Sleep Duration, Sleep Quality, and Biomarkers of Inflammation in a Taiwanese Population
Introduction
Experimental and observational data indicate that sleep duration and other sleep characteristics are associated with a wide array of health outcomes including all-cause mortality, cardiovascular disease, diabetes, and obesity 1, 2, 3. Recent work has begun to investigate the role of inflammation in mediating associations between sleep and health outcomes 4, 5, 6, 7. Experimentally, sleep deprivation is associated with acute elevation of both C-reactive protein (CRP) and interleukin-6 (IL-6) 8, 9, but findings in nonexperimental settings have been mixed 5, 6, 7, 10, 11, 12. Associations between overall sleep quality and inflammatory markers have been more consistent but have still produced diverse findings (13). This study examined associations between self-reported sleep duration, sleep quality, and biomarkers of inflammation in a middle-aged and elderly cohort of Taiwanese adults.
Biologically, there are plausible mechanisms linking inflammation and sleep in both causal directions (14). Activation of the autonomic nervous system and elevated catecholamines during sleep deprivation can stimulate production of inflammatory mediators (10). Sleep deprivation also leads to blood pressure elevations that may increase endothelial shear stress (the force of flowing blood over the surface of the endothelium) (15), resulting in endothelial production of inflammatory mediators such as IL-6 and adhesion molecules such as e-selectin and soluble intercellular adhesion molecule-1 (sICAM-1) 10, 16. In the reverse direction, cytokines may have direct effects on the brain, including the regions involved in sleep regulation 14, 17. Cytokines are important regulators of host defense to infection, and the sleep-inducing impact of cytokines such as IL-6, as well as other immune cells that increase expression of these cytokines, may predispose persons with elevated levels of inflammation to longer sleep durations (18).
This study seeks to fill several gaps in the current literature. First, although studies of sleep duration and outcomes such as obesity, diabetes, and mortality have focused on the U-shaped risk of both short and long sleep, studies on sleep duration and inflammation have focused either on short sleep duration or modeled sleep duration linearly, both approaches potentially missing an effect at longer durations. Second, the majority of existing studies of sleep characteristics and inflammation have examined Western populations. A biological necessity, sleep is also a complex behavior influenced by cultural and social factors, such as the encouragement or discouragement of naps, traditional care giving roles, or the amount of time typically devoted to work. Thus, cross-cultural studies may help elucidate disease etiology in settings where the determinants of sleep habits differ (19). Last, most studies on sleep characteristics and inflammation have looked at young adult populations, but differences in these relationships may emerge in older populations, among whom chronic disease and higher levels of inflammation are more prevalent 20, 21. It is possible that the mechanisms through which sleep affects inflammatory processes (and vice versa) vary across the life span. In particular, long sleep is most prevalent in those over age 60, and a lengthening of sleep duration may coincide with the aging process and declining health 22, 23, 24.
Section snippets
Sample
Data are from the 2000 and 2006 Social Environment and Biomarkers of Aging Study (SEBAS) of Taiwanese adults 53 years of age and over in 2006. All participants were part of the ongoing Taiwan Longitudinal Study of Aging (TLSA) initiated in 1989, with interviews conducted every 3–4 years and with periodic inclusion of younger refresher cohorts (25). In 2000, a demographic and health update, blood and urine specimens, and a medical examination were collected on a subset of respondents (SEBAS I,
Sleep
Sleep questions were asked for the first time in 2006. A shortened version of the Pittsburgh Sleep Quality Index (PSQI) captured five dimensions of sleep over the month before interview (30): subjective sleep quality, sleep latency (time to fall asleep), sleep duration (during the night), sleep efficiency (hr asleep/hr in bed), and sleep dysfunction (daytime sleepiness). The original PSQI contains two additional subcomponents: sleep disturbances and use of sleep medication (30). Subsequent
Results
The average age of the sample was 66 years, with 6.4 average hours of reported sleep (Table 1). Overall, there were few associations between the inflammatory markers and the PSQI subcomponents or the overall PSQI (Table 2). There were no significant associations for CRP, IL-6, fibrinogen, WBC, or albumin. sICAM-1 showed marginally significant positive associations with the overall index (p ≈ 0.057), sleep efficiency (p ≈ 0.092), and a significant association with the index measure of short
Discussion
From our cross-sectional data, we found virtually no relationship between biomarkers of inflammation and the overall sleep quality index or its subcomponents. In contrast, we found a strong relationship between long sleep duration and most markers of inflammation, with little evidence of associations between short sleep duration and inflammation. Increases in inflammation between 2000 and 2006, determined from longitudinal data, were associated with an increased relative risk of long sleep
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