Yin · Journal of the American Heart Association 2017 · systematic review and dose-response meta-analysis of prospective cohort studies · n=?

Relationship of Sleep Duration With All-Cause Mortality and Cardiovascular Events: A Systematic Review and Dose-Response Meta-Analysis of Prospective Cohort Studies.

Cited 724 times in the scientific literature.

Level 1 - systematic review of randomized trials

Systematic review and meta-analysis of prospective cohort studies for an etiological/prognostic question

PubMed 28889101 · doi:10.1161/JAHA.117.005947 · record verified 2026-08-26

What was done

PubMed and Embase were systematically searched through December 1, 2016, for prospective cohort studies examining the dose-response associations between sleep duration and risk of all-cause mortality, total cardiovascular disease (CVD), coronary heart disease (CHD), and stroke in generally healthy populations.

What was found

A U-shaped association was observed for all outcomes, with the lowest risk at approximately 7 hours of sleep per day regardless of sex. - All-cause mortality: For <7 hours/day, pooled relative risk (RR) was 1.06 (95% CI, 1.04–1.07) per 1-hour reduction; for >7 hours/day, pooled RR was 1.13 (95% CI, 1.11–1.15) per 1-hour increment. - Total CVD: Pooled RR was 1.06 (95% CI, 1.03–1.08) per 1-hour reduction and 1.12 (95% CI, 1.08–1.16) per 1-hour increment. - Coronary heart disease: Pooled RR was 1.07 (95% CI, 1.03–1.12) per 1-hour reduction and 1.05 (95% CI, 1.00–1.10) per 1-hour increment. - Stroke: Pooled RR was 1.05 (95% CI, 1.01–1.09) per 1-hour reduction and 1.18 (95% CI, 1.14–1.21) per 1-hour increment.

Why it matters

This meta-analysis quantifies a consistent U-shaped risk curve, establishing 7 hours per day as the reference nadir for cardiovascular and all-cause mortality risk.

Limits

The abstract does not state the number of included studies, overall participant sample size, or follow-up durations. Because the underlying data come from observational cohort studies, residual confounding and reverse causation (e.g., pre-existing subclinical disease causing longer sleep duration) cannot be excluded, and sleep duration was likely assessed via self-report rather than objective actigraphy or polysomnography.

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