Alcohol intake → Major cardiovascular events
Higher Alcohol intake increases Major cardiovascular events.
Holmes 2014 found that a gene variant that cuts weekly drinking by 17 percent also cut the odds of coronary heart disease by 10 percent in 261,991 European adults (odds ratio 0.90, 0.84 to 0.96). Millwood 2019 found genetically predicted drinking raised stroke in Chinese men and left heart attack unmoved.
Mendelian randomization · Moderate · N=261991
Mendelian randomization. It's a great tool for ruling out environmental factors, though it has its own genetic limitations.
Mechanism
People who drink a little often look safer than people who drink nothing. Sick quitters, money, and smoking sit on that backdoor. Researchers use a genetic shortcut called Mendelian randomization. It is good at ruling out diet and income. It can still be fooled when one gene affects two traits. Holmes, Dale, Zuccolo and colleagues (2014) used ADH1B rs1229984 in 261,991 European adults from 56 studies (20,259 coronary cases, 10,164 strokes). The A-allele cut weekly units by 17.2 percent and cut coronary heart disease (odds ratio 0.90, 0.84 to 0.96). Combined stroke was null. Ischaemic stroke was 0.83 (0.72 to 0.95). Millwood, Walters, Mei and colleagues (2019) followed 512,715 adults in China for about ten years and genotyped 161,498 for ALDH2 rs671 and ADH1B rs1229984. Self-report was U-shaped. Genotype-predicted male intake was not. Per 280 g a week, haemorrhage relative risk was 1.58 (1.36 to 1.84) and ischaemic stroke 1.27 (1.13 to 1.43). Myocardial infarction was 0.96 (0.78 to 1.18). Women drank little and the same genes did not move events. Larsson, Burgess, Mason and Michaëlsson (2021) used up to 94 SNPs. Stroke odds per 1-SD log drinks were 1.27 (1.12 to 1.45). Peripheral artery disease was 3.05. Coronary disease was 1.16 (1.00 to 1.36). Smoking-adjusted estimates were weaker. Rosoff, Davey Smith, Mehta, Clarke and Lohoff (2021) found univariable Mendelian randomization raised myocardial infarction (1.24) and coronary disease (1.21). A smoking adjustment attenuated both. They found no protection. Lankester, Zanetti, Ingelsson and Assimes (2021) used ADH1B plus up to 24 SNPs in UK Biobank. An extra daily drink tracked higher pressure, haemorrhagic stroke (2.25, 1.41 to 3.60), and atrial fibrillation (1.26). A heart-attack signal did not hold after pressure. Two-sample work was mostly null. No analysis found protection.
Caveats
This page is adult alcohol intake and later coronary disease or stroke. It is not all-cause death. That pair is the alcohol-and-death page. Holmes is European and one SNP. Millwood is Chinese men who drink spirits. Women are the negative control. Larsson, Rosoff, and Lankester are mostly European summary statistics and UK Biobank. Mendelian randomization assumes no pleiotropy. Alcohol instruments often travel with smoking. Rosoff's coronary signal shrank after a smoking adjustment. Lankester's heart-attack signal shrank after blood pressure. Millwood's heart-attack estimate is null. Combined stroke in Holmes was null. The designs are Mendelian randomization, a genetic shortcut that can still be fooled when one gene affects two traits. N=261,991 is from Holmes. Wood 2018 is an observational pool of current drinkers. Hoek 2022 and Goel 2019 are reviews. Ahmed 2024 is liver fat, not drinks. Hisamatsu 2022 is coronary calcium and a revascularization case-control in Japanese men, not incident events. Bouajila 2024 is a review. Those files stay off this page. This is not medical advice and not a recommendation to drink, to abstain, or to treat a number.
Effect
odds_ratio = 0.9. Holmes 2014: ADH1B A-allele (17% fewer units/week) CHD OR 0.90 (0.84-0.96). More genetically predicted alcohol, more CHD. Millwood stroke RR 1.27-1.58 per 280 g/week; MI null.
Nodes
Named confounders
Cite this page
What Causes What. “Alcohol intake → Major cardiovascular events.” https://whatcauseswhat.org/edges/e-alcohol-cv (atlas updated 2026-09-02).
Papers
- Association between alcohol and cardiovascular disease: Mendelian randomisation analysis based on individual participant data.
MV Holmes, CE Dale, L Zuccolo, RJ Silverwood, Y Guo, Z Ye, D Prieto-Merino, A Dehghan · 2014 · BMJ (Clinical research ed.)
- Conventional and genetic evidence on alcohol and vascular disease aetiology: a prospective study of 500 000 men and women in China.
IY Millwood, RG Walters, XW Mei, Y Guo, L Yang, Z Bian, DA Bennett, Y Chen · 2019 · Lancet (London, England)
- Alcohol Consumption and Cardiovascular Disease: A Mendelian Randomization Study.
SC Larsson, S Burgess, AM Mason, K Michaëlsson · 2021 · Circulation. Genomic and precision medicine
- Evaluating the relationship between alcohol consumption, tobacco use, and cardiovascular disease: A multivariable Mendelian randomization study.
DB Rosoff, G Davey Smith, N Mehta, TK Clarke, FW Lohoff · 2021 · PLoS medicine
- Alcohol use and cardiometabolic risk in the UK Biobank: A Mendelian randomization study.
J Lankester, D Zanetti, E Ingelsson, TL Assimes · 2021 · PloS one