Peripheral arterial disease (PAD) is defined as an atherosclerotic disease in the lower extremities and is characterized by its symptom of intermittent claudication with discomfort and pain at posterior cruris. Various abnormalities of vascular endothelial cells, smooth muscle cells and platelets induced by risk factors of PAD are involved in its pathogenesis. The most important risk factors are ageing, smoking and diabetes mellitus. Dyslipidemia and hypertension are also classical risk factors of PAD. A lesion of PAD in the lower extremity is prone to be more distal in patients with diabetes than in non-diabetics and to be more proximal in smokers than in nonsmokers. In addition, race/ethnicity, increased inflammatory marker levels, homocysteinemia and abdominal obesity are known to be risk factors of PAD. Light-to-moderate alcohol drinking has been demonstrated to reduce the risks of coronary artery disease and ischemic type of stroke, while excessive alcohol drinking increases the risks of hemorrhagic type of stroke (cerebral hemorrhage and subarachnoid hemorrhage), hypertension, cardiac arrhythmia and sudden cardiac death. In most previous epidemiological studies, the risk of PAD has been shown to be lower in light-to-moderate drinkers than in abstainers. Moreover, drinkers with PAD reportedly showed lower mortality than did nondrinkers with PAD. On the other hand, heavy drinking has been reported to be positively associated with the risk of PAD. Increase in HDL cholesterol, decrease in LDL cholesterol, inhibition of platelet aggregation, decrease in blood coagulability, increase in blood fibrinolitic activity, and increase in insulin sensitivity are known as mechanisms for suppression of atherosclerosis by alcohol drinking. These mechanisms are also thought to contribute to reduction of the risk of PAD by alcohol drinking. Further studies are needed to clarify pathophysiological mechanisms for dose-dependent diverse effects of alcohol on the risk of PAD.