioid antagonist naltrexone in overweight/obese women (mean BMI = 31.1 ± 4.8) prior to the start of a mindful eating intervention to reduce stress eating. In addition, we assessed indices of hedonic-related eating, including eating behaviors (binge eating, emotional eating, external eating, restraint) and intake of sweets/desserts and carbohydrates (Block Food Frequency); interoceptive awareness (which is associated with dysregulated eating behavior); and level of adiposity at baseline. Naltrexone-induced increases in cortisol were associated with greater emotional and restrained eating and lower interoceptive awareness. Naltrexone-induced nausea was associated with binge eating and higher adiposity. Furthermore, in a small exploratory analysis, naltrexone-induced nausea predicted treatment response to the mindful eating intervention, as participants with more severe nausea at baseline maintained weight whereas those without nausea responses tended to gain weight. These preliminary data suggest that naltrexone-induced cortisol release and nausea may help identify individuals who have greater underlying food reward dependence, which leads to an excessive drive to eat. Future research is needed to confirm this finding and to test if these markers of opioidergic tone might help predict success in certain types of weight management programs.

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“…However, after more prolonged periods of abstinence, cocaine addicts exhibit decreased acoustic startle compared with healthy controls, suggesting a dampened stress response [111]. Additionally, stimulant dependent individuals exhibit decreased cortisol response to a stressful situation, as do alcoholics after longer periods of abstinence [94, 112, 113]. However, when marijuana dependence is added to the equation, the results are quite different.…”

Section: Clinical Studies Of Substance Use and Stress Responsivitymentioning

confidence: 99%

Substance use modulates stress reactivity: Behavioral and physiological outcomes

Fosnocht

Briand

2016

Physiology & Behavior

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Drug addiction is a major public health concern in the United States costing taxpayers billions in health care costs, lost productivity and law enforcement. However, the availability of effective treatment options remains limited. The development of novel therapeutics will not be possible without a better understanding of the addicted brain. Studies in both clinical and preclinical models indicate that chronic drug use leads to alterations in the body and brain’s response to stress. Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis may shed light on the ability of stress to increase vulnerability to relapse. Further, within both the HPA axis and limbic brain regions, corticotropin-releasing factor (CRF) is critically involved in the brain’s response to stress. Alterations in both central and peripheral CRF activity seen following chronic drug use provide a mechanism by which substance use can alter stress reactivity, thus mediating addictive phenotypes. While many reviews have focused on how stress alters drug-mediated changes in physiology and behavior, the goal of this review is to focus on how substance use alters responses to stress.

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Cortisol and β-endorphin response in alcoholics and alcohol abusers following a high naloxone dosage

Cited by 32 publications

References 29 publications

Stress Hormone Dysregulation at Rest and After Serotonergic Stimulation Among Alcohol‐Dependent Men With Extended Abstinence and Controls

Stress Hormone Dysregulation at Rest and After Serotonergic Stimulation Among Alcohol‐Dependent Men With Extended Abstinence and Controls

A new biomarker of hedonic eating? A preliminary investigation of cortisol and nausea responses to acute opioid blockade

Substance use modulates stress reactivity: Behavioral and physiological outcomes

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