Autonomic, Endothelial, and Inflammatory Correlates of Sleep Duration

描述(由申请人提供)：睡眠时间短(&lt；6小时/晚)与高血压、糖尿病和超重/肥胖的患病率和发病率较高有关，所有这些都可能导致冠心病。在睡眠呼吸紊乱(SDB)的背景下，即睡眠呼吸暂停，或在睡眠限制的实验研究中，已经确定了可以解释这些关联的病理生理机制，如自主神经系统功能障碍、内皮功能障碍、炎症和胰岛素抵抗。然而，超过90%的成年人没有SDB，完全限制睡眠的情况很少见。相反，一个重要的公共卫生问题是，这些病理生理机制是否与没有SDB的人的睡眠时间短有关。本次流行病学研究将从伊利诺伊州芝加哥地区招募年龄为35-的成年人500名，通过有效筛查问卷和居家过夜多导睡眠图确定他们没有SDB。一半的人口将是女性，25%的人将分别是高加索人、非裔美国人、亚洲人和拉丁裔人。没有SDB的参与者将在他们正常的家庭环境中接受腕部动作描记，以测量7天的睡眠时间。他们将接受2.5小时的临床检查，测量静息副交感神经功能，并检测空腹血中血管内皮细胞功能的生物标记物(von Willebrand因子和E-选择素)以及代表胰岛素抵抗的脂肪细胞因子(脂联素、瘦素、抵抗素、肿瘤坏死因子-1、纤溶酶原激活物抑制物-1)和炎症(C-反应蛋白)。代谢综合征成分(血压、血脂、血糖、人体测量学)、情绪障碍的患病率、病史和健康行为将使用标准的临床程序和问卷来确定。利用这些信息，研究人员将检验这一假设，即在缺乏SDB的情况下，睡眠时间缩短与静息副交感神经功能降低、内皮功能障碍、胰岛素抵抗和炎症有关。利用收集到的大量数据，研究人员将探索人口统计特征、体力活动和抑郁症状对任何观察到的关联的混淆和修正效应。这项横断面流行病学研究的主要创新是能够研究在正常人群范围内客观测量的睡眠时间与与代谢综合征组成部分相关的病理生理机制的关联。我们的基于人群的抽样方法允许将我们的发现推广到具有已知睡眠时间和代谢性疾病变化的种族/民族多样化的人群。这项横断面研究的结果将为解释先前观察到的睡眠时间与心血管疾病风险因素之间的关联提供机制。与公共健康相关：每晚睡眠时间较少的人的健康状况较差，其特点是高血压、糖尿病和心脏病(即心血管疾病)的发病率较高。对睡眠呼吸暂停等睡眠呼吸障碍(SDB)患者的研究和限制睡眠的实验研究发现了许多可以解释这种联系的机制。没有研究测试这些机制是否与没有SDB的人的观察环境中测量的(即，不是自我报告的)睡眠持续时间有关。本研究将从伊利诺伊州芝加哥招募年龄在35-之间的500名成年人(女性占50%，高加索人、非裔美国人/黑人、亚裔和拉丁裔各占25%)，并使用家庭多导睡眠图对他们进行SDB筛查。没有SDB的成年人将佩戴便携式手腕监测器7天来测量睡眠时间。参与者将参加一项简短的临床检查，以衡量上述机制和传统的心血管疾病危险因素。研究人员假设，睡眠时间较短与自主神经系统功能障碍、内皮功能障碍、炎症和胰岛素抵抗有关。这项研究的发现将为解释先前观察到的睡眠时间与心血管疾病风险因素之间的关联提供机制。

DESCRIPTION (provided by applicant): 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. PUBLIC HEALTH RELEVANCE: 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.