Effects of at-risk alcohol use on nighttime blood pressure, urinary catecholamines, and sleep quality in midlife adults.

Abstract

Background: The association between alcohol and hypertension has been predominantly based on office blood pressure (BP) measurements. However, little is known about the effect of alcohol use on nighttime BP and the underlying mechanisms. The purpose of this study was to investigate the effects of at-risk alcohol use on nighttime BP, urinary catecholamines, and sleep quality in midlife adults.

Methods: A total of 32 midlife men and 30 postmenopausal women, free of major clinical diseases and nonsmokers (age: 58 ± 4; mean ± SD), were included. Among all participants, 22 were currently taking antihypertensive medications. At-risk drinkers were defined as those who had a dried blood spot phosphatidylethanol level ≥20 ng/mL. All participants completed 24-h ambulatory BP monitoring and urine collection to determine nighttime (or asleep) BP and nighttime urinary catecholamine levels. Sleep quality was determined by using the Pittsburgh Sleep Quality Index.

Results: In midlife adults free of antihypertensive medications, at-risk drinkers had a higher nighttime systolic (118 ± 14 vs. 107 ± 14 mmHg, p = 0.02) and diastolic BP (70 ± 9 vs. 62 ± 9 mmHg, p = 0.003) than low-risk drinkers with no between-group differences in sleep quality component scores (p ≥ 0.14). In midlife adults taking antihypertensive medications, no difference in nighttime BP was found between at-risk drinkers and low-risk drinkers (p ≥ 0.68), with a higher score for the "use of sleeping medication" component in high-risk drinkers (p = 0.02). Regardless of antihypertensive medication use, no difference between at-risk drinkers and low-risk drinkers was found in nighttime urinary catecholamine levels (p ≥ 0.19).

Conclusions: Our findings suggest that in midlife adults free of antihypertensive medication use, at-risk alcohol use is associated with an increase in nighttime BP, and the increase in nighttime BP may be mediated by mechanisms other than increased catecholamines and poor sleep quality.