Drinking alcohol even in small amounts has been found to raise blood pressure (BP) levels over time for both men and women, with no threshold below which the risk of BP elevation is negligible.
Pooled data from seven studies involving 19,548 participants with a median follow-up of 5.3 years showed that the higher an individual’s baseline alcohol consumption, the greater the increase in their BP over time. This association was stronger for systolic BP (SBP) than for diastolic BP (DBP). [Hypertension 2023;80:1961-1969]
Compared with nonconsumption, a daily intake of alcohol as little as 12 g was associated with 1.25-mm Hg (95 percent confidence interval [CI], 0.49–2.01) increase in SBP and 1.14-mm Hg (95 percent CI, 0.60–1.68) increase in DBP.
The corresponding differences in SBP and DBP associated with greater levels of alcohol intake vs nonconsumption were 2.48 (95 percent CI, 1.40–3.56) and 2.03 (95 percent CI, 1.19–2.86) mm Hg for 24 g/day, and 4.90 (95 percent CI, 3.71–6.08) and 3.10 (95 percent CI, 1.88–4.33) mm Hg for 48 g/day.
Subgroup analyses by sex showed that in men, the greater the alcohol consumed, the greater the increase in SBP and DBP over time. In women, alcohol intake had a linear, positive association with SBP that was similar to that observed in men, but the association for DBP followed a U-shaped pattern. That is, women who drank a moderate amount of alcohol had lower DBP change than women with higher or lower intake levels.
Further analysis showed that drinking alcohol was positively associated with BP changes in both Asians and North Americans, apart from DBP in the latter group.
The sex- and race/ethnicity-related differences in the pattern of the association may be related to a causal role of factors such as sex hormones and to known differences in alcohol metabolizing enzymes such as alcohol dehydrogenase and aldehyde dehydrogenase between Asians and North Americans. It is also possible that the differences between men and women may have resulted from a bias such as enhanced misclassification of the exposure and outcome values in women consuming high levels of alcohol, the investigators pointed out.
“To the best of our knowledge, this is the first dose-response meta-analysis assessing the relationship between usual baseline alcohol consumption and BP levels in nonexperimental cohort studies, this being its major strength,” they said.
What the findings point to is that “there is no threshold below which no association exists between alcohol consumption and a higher SBP,” according to the investigators, adding that the 1.25-mm Hg increase in SBP associated with an intake of alcohol as little as 12 g/day might have a meaningful adverse impact on cardiovascular morbidity on a population basis.
Likewise, even small reductions in BP have been shown to have a big impact on health, helping prevent hypertension and cardiovascular events. For example, a study of people in the Multiple Risk Factor Intervention Trial (MRFIT) found that a 2-mm Hg reduction in systolic blood pressure led to a 6-percent reduction in annual mortality from stroke, a 4-percent reduction in annual mortality from coronary heart disease, and a 3-percent reduction in all-cause annual mortality. Another study, the Atherosclerosis Risk in Communities (ARIC) Study, found that a 1-mm Hg reduction in SBP correlated with 13.5 and 9.0 fewer coronary heart disease events per 100,000 person-years in African Americans and Whites, respectively. [Hypertension 1991;17:I16-I20; J Am Heart Assoc 2015;4:e002276]
The investigators argued that consumption of any alcohol should be considered a risk factor for high SBP, with important preventive and therapeutic implications.