Heavy alcohol use as well as alcohol dependence (AD) have been associated with dysregulation of the hypothalamic–pituitary–adrenal (HPA)-axis and the autonomic nervous system (ANS). However, the relative contribution of alcohol use and AD is unclear.
Baseline data were derived from 2947 persons of the Netherlands Study of Depression and Anxiety (NESDA), including non-drinkers (n = 498), moderate drinkers (n = 2112) and heavy drinkers (n = 337). We also distinguished between persons with no lifetime DSM-IV AD (n = 2496), remitted AD (>1 year; n = 243), and current AD (≤1 year; n = 208). ANS measures included ECG-based heart rate (HR), respiratory sinus arrhythmia (RSA, high RSA reflecting high cardiac parasympathetic control) and pre-ejection period (PEP, high PEP reflecting low cardiac sympathetic control). HPA-axis measures included the cortisol awakening response (area under the curve with respect to the ground [AUCg] and increase [AUCi]), evening cortisol and a 0.5 mg dexamethasone suppression test, all measured in saliva.
Heavy drinkers showed higher basal cortisol levels (AUCg: p = .02; evening cortisol: p = .006) and increased cardiac sympathetic control (higher HR: p = .04; lower PEP: p = .04) compared to moderate drinkers. Persons with current or remitted AD did not differ from persons without lifetime AD on any of the HPA-axis or ANS indicators (all p > .33). Similar patterns of HPA-axis and ANS activity across alcohol use groups were found in persons with and without lifetime AD.
Our findings suggest that current heavy alcohol use, rather than current or remitted AD, is associated with hyperactivity of the HPA-axis and increased cardiac sympathetic control.
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Baseline data were derived from 2947 persons of the Netherlands Study of Depression and Anxiety (NESDA), including non-drinkers (n = 498), moderate drinkers (n = 2112) and heavy drinkers (n = 337). We also distinguished between persons with no lifetime DSM-IV AD (n = 2496), remitted AD (>1 year; n = 243), and current AD (≤1 year; n = 208). ANS measures included ECG-based heart rate (HR), respiratory sinus arrhythmia (RSA, high RSA reflecting high cardiac parasympathetic control) and pre-ejection period (PEP, high PEP reflecting low cardiac sympathetic control). HPA-axis measures included the cortisol awakening response (area under the curve with respect to the ground [AUCg] and increase [AUCi]), evening cortisol and a 0.5 mg dexamethasone suppression test, all measured in saliva.
Heavy drinkers showed higher basal cortisol levels (AUCg: p = .02; evening cortisol: p = .006) and increased cardiac sympathetic control (higher HR: p = .04; lower PEP: p = .04) compared to moderate drinkers. Persons with current or remitted AD did not differ from persons without lifetime AD on any of the HPA-axis or ANS indicators (all p > .33). Similar patterns of HPA-axis and ANS activity across alcohol use groups were found in persons with and without lifetime AD.
Our findings suggest that current heavy alcohol use, rather than current or remitted AD, is associated with hyperactivity of the HPA-axis and increased cardiac sympathetic control.
Read Full Abstract
Request Reprint E-Mail: l.boschloo@ggzingeest.nl
