Longer Sleep Duration and Endothelial Cell Health Among a Multiethnic Sample of Adolescents.

Abstract

Adverse endothelial cell health, an early pathogenic process underlying atherosclerosis and cardiovascular disease, is evident in childhood and adolescence. Sleep duration, a modifiable cardiovascular health behavior, may be an important cardiovascular disease prevention target that may affect endothelial cell health. We examined the associations of longer sleep duration with endothelial cell injury among youth. In a multiethnic sample of 235 children (63.0% female, mean age = 13.9 years), we conducted multivariable linear regressions to test the cross-sectional association of sleep duration and circulating levels of endothelial cell-derived microparticles (EMPs), phenotypic for endothelial cell activation and apoptosis (CD62E+ EMPs, CD31+/CD42b- EMPs, and CD31+/Annexin V+ EMPs). Sleep duration and EMPs were both treated as continuous variables. Models were adjusted for age, sex, race, pubertal status, household economic resources, and waist circumference. Overall, 69.2% had short sleep duration (<8 hours of sleep per night). Longer sleep duration was significantly associated with lower levels of CD62E+ EMPs and CD31+/CD42b- EMPs. A 60-minute increase in sleep duration was associated with an 8.40 (95% confidence interval = -205.20 to -1.80, p = .046) decrease in CD62E+ EMPs and a 9.00 (95% confidence interval = -153.60 to -9.60, p = .027) decrease in CD31+/CD42b- EMPs. Sleep duration was not associated with CD31+/Annexin V+ EMPs. Our results support the hypothesis that sleeping longer has beneficial effects on endothelial cell health during childhood. Primordial prevention efforts might incorporate sleep extension to offset cardiovascular risk in youth.