Background: Existing evidence suggested that sleep duration may be involved in hypertension; however, the conclusions were still controversial. This study aimed to examine the association of longitudinal trajectory of sleep duration with hypertension and to explore the role of the inflammation in such associations.
Methods: A total of 3178 subjects over 30 years of age without hypertension were enrolled in 2004, and they were followed until 2009. Self-reported sleep duration was recorded, and inflammation was measured by highly sensitive C reactive protein (hs-CRP). Log-binomial regression models were applied to examine the association of sleep duration trajectory and inflammation with the risk of hypertension. The mediating effect of elevated hs-CRP was examined by the bootstrap and the process software.
Results: The prevalence of persistent short (≤ 7 hours/day), normal (8– 9 hours/day), and long (> 9 hours/day) sleep duration over 5 years were 9.1%, 37.7%, and 2.3%, respectively. The incidence of hypertension was 26.6% during the follow-up period. Compared with those who persistently slept 8– 9 hours/day from baseline to follow-up, those who persistently slept ≤ 7 hours/day, persistently slept ≥ 10 hours/day, and those whose sleep duration changed have higher risks of hypertension by 1.375-fold (95% CI: 1.121, 1.686), 1.557-fold (95% CI: 1.171, 2.069) and 1.299-fold (95% CI: 1.135, 1.487), respectively. In addition, persistently slept ≤ 7 hours/day was found to be associated with higher risk of inflammation (RR: 1.285, 95% CI: 1.008, 1.638). The mediation analysis did not find significant mediating effect of elevated CRP on the association between sleep duration trajectory and hypertension.
Conclusion: Experiencing both a short or long sleep duration, especially for a long time, could lead to higher risk of hypertension. Persistent exposure to short sleep duration was also associated with inflammation. However, the higher risk of hypertension caused by persistent short sleep duration does not seem to be directly mediated through inflammation.
Keywords: sleep duration, trajectory, inflammation, hypertension, longitudinal study