0138 Behaviorally Assessed Sleep Duration and Oxidative Stress

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Abstract Introduction Sleep may promote health by acting as an antioxidant, thereby increasing the body’s resistance to oxidative stress. Lipid peroxidation, a marker of oxidative stress, is one of the key early events in the development of atherosclerosis, the pathologic condition that underlies cardiovascular disease (CVD). Short sleep duration is prevalent in the general population and associated with CVD risk. However, the mechanisms linking short sleep to CVD are not well understood. Methods To test the hypothesis that short sleep duration would be associated with higher levels of oxidative stress, we conducted secondary data analysis on a diverse sample of participants (N= 81; Mage = 30.1(SD=10.9); 57% Male; 27% African American) from Pittsburgh, Pennsylvania. Participants wore actigraphs on their non-dominant wrists for 7 days to collect rest and activity data, which were used to derive average sleep duration. Participants provided urine samples and self-reported demographic data, along with daily mood, alcohol use, and physical activity. Oxidative stress was quantified as urinary concentrations of 15-F2t-isoprostane (15-F2-IsoP). Levels of 15-F2-IsoP were measured with a competitive enzyme linked-immunosorbent assay (ELISA) in duplicate. Urinary 15-F2-IsoP was adjusted by urinary creatinine to create an index of oxidative stress that took into account a measure of antioxidant defenses. Results Sleep duration was inversely correlated with oxidative stress (b= -.24, p=.03). In multiple regression analyses that controlled for age, sex, race, body mass index, alcohol use, physical activity, and depressed mood, sleep duration remained significantly negatively associated with oxidative stress, β = -.16, t = -2.33, p = .02, R2= .20. Conclusion These findings are important because they suggest that a relationship exists between short sleep and increased oxidative damage to lipids. Increasing our understanding of this relationship could motivate new CVD prevention strategies that target the inhibition of oxidative stress through sleep interventions. Support This study was supported by a grant from the National Center for Complementary and Integrative Health (AT006694); a grant from the National Institute of Allergy and Infectious Diseases (R01 AI066367); grants from the National Institutes of Health (UL1 RR024153 and UL1 RT000005); and by the John D. and Catherine T. MacArthur Foundation.

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