1. The regular consumption of alcohol elevates blood pressure, with global estimates that the attributable risk for hypertensive disease from alcohol is 16%. 2. The increase in blood pressure is approximately 1 mmHg for each 10 g alcohol consumed and is largely reversible within 2-4 weeks of abstinence or a substantial reduction in alcohol intake. 3. This increase in blood pressure occurs irrespective of the type of alcoholic beverage. In particular, the postulated effects of vasodilator flavonoid components of red wine to lessen or reverse alcohol-related hypertension have not been borne out in intervention studies. 4. Heavy drinking, especially a binge pattern of drinking, is linked to a higher incidence of cerebral thrombosis, cerebral haemorrhage and coronary artery disease deaths, although a role for alcohol-related hypertension in the causal pathway is not well defined. 5. In contrast, the light to moderate intake of alcohol has been consistently linked to a reduced risk of atherosclerotic vascular disease end-points. Such a protective effect may also extend to hypertensive subjects. 6. However, the magnitude of any protective effect appears to have been exaggerated because of unmeasured confounders, especially diet, lifestyle and patterns of drinking. Furthermore, a decrease in overall mortality with drinking appears confined to older subjects and to populations with a high background cardiovascular risk profile. 7. Any putative cardiovascular benefits from drinking need to be carefully considered against the effects of alcohol to elevate blood pressure, together with many other adverse health consequences from drinking. Maximum cardiovascular benefit occurs at relatively low levels of consumption (i.e. one to two standard drinks a day in men (10-20 g alcohol) and up to one a day in women (10 g alcohol)). In hypertensive subjects, consumption beyond these levels would be unwise.