This study used Mendelian randomization (MR) to investigate the causal relationship between alcohol consumption and 8 cardiovascular diseases (CVDs). Genetic variants associated with alcohol consumption were used as instrumental variables, and data from large-scale consortia and UK Biobank were analyzed. The study found that genetically predicted alcohol consumption was consistently associated with an increased risk of stroke and peripheral artery disease. The odds ratios (ORs) per 1-SD increase in log-transformed alcoholic drinks per week were 1.27 (95% CI, 1.12–1.45; P=2.87×10⁻⁴) for stroke and 3.05 (95% CI, 1.92–4.85; P=2.30×10⁻⁶) for peripheral artery disease in the inverse variance-weighted analysis. Some evidence suggested positive associations with coronary artery disease, atrial fibrillation, and abdominal aortic aneurysm, though these associations were somewhat attenuated after adjusting for smoking. No significant associations were found with heart failure, venous thromboembolism, or aortic valve stenosis. The study provides evidence of a causal relationship between higher alcohol consumption and increased risk of stroke and peripheral artery disease. The causal role of alcohol consumption for other CVDs requires further research. The study highlights the importance of distinguishing risks and benefits of alcohol consumption at a population level, as observational studies have shown mixed results. MR is less vulnerable to bias from confounding, reverse causation, and measurement error compared with conventional observational studies. The study used multiple SNPs as instrumental variables and found that alcohol consumption was associated with higher blood pressure and high-density lipoprotein cholesterol levels, and lower triglyceride levels. The study also found that the association between alcohol consumption and CVD may be mediated through blood pressure and lipid levels. The study's strengths include the use of large datasets and multiple SNPs as instrumental variables, while limitations include potential population stratification and the inability to investigate potential U-shaped or J-shaped associations. The study concludes that higher alcohol consumption may be causally associated with increased risk of stroke and peripheral artery disease, but the causal role of alcohol consumption for other CVDs requires further research.This study used Mendelian randomization (MR) to investigate the causal relationship between alcohol consumption and 8 cardiovascular diseases (CVDs). Genetic variants associated with alcohol consumption were used as instrumental variables, and data from large-scale consortia and UK Biobank were analyzed. The study found that genetically predicted alcohol consumption was consistently associated with an increased risk of stroke and peripheral artery disease. The odds ratios (ORs) per 1-SD increase in log-transformed alcoholic drinks per week were 1.27 (95% CI, 1.12–1.45; P=2.87×10⁻⁴) for stroke and 3.05 (95% CI, 1.92–4.85; P=2.30×10⁻⁶) for peripheral artery disease in the inverse variance-weighted analysis. Some evidence suggested positive associations with coronary artery disease, atrial fibrillation, and abdominal aortic aneurysm, though these associations were somewhat attenuated after adjusting for smoking. No significant associations were found with heart failure, venous thromboembolism, or aortic valve stenosis. The study provides evidence of a causal relationship between higher alcohol consumption and increased risk of stroke and peripheral artery disease. The causal role of alcohol consumption for other CVDs requires further research. The study highlights the importance of distinguishing risks and benefits of alcohol consumption at a population level, as observational studies have shown mixed results. MR is less vulnerable to bias from confounding, reverse causation, and measurement error compared with conventional observational studies. The study used multiple SNPs as instrumental variables and found that alcohol consumption was associated with higher blood pressure and high-density lipoprotein cholesterol levels, and lower triglyceride levels. The study also found that the association between alcohol consumption and CVD may be mediated through blood pressure and lipid levels. The study's strengths include the use of large datasets and multiple SNPs as instrumental variables, while limitations include potential population stratification and the inability to investigate potential U-shaped or J-shaped associations. The study concludes that higher alcohol consumption may be causally associated with increased risk of stroke and peripheral artery disease, but the causal role of alcohol consumption for other CVDs requires further research.