A meta-analysis on the relation between acute stress exposure, alcohol consumption and cortisol levels in individuals with a personal, familial or no alcohol use disorder

Aims: To investigate the relation between acute stress exposure, acute alcohol consumption, and corti-sol levels among individuals with varying statuses of alcohol use disorder (AUD) and family histories of AUD.Design: We conducted a systematic search for primary studies registered in the PubMed/Medline, Web of Science, and PsycInfo databases up to July 31, 2023, providing data on the volume of alcohol consumed in millilitre after stress compared to control procedures, or on the effect of acute alcohol consumption, with or without simultaneous stress exposure, on minimal (CMin indicating cortisol recovery) and differ-ences between minimal and maximal cortisol levels (CMaxMin indicating cortisol reactivity). The samples’ AUD status was categorized as actively drinking individuals meeting AUD criteria (including abuse and dependence; AUD+), abstinent individuals who previously met the criteria, or individuals with no AUD di-agnosis. The samples’ family history of AUD status was extracted or approximated on lifetime prevalence rates of AUD for the respective country or cultural area. Findings: We integrated data from 53 experimental and 31 observational studies. Our meta-analysis suggests that acute stress exposure increases alcohol consumption only when small study effects are not accounted for (gREE=0.25 vs. gPEESE= 0.02; CI95% = -0.19-0.23). Acute alcohol consumption decreases corti-sol recovery (CMin↑; gREE= 0.15; CI95%= -0.02-0.31), particularly in actively drinking individuals with AUD+ (gREE= 0.46; CI95%= 0.03-0.90) and those with a familial history of AUD (gREE= 0.16; CI95%= -0.08-0.39). Acute alcohol consumption does not significantly alter cortisol reactivity (β= -0.01; CI95%= -0.14-0.12), with divergent effects observed in individuals with AUD+ (CMaxMin↑) or familial AUD history (CMaxMin↓).Conclusions: The evidence presented suggests that acute stress does not substantially increase alcohol consumption, and that alcohol consumption does not effectively regulate reactive cortisol stress re-sponses. Minimal cortisol levels may be more suitable indicators for detecting alcohol-related changes in the cortisol stress processing system.