Alcohol self-administration, craving and HPA-axis activity: an intriguing relationship

Kiefer, Falk; Jahn, Holger; Schick, Mildred; Wiedemann, Klaus

doi:10.1007/s00213-002-1255-3

Cited by 48 publications

(44 citation statements)

References 13 publications

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“…Plasma ACTH decreased significantly from baseline to week 12 in the placebo group, but not during active treatment with naltrexone, acamprosate, or both compounds combined (Kiefer et al, 2002). After 12 weeks of treatment, ACTH was significantly higher in the naltrexone group and in the combined treatment group compared to placebo.…”

Section: Hpa-axis Activation As a Key Mechanism Of Pharmacological Anmentioning

confidence: 81%

“…Moreover, a direct relation with abstinence duration was also observed. The subanalysis of the placebo-treated patients revealed basal concentrations of serum cortisol and ACTH that were significantly lower in those patients that subsequently relapsed than in those that remained abstinent (t-test; p < 0.05; Kiefer et al, 2002). Moreover, no such association was detectable in groups that received the active treatments.…”

Section: Hpa-axis Activation As a Key Mechanism Of Pharmacological Anmentioning

confidence: 92%

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Suppression of the HPA Axis Stress‐Response: Implications for Relapse

Adinoff

Junghanns

Kiefer

et al. 2005

Alcoholism Clin & Exp Res

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181

161

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This article presents the proceedings of a symposium held at the meeting of the International Society for Biomedical Research on Alcoholism (ISBRA) in Mannheim, Germany, in October 2004. This symposium explored the potential role of hypothalamic-pituitary-adrenal (HPA) axis dysregulation upon relapse. HPA axis stimulation induces the release of the glucocorticoid cortisol, a compound with profound effects upon behavior and emotion. Altered stress-responses of the HPA axis in abstinent alcohol-dependent subjects, therefore, may influence their affective and behavioral regulation, thus impacting their potential for relapse. Bryon Adinoff began the symposium with a review of HPA axis dysfunction in alcohol-dependent subjects, including recent studies from his lab demonstrating an attenuated glucocorticoid response to both endogenous and exogenous stimulation in one-month abstinent men. Klaus Junghanns presented his work demonstrating that a blunted ACTH or cortisol response to subjective stressors (social stressor or alcohol exposure) is predictive of a return to early drinking. The final two presenters examined the interaction between naltrexone and HPA responsiveness in alcohol-dependent or at-risk subjects, as naltrexone induces an increase in ACTH and cortisol. Falk Kiefer discussed the relationship between basal HPA axis responsivity and clinical outcome following treatment with naltrexone or acamprosate. Plasma ACTH significantly decreased over the course of the study in the medication groups, but not the placebo group. Lower basal concentrations of ACTH and cortisol were associated with quicker relapse in the placebo group only. Suchitra Krishnan-Sarin described her preliminary work, in which family-history positive (FH+) and family history negative (FH-) subjects were administered naltrexone, followed by an assessment of alcohol-induced craving. The cortisol response to alcohol was significantly and inversely related to craving in the FH+, but not the FH-, subjects. Alterations in HPA axis responsivity may therefore have a negative impact upon clinical outcome in alcohol-dependent subjects, and disinhibition of the axis with medication may have therapeutic potential. KeywordsAdrenal Cortex; Alcoholism; Pituitary-Adrenal System; Naltrexone Hypothalamic-pituitary-adrenal (HPA AXIS) activation is a key component of the physiological response to stress, particularly stress accompanied by anxiety or fear. Stress initiates a cascade of events, beginning with central nervous system stimulation of

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Section: Hpa-axis Activation As a Key Mechanism Of Pharmacological Anmentioning

confidence: 81%

Section: Hpa-axis Activation As a Key Mechanism Of Pharmacological Anmentioning

confidence: 92%

Suppression of the HPA Axis Stress‐Response: Implications for Relapse

Adinoff

Junghanns

Kiefer

et al. 2005

Alcoholism Clin & Exp Res

Self Cite

181

161

View full text Add to dashboard Cite

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“…The natriuretic peptide ANP is tightly interwoven into side effects observed during detoxification treatment [11, 12]. ANP is involved in the regulation of the HPA system [10, 11].…”

Section: Discussionmentioning

confidence: 99%

“…Koopmann et al [8, 9] demonstrated a converse correlation of ANP plasma levels and craving in early abstinent alcohol-dependent patients and concluded that ANP plasma levels affect craving indirectly through their influence on patients’ perceived stress. Kiefer et al [10, 11] demonstrated lower plasma concentrations of ANP in alcohol-dependent patients during withdrawal compared to healthy controls. Considering epigenetic changes as an important mode of regulation for ANP, our group demonstrated significant changes in the methylation status of individual cytosine-phosphatidyl-guanine (CpG) sites of ANP during alcohol withdrawal.…”

Section: Introductionmentioning

confidence: 99%

Smoking and Promoter-Specific Deoxyribonucleic Acid Methylation of the Atrial Natriuretic Peptide Gene: Methylation of Smokers and Non-Smokers Differs Significantly during Withdrawal

et al. 2017

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Background: Atrial natriuretic peptide (ANP) is well known in psychiatric disorders to modulate hypothalamic-pituitary-adrenal axis activity. Disturbances of ANP have been described in early abstinent alcohol-dependent patients. This is the first longitudinal investigation on cytosine-phosphatidyl-guanine (CpG)-island promoter methylation of the ANP gene in the blood of tobacco-dependent patients. Methods: In a longitudinal approach, we investigated whether changes in ANP serum levels correlated to CpG methylation of the respective gene promoters on days 1, 7, and 14 of tobacco withdrawal. Results and Conclusion: Compared to non-smokers, promoter-related deoxyribonucleic acid methylation of the ANP promoter was significantly elevated on days 7 and 14 of withdrawal in tobacco-dependent patients. Baseline methylation status of the ANP promoter was not significantly different from controls, arguing for an impaired regulation during withdrawal.

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“…The derivatives of POMC, especially the melanocortin hormones adrenocorticotropic hormone and alpha-melanocyte-stimulating-hormone (alpha-MSH), are current subjects of research in the context of alcohol addiction [11]. Leptin has an inhibiting effect on the central actors of the HPA axis, the corticotropin-releasing factor expression in hypothalamus as well as adrenocorticotropic hormone expression in the anterior lobe of pituitary gland [12,13], which are known to be associated with higher craving for alcohol when diminished [14,15]. Long-term ethanol consumption is associated with increased levels of leptin in plasma compared to healthy controls [16], whereas leptin levels normalize during abstinence [17].…”

Section: Doi: 101159/000496111mentioning

confidence: 99%

DNA Methylation of the Leptin Gene Promoter is Altered by Chronic Alcohol Exposure in an Animal Model for Alcohol Dependence

et al. 2019

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Appetite-regulating peptides, such as leptin, are linked to craving and have been in the focus of alcohol dependence research for years. The objective of our study was to investigate the dynamics of leptin gene promoter methylation during alcohol withdrawal and specific treatment in a rodent (rat) model for alcohol dependence. DNA methylation was measured using direct bisulfite sequencing at 0 h, 24 h, and 6 days of alcohol withdrawal as well as after treatment with alpha-melanocyte-stimulating hormone (alpha-MSH), Beta-Endorphin, or saline. We found significantly lower methylation levels in alcohol-consuming animals compared to alcohol-naïve animals. During 6 days of alcohol deprivation, this difference in methylation vanished. Leptin methylation of the alpha-MSH-treated group and 6 days alcohol-deprived animals was significantly higher than that in saline-treated animals, possibly indicating compensatory effects of the treatment. Our results further expand on previous findings from human studies that explain leptin’s role in bridging the gap between alcohol consumption and appetite regulation.

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Alcohol self-administration, craving and HPA-axis activity: an intriguing relationship

Cited by 48 publications

References 13 publications

Suppression of the HPA Axis Stress‐Response: Implications for Relapse

Suppression of the HPA Axis Stress‐Response: Implications for Relapse

Smoking and Promoter-Specific Deoxyribonucleic Acid Methylation of the Atrial Natriuretic Peptide Gene: Methylation of Smokers and Non-Smokers Differs Significantly during Withdrawal

DNA Methylation of the Leptin Gene Promoter is Altered by Chronic Alcohol Exposure in an Animal Model for Alcohol Dependence

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