Zarezadeh · Ageing research reviews 2024 · systematic review and dose-response meta-analysis · n=17 studies

Alcohol consumption in relation to cognitive dysfunction and dementia: A systematic review and dose-response meta-analysis of comparative longitudinal studies.

Cited 33 times in the scientific literature.

Level 3 - non-randomized controlled study

Systematic review and meta-analysis of observational cohort and case-control studies.

PubMed 39038743 · doi:10.1016/j.arr.2024.102419 · record verified 2026-08-29

What was done

Authors conducted a systematic search across PubMed/MEDLINE, Scopus, Embase, PsychInfo, and Google Scholar up to April 2023 for comparative longitudinal cohort and case-control studies. A dose-response meta-analysis using restricted cubic spline regression and random-effects models was performed to evaluate non-linear relationships between daily alcohol intake and risk of cognitive dysfunction and dementia. Heterogeneity, small-study effects, and subgroups by age and follow-up duration were assessed.

What was found

Seventeen studies were included (80,680 participants with 4,929 cases for dementia; 13,530 participants with 1,579 cases for cognitive dysfunction). Both outcomes showed significant J-shaped relationships compared to 0 g/day: - Cognitive dysfunction: Reduced risk at 1–30.5 g/day (RR 0.97, 95% CI 0.95–0.99) and increased risk at >30.5 g/day (RR 1.07, 95% CI 1.01–1.15), with nadir at ~30 g/day. - Dementia: Reduced risk at 1–17.5 g/day (RR 0.92, 95% CI 0.88–0.96) and increased risk at >17.5 g/day (RR 1.23, 95% CI 1.09–1.35), with nadir at ~15 g/day. The J-shaped pattern held across age subgroups (≤65 and >65 years) and follow-up duration (<10 and ≥10 years) for dementia, and within age >65 and duration <10 years for cognitive dysfunction.

Why it matters

This review quantifies empirical intake thresholds where alcohol shifts from an inverse association to an increased risk of cognitive decline and dementia, clarifying dose-dependent boundaries in observational literature.

Limits

All included studies were observational, preventing causal conclusions. The abstract does not indicate whether lifetime abstainers were distinguished from ex-drinkers (sick quitter bias), nor how key confounders such as socioeconomic status, smoking, or binge drinking patterns were adjusted. Specific DSM-defined cognitive subdomains were not evaluated.

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