What question did this study set out to answer?

This study aims to reassess the relationship between alcohol consumption and cardiovascular disease by minimizing biases.

February 6, 2026

Reassessing alcohol consumption and cardiovascular disease by addressing bias: the Multi-Ethnic Study of Atherosclerosis

Puntos clave

This study aims to reassess the relationship between alcohol consumption and cardiovascular disease by minimizing biases.
Prospective cohort study of 6,814 participants aged 45-84 years without baseline cardiovascular disease.
Evaluation of alcohol use categorized into lifetime abstainers, former drinkers, and current drinkers based on consumption levels.
Use of multinomial logistic regression for coronary artery calcium and Cox proportional hazards models for clinical outcomes.
Comparison of conventional models with those using occasional drinkers as reference instead of lifetime abstainers.
Increasing alcohol consumption correlated with a dose-response increase in coronary artery calcium scores.
Heavy drinking was associated with severe coronary artery calcium (>300).
Light drinking was linked to increased risk for myocardial infarction, stroke, major adverse cardiovascular events, and heart failure in fully adjusted models.
Traditional models claimed moderate drinking offered protective effects, but these were less significant when adjusted.

Resumen

Abstract Background Alcohol consumption and its relationship with cardiovascular disease (CVD) remains controversial. Observational studies have reported J-shaped associations suggesting cardioprotective effects of moderate drinking, while other observational and Mendelian Randomization studies have found dose-response harm. Biases such as abstainer misclassification, sick quitter effects, and residual confounding may obscure true associations. This study aimed to reassess alcohol’s impact on CVD using novel methods to minimize bias. Purpose We evaluated the relationship between alcohol and subclinical (coronary artery calcium CAC) and clinical (myocardial infarction MI, stroke, cardiovascular death, major adverse cardiovascular events MACE, and heart failure) outcomes in the Multi-Ethnic Study of Atherosclerosis (MESA). We compared conventional models with those using (1) occasional drinkers as the reference group instead of lifetime abstainers and (2) intention-to-treat (ITT) reallocation of former drinkers based on past drinking patterns. Methods MESA is a prospective cohort study of 6,814 participants aged 45-84 years without baseline CVD. Alcohol use was classified as lifetime abstainer, former drinker, or current drinker (occasional ≤1 drink/week, light 2-7 drinks/week, moderate 8-14 drinks/week, heavy 14 drinks/week). We used multinomial logistic regression for CAC and Cox proportional hazards models for clinical outcomes across four models: (1) non-drinker reference, (2) lifetime abstainer reference, (3) occasional drinker reference, and (4) occasional drinker reference with ITT reallocation of former drinkers to their previous drinking levels. Results Increasing alcohol consumption correlated with a dose-response increase in CAC. Heavy drinking was consistently associated with severe CAC (300). In fully adjusted models, light (OR: 1.23, 95% CI: 1.02-1.48), moderate (OR: 1.27, 95% CI: 1.04-1.55), and heavy drinking (OR: 1.42, 95% CI: 1.12-1.78) were associated with higher CAC scores compared to occasional drinkers. Traditional models replicated protective effects of moderate drinking for MI and cardiovascular mortality. However, these associations attenuated in adjusted models. Moderate drinking showed an attenuated, non-significant benefit for MI (HR: 0.64, 95% CI: 0.38-1.06) and cardiovascular mortality (HR: 0.81, 95% CI: 0.53-1.25) in fully adjusted models. Light drinking shifted from null to increased risk for MI (HR: 1.46, 95% CI: 1.11-1.92), stroke (HR: 1.54, 95% CI: 1.17-2.03), MACE (HR: 1.33, 95% CI: 1.12-1.57), and heart failure (HR: 1.42, 95% CI: 1.10-1.84). Conclusion Adjusting for abstainer and sick quitter biases altered the observed relationship between alcohol and CVD, showing increased harm with light drinking, attenuated protective effects of moderate drinking, and a dose-response relationship for CAC in bias-adjusted models. These findings illustrate the importance of methodology in alcohol-CVD relationships.

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