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

Stranges, Saverioa,b; Dorn, Joan Mb,c; Cappuccio, Francesco Pd; Donahue, Richard Pb; Rafalson, Lisa Be; Hovey, Kathleen Mb; Freudenheim, Jo Lb; Kandala, Ngianga-Bakwind; Miller, Michelle Ad; Trevisan, Mauriziob,f

doi: 10.1097/HJH.0b013e328335d076
Original papers: Epidemiology
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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.

aHealth Sciences Research Institute, University of Warwick Medical School, Coventry, United Kingdom

bDepartment of Social and Preventive Medicine, USA

cDepartment of Exercise and Nutrition Sciences, School of Public Health and Health Professions, State University of New York (SUNY) at Buffalo, Buffalo, New York, USA

dClinical Sciences Research Institute, University of Warwick Medical School, Coventry, United Kingdom

eDepartment of Family Medicine, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, New York, USA

fHealth Sciences System, Nevada System of Higher Education, Las Vegas, Nevada, USA

Received 4 August, 2009

Revised 11 November, 2009

Accepted 22 November, 2009

Correspondence to Saverio Stranges, MD, PhD, Associate Clinical Professor of Cardiovascular Epidemiology, Health Sciences Research Institute, University of Warwick Medical School, Medical School Building, Room A105, Gibbet Hill Campus, Coventry CV4 7AL, UK Tel: + 44 2476151153; fax:+ 44 2476528375; e-mail: S.Stranges@warwick.ac.uk

© 2010 Lippincott Williams & Wilkins, Inc.