Objective: We investigated the association between sleep duration and the risk of all-cause and cardiovascular death, and explored the potential mediators of atherosclerotic markers in causal effect to identify potential biological pathways. Design and method: We used data from the Chin-Shan Community Cardiovascular Cohort in Taiwan, a prospective study. After excluding individuals with incomplete data and those with cardiovascular diseases, 3,305 participants were included. Participants were classified into three sleep duration groups as short (=9 hours) through structured questionnaires. Cox proportional hazard models and restricted cubic splines assessed the associations and non-linear trends. Causal mediation analysis was performed to identify potential mediators. Results: During a median of 30.8 years of follow-up, after adjusting for potential confounding factors, long sleep duration was significantly associated with increased risks of all-cause mortality (adjusted hazard ratio aHR: 1.17, 95% confidence interval CI: 1.01, 1.35), while short sleep duration showed no significant difference. However, long sleep duration was not significantly associated with cardiovascular mortality (aHR: 1.18, 95% CI: 0.89, 1.56). However, short sleep duration was no significant associated with either outcome. In addition, Subgroup analysis showed the effects were consistent across age, sex, body mass index, hypertension, and diabetes. Moreover, Systolic blood pressure was identified as a potential mediator between long sleep duration and all-cause mortality, with indirect effects of 1.03 (95% CI: 1.00, 1.06). Conclusions: We clearly demonstrated that a longer sleep duration increased the risk of all-cause mortality, and systolic blood pressure played a significant mediator for the effect.
Chien et al. (Fri,) studied this question.