A population-based study of reduced sleep duration and hypertension: the strongest association may be in premenopausal women

Saverio Stranges, Joan M Dorn, Francesco P Cappuccio, Richard P Donahue, Lisa B Rafalson, Kathleen M Hovey, Jo L Freudenheim, Ngianga-Bakwin Kandala, Michelle A Miller, Maurizio Trevisan, Saverio Stranges, Joan M Dorn, Francesco P Cappuccio, Richard P Donahue, Lisa B Rafalson, Kathleen M Hovey, Jo L Freudenheim, Ngianga-Bakwin Kandala, Michelle A Miller, Maurizio Trevisan

Abstract

Objectives: Recent evidence indicates that reduced sleep duration may be associated with an increased risk of hypertension with possibly stronger effects among women than men. We therefore examined cross-sectional sex-specific associations of sleep duration with hypertension in a large population-based sample from the Western New York Health Study (1996<2001).

Methods: Participants were 3027 white men (43.5%) and women (56.5%) without prevalent cardiovascular disease (median age 56 years). Hypertension was defined as blood pressure at least 140 or at least 90&mmHg or regular use of antihypertensive medication. Multivariate logistic regression analyses were performed to estimate odds ratios (ORs) of hypertension comparing less than 6&h of sleep per night versus the reference category (&6&h) while accounting for a number of potential confounders.

Results: In multivariate analyses, less than 6&h of sleep was associated with a significant increased risk of hypertension compared to sleeping at least 6&h per night, only among women [OR&=&1.66 (1.09 to 2.53)]. No significant association was found among men [OR&=&0.93 (0.62 to 1.41)].In subgroup analyses by menopausal status, the effect was stronger among premenopausal women [OR&=&3.25 (1.37 to 7.76)] than among postmenopausal women [OR&=&1.49 (0.92 to 2.41)].

Conclusion: Reduced sleep duration, by increasing the risk of hypertension, may produce detrimental cardiovascular effects among women. The association is independent of socioeconomic status, traditional cardiovascular risk factors, and psychiatric comorbidities, and is stronger among premenopausal women. Prospective and mechanistic evidence is necessary to support causality.

Source: PubMed

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