Increasing evidence suggests an association between both short and long duration of habitual sleep with adverse health outcomes. To assess whether the population longitudinal evidence supports the presence of a relationship between duration of sleep and all-cause mortality, to investigate both short and long sleep duration and to obtain an estimate of the risk. We performed a systematic search of publications using MEDLINE (1966–2009), EMBASE (from 1980), the Cochrane Library, and manual searches without language restrictions. We included studies if they were prospective, had follow-up >3 years, had duration of sleep at baseline, and all-cause mortality prospectively. We extracted relative risks (RR) and 95% confidence intervals (CI) and pooled them using a random effect model. We carried out sensitivity analyses and assessed heterogeneity and publication bias. Overall, the 16 studies analyzed provided 27 independent cohort samples. They included 1,382,999 male and female participants (follow-up range 4 to 25 years), and 112,566 deaths. Sleep duration was assessed by questionnaire and outcome through death certification. In the pooled analysis, short duration of sleep was associated with a greater risk of death (RR: 1.12; 95% CI 1.06 to 1.18; P < 0. 01) with no evidence of publication bias (P = 0.74) but heterogeneity between studies (P = 0.02). Long duration of sleep was also associated with a greater risk of death (1.30; [1.22 to 1.38]; P < 0.0001) with no evidence of publication bias (P = 0.18) but significant heterogeneity between studies (P < 0.0001). Conclusion: Both short and long duration of sleep are significant predictors of death in prospective population studies.

To assess the relationship between duration of sleep and morbidity and mortality from coronary heart disease (CHD), stroke, and total cardiovascular disease (CVD). We performed a systematic search of publications using MEDLINE (1966–2009), EMBASE (from 1980), the Cochrane Library, and manual searches without language restrictions. Studies were included if they were prospective, follow-up >3 years, had duration of sleep at baseline, and incident cases of CHD, stroke, or CVD. Relative risks (RR) and 95% confidence interval (CI) were pooled using a random-effect model. Overall, 15 studies (24 cohort samples) included 474 684 male and female participants (follow-up 6.9–25 years), and 16 067 events (4169 for CHD, 3478 for stroke, and 8420 for total CVD). Sleep duration was assessed by questionnaire and incident cases through certification and event registers. Short duration of sleep was associated with a greater risk of developing or dying of CHD (RR 1.48, 95% CI 1.22–1.80, P < 0.0001), stroke (1.15, 1.00–1.31, P = 0.047), but not total CVD (1.03, 0.93–1.15, P = 0.52) with no evidence of publication bias (P = 0.95, P = 0.30, and P = 0.46, respectively). Long duration of sleep was also associated with a greater risk of CHD (1.38, 1.15–1.66, P = 0.0005), stroke (1.65, 1.45–1.87, P < 0.0001), and total CVD (1.41, 1.19–1.68, P < 0.0001) with no evidence of publication bias (P = 0.92, P = 0.96, and P = 0.79, respectively). Both short and long duration of sleep are predictors, or markers, of cardiovascular outcomes.

Recent epidemiological studies suggest that short sleep duration may be associated with the development of obesity from childhood to adulthood. To assess whether the evidence supports the presence of a relationship between short sleep duration and obesity at different ages, and to obtain an estimate of the risk. We performed a systematic search of publications using MEDLINE (1996–2007 wk 40), EMBASE (from 1988), AMED (from 1985), CINHAL (from 1982) and PsycINFO (from 1985) and manual searches without language restrictions. When necessary, authors were contacted. Criteria for inclusion were: report of duration of sleep as exposure, BMI as continuous outcome and prevalence of obesity as categorical outcome, number of participants, age, and gender. Results were pooled using a random effect model. Sensitivity analysis was performed, heterogeneity and publication bias were also checked. Results are expressed as pooled odds ratios (OR [95% confidence intervals, CIs]) and as pooled regression coefficients (β 95% CIs). Of 696 studies identified, 45 met the inclusion criteria (19 in children and 26 in adults) and 30 (12 and 18, respectively) were pooled in the meta-analysis for a total of 36 population samples. They included 634,511 participants (30,002 children and 604,509 adults) from around the world. Age ranged from 2 to 102 years and included boys, girls, men and women. In children the pooled OR for short duration of sleep and obesity was 1.89 (1.46 to 2.43; P < 0.0001). In adults the pooled OR was 1.55 (1.43 to 1.68; P < 0.0001). There was no evidence of publication bias. In adults, the pooled β for short sleep duration was −0.35 (−0.57 to −0.12) unit change in BMI per hour of sleep change. Cross-sectional studies from around the world show a consistent increased risk of obesity amongst short sleepers in children and adults. Causal inference is difficult due to lack of control for important confounders and inconsistent evidence of temporal sequence in prospective studies.

OBJECTIVE: To assess the relationship between habitual sleep disturbances and the incidence of type 2 diabetes and to obtain an estimate of the risk. RESEARCH DESIGN AND METHODS: We conducted a systematic search of publications using MEDLINE (1955–April 2009), EMBASE, and the Cochrane Library and manual searches without language restrictions. We included studies if they were prospective with follow-up >3 years and had an assessment of sleep disturbances at baseline and incidence of type 2 diabetes. We recorded several characteristics for each study. We extracted quantity and quality of sleep, how they were assessed, and incident cases defined with different validated methods. We extracted relative risks (RRs) and 95% CI and pooled them using random-effects models. We performed sensitivity analysis and assessed heterogeneity and publication bias. RESULTS: We included 10 studies (13 independent cohort samples; 107,756 male and female participants, follow-up range 4.2–32 years, and 3,586 incident cases of type 2 diabetes). In pooled analyses, quantity and quality of sleep predicted the risk of development of type 2 diabetes. For short duration of sleep (≤5–6 h/night), the RR was 1.28 (95% CI 1.03–1.60, P = 0.024, heterogeneity P = 0.015); for long duration of sleep (>8–9 h/night), the RR was 1.48 (1.13–1.96, P = 0.005); for difficulty in initiating sleep, the RR was 1.57 (1.25–1.97, P < 0.0001); and for difficulty in maintaining sleep, the RR was 1.84 (1.39–2.43, P < 0.0001). CONCLUSIONS: Quantity and quality of sleep consistently and significantly predict the risk of the development of type 2 diabetes. The mechanisms underlying this relation may differ between short and long sleepers.

Sleep deprivation (≤5 hour per night) was associated with a higher risk of hypertension in middle-aged American adults but not among older individuals. However, the outcome was based on self-reported diagnosis of incident hypertension, and no gender-specific analyses were included. We examined cross-sectional and prospective associations of sleep duration with prevalent and incident hypertension in a cohort of 10 308 British civil servants aged 35 to 55 years at baseline (phase 1: 1985–1988). Data were gathered from phase 5 (1997–1999) and phase 7 (2003–2004). Sleep duration and other covariates were assessed at phase 5. At both examinations, hypertension was defined as blood pressure ≥140/90 mm Hg or regular use of antihypertensive medications. In cross-sectional analyses at phase 5 (n=5766), short duration of sleep (≤5 hour per night) was associated with higher risk of hypertension compared with the group sleeping 7 hours, among women (odds ratio: 2.01; 95% CI: 1.13 to 3.58), independent of confounders, with an inverse linear trend across decreasing hours of sleep ( P =0.003). No association was detected in men. In prospective analyses (mean follow-up: 5 years), the cumulative incidence of hypertension was 20.0% (n=740) among 3691 normotensive individuals at phase 5. In women, short duration of sleep was associated with a higher risk of hypertension in a reduced model (age and employment) (6 hours per night: odds ratio: 1.56 [95% CI: 1.07 to 2.27]; ≤5 hour per night: odds ratio: 1.94 [95% CI: 1.08 to 3.50] versus 7 hours). The associations were attenuated after accounting for cardiovascular risk factors and psychiatric comorbidities (odds ratio: 1.42 [95% CI: 0.94 to 2.16]; odds ratio: 1.31 [95% CI: 0.65 to 2.63], respectively). Sleep deprivation may produce detrimental cardiovascular effects among women.

Although sleep curtailment has become widespread in industrialised societies, little work has examined the effects on mortality of change in sleep duration. We investigated associations of sleep duration and change in sleep duration with all-cause, cardiovascular, and non-cardiovascular mortality. Prospective cohort study. Data are from baseline (Phase 1, 1985–88) and Phase 3 (1991–93), with mortality follow-up of 17 and 12 years respectively. The Whitehall II study of 10,308 white-collar British civil servants aged 35–55 at baseline. 9,781 participants with complete data were included in the analyses at Phase 1, and 7,729 of the same participants were included in the analyses at Phase 3 and the analyses of change in sleep duration. None. U-shaped associations were observed between sleep (≤5, 6, 7, 8, ≥9 hours) at Phase 1 and Phase 3 and subsequent all-cause, cardiovascular, and non-cardiovascular mortality. A decrease in sleep duration among participants sleeping 6, 7, or 8 hours at baseline was associated with cardiovascular mortality, hazard ratio 2.4 (95% confidence intervals 1.4–4.1). However, an increase in sleep duration among those sleeping 7 or 8 hours at baseline was associated with non-cardiovascular mortality, hazard ratio 2.1 (1.4–3.1). Adjustment for the socio-demographic factors, existing morbidity, and health-related behaviours measured left these associations largely unchanged. This is the first study to show that both a decrease in sleep duration and an increase in sleep duration are associated with an increase in mortality via effects on cardiovascular death and non-cardiovascular death respectively.