Short sleep duration (<6 hours/night) is associated with a higher prevalence and incidence of hypertension, diabetes, and overweight/obesity, all of which can contribute to coronary heart disease. Pathophysiologic mechanisms that could explain these associations such as autonomic nervous system dysfunction, endothelial dysfunction, inflammation, and insulin resistance have been identified in the setting of sleep disordered breathing (SDB), namely sleep apnea, or in experimental studies of sleep restriction. However, over 90% of adults do not suffer from SDB, and complete sleep restriction is rare. Rather, an important public health concern is whether these pathophysiologic mechanisms are apparent in association with short sleep duration in persons without SDB. The present epidemiologic study will recruit a sample of 500 adults aged 35-64 from the Chicago, IL area who do not have SDB as determined by validated screening questionnaires and in-home overnight polysomnography. Half of the population will be female and 25% each will be of Caucasian, African- American, Asian, and Latino race/ethnicity. Participants free from SDB will undergo wrist actigraphy to measure sleep duration for 7-days in their regular home environment. They will undergo a 2.5-hour clinical examination to have resting parasympathetic function measured, and biomarkers of endothelial function (von Willebrand factor and E-selectin) and adipocytokines that represent insulin resistance (adiponectin, leptin, resistin, tumor necrosis factor-1, plasminogen activator inhibitor-1) and inflammation (C-reactive protein) measured in fasting blood. Metabolic syndrome components (blood pressure, lipids, glucose, anthropometrics), the prevalence of mood disorders, medical history, and health behaviors will be determined using standard clinical procedures and questionnaires. Using this information, the investigators will test the hypothesis that shortened sleep duration, in the absence of SDB, is associated with lower resting parasympathetic function, endothelial dysfunction insulin resistance, and inflammation. Using the wealth of assembled data, investigators will explore the confounding and modifying effects of demographic characteristics, physical activity and depressive symptoms on any observed associations. The primary innovation of this cross-sectional epidemiologic study is the ability to study the association of objectively- measured sleep duration within the normal population range on pathophysiologic mechanisms associated with metabolic syndrome components. Our population-based sampling method permits generalizability of our findings to the race/ethnically diverse population with known variations in sleep duration and metabolic disease. Findings from this cross-sectional study will suggest mechanisms to explain the prior observed associations between sleep duration and cardiovascular disease risk factors.
Persons who sleep for less time each night have worse health profiles characterized by higher rates of hypertension, diabetes, and heart disease (i.e., cardiovascular diseases [CVD]). Studies in persons with sleep disordered breathing (SDB) conditions such as sleep apnea and experimental studies that restrict sleep have identified a number of mechanisms that could explain this association. No studies have tested whether these mechanisms are present in relation to measured (i.e., not self-reported) sleep duration in an observational setting of persons who do not have SDB. The present study will recruit a sample of 500 adults (50% women and 25% each Caucasian, African-American/Black, Asian, and Latino) ages 35-64 years from Chicago, IL and screen them for SDB using in-home polysomnography. Adults without SDB will wear portable wrist monitors for 7 days to measure sleep duration. Participants will attend a brief clinical examination to measure the mechanisms above and traditional CVD risk factors. The investigators hypothesize that shorter sleep duration is associated with autonomic nervous system dysfunction, endothelial dysfunction, inflammation, and insulin resistance. Findings from this study will suggest mechanisms to explain the prior observed associations between sleep duration and CVD risk factors.
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