Xie · Geriatrics & gerontology international 2022 · systematic review and dose-response meta-analysis · n=13 studies (6 in dose-response meta-analysis)

Alcohol consumption and risk of Alzheimer's disease: A dose-response meta-analysis.

Cited 23 times in the scientific literature.

Level 3 - non-randomized controlled study

Systematic review and meta-analysis of observational studies

PubMed 35171516 · doi:10.1111/ggi.14357 · record verified 2026-08-31

What was done

Authors conducted a systematic review and dose-response meta-analysis searching PubMed and Web of Science through September 1, 2019, examining the association between alcohol consumption and Alzheimer's disease (AD) risk. They calculated pooled relative risks (RR) with 95% confidence intervals, performed subgroup analyses across alcohol type, ethnicity, study design, and sex, and modeled non-linear dose-response curves.

What was found

Across 13 included studies, alcohol drinkers had a lower risk of AD compared with non-drinkers (RR 0.68, 95% CI 0.53–0.87; I² = 87.9%, P < 0.001). Wine consumption was specifically associated with reduced risk (RR 0.71, 95% CI 0.51–0.96). Stratification by ethnicity, sex, or study design yielded no statistically significant associations. In the dose-response analysis (6 studies), the overall association was non-linear but non-significant. However, sex-stratified dose modeling showed excess AD risk in men starting from 14.8 drinks per week (overall P = 0.023; non-linearity P = 0.025), whereas intake under 16.9 drinks per week in women showed a significant non-linear association with reduced AD risk (overall P = 0.002; non-linearity P = 0.019).

Why it matters

This study highlights potential sex-specific thresholds in alcohol's relationship with AD, suggesting protective associations at moderate levels in women and elevated risk beyond ~15 drinks weekly in men.

Limits

The analysis is constrained by high statistical heterogeneity (I² = 87.9%) and reliance on observational studies vulnerable to residual confounding, misclassification of intake, and 'sick quitter' bias in non-drinker reference groups. Only 6 of the 13 studies provided adequate data for dose-response modeling.

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