Examining the reciprocal effects of racial discrimination and sleep on cardiovascular functioning: An experimental approach

项目摘要/摘要 非裔美国人不成比例地背负着临床和亚临床心血管疾病的负担 (CVD)与欧洲裔美国人(EA)相比，虽然种族歧视的经历 与心血管疾病的发病率有关，包括白天和夜间血压偏高， 这些关联背后的机制尚不清楚。睡眠质量差，如睡眠时间短、睡眠质量差 睡眠连续性，可能是一种新的途径；然而，这种可能性还没有得到严格的测试。而当 睡眠不佳在腹主动脉硬化中更为常见，这一发现前瞻性地预测了心血管疾病的发病率和死亡率 种族歧视会影响睡眠，推测的心血管途径也是复杂的。与种族有关的证据 歧视和睡眠来自于横断面研究，研究人员在很大程度上忽略了 互惠效应的可能性。虽然种族歧视的经历可能会影响夜间睡眠，但睡眠不佳 可能会增加一个人将模棱两可的刺激解释为歧视性或威胁性的倾向并对其做出反应的倾向。仅限 实验设计可以证明种族歧视对睡眠的因果影响，反之亦然。这个 这项提案的首要目标是系统地剖析种族歧视和 睡眠对心血管功能的影响，包括血压调节，并确定关键机制和 歧视-睡眠链接的主持人。 为了实现这一目标，我们提出了两项实验研究。在研究1中，我们将随机选择80个AA 和80个EA使用我们经过充分验证的基于种族的社会拒绝范例来反对种族歧视(即， 被外群体成员拒绝)或同一种族的社会排斥，以测试种族的因果影响 多导睡眠图测量的客观睡眠参数与夜间心血管疾病的辨别 功能，包括夜间血压。在研究2中，我们将测试睡眠不足对 以睡眠限制为实验对象对种族歧视的认知和生理反应 探测器。在这里，我们将随机将80名AA分为部分睡眠限制条件(2晚4小时/晚) 或在我们的睡眠实验室中正常睡眠，然后进行一系列实验室任务，以评估一个人的倾向 将模棱两可的刺激视为歧视性的、交感神经激活/副交感神经退缩的幅度 在种族间的互动中，对外群成员保持注意警惕。建议的情感， 将检查认知和生理机制，以及潜在的调节因素(例如，社会经济 状态和基于种族的拒绝敏感性)。这些研究将填补科学文献中的基本空白。 并提供必要的关键的因果和机械证据，以解决睡眠和睡眠中的种族差异 心血管风险。

Project Summary/Abstract African Americans (AAs) are disproportionately burdened by clinical and subclinical cardiovascular disease (CVD) when compared to European Americans (EAs), and while experiences of racial discrimination have been associated with CVD morbidity among AAs, including high daytime and nighttime blood pressure, the mechanisms underlying these associations are unclear. Poor sleep, such as short sleep duration and poor sleep continuity, may serve as a novel pathway; however, this possibility has not been rigorously tested. While poor sleep, which is more common among AAs, prospectively predicts CVD morbidity and mortality, findings that racial discrimination affects sleep and putative cardiovascular pathways are mixed. Evidence linking racial discrimination and sleep are derived from cross-sectional studies, and researchers have largely ignored the possibility of reciprocal effects. While experiences of racial discrimination may impair nightly sleep, poor sleep may increase one's tendency to interpret and react to ambiguous stimuli as discriminatory or threatening. Only experimental designs can demonstrate causal influences of racial discrimination on sleep and vice versa. The overarching goal of this proposal is to systematically dissect the reciprocal effects of racial discrimination and sleep on cardiovascular functioning, including blood pressure regulation, and identify key mechanisms and moderators of the discrimination-sleep link. To accomplish this goal, we propose two experimental studies. In Study 1 we will to randomize 80 AAs and 80 EAs to either racial discrimination using our well-validated race-based social rejection paradigm (i.e., being rejected by an outgroup member) or same-race social rejection to test the causal influences of racial discrimination on objective sleep parameters, measured using polysomnography, and nocturnal cardiovascular functioning, including nocturnal blood pressure. In Study 2 we will test the causal influences of sleep loss on perceptions of and physiological reactions to racial discrimination by using sleep restriction as an experimental probe. Here, we will randomize 80 AAs to either a partial sleep restriction condition (2 nights of 4 hours/night) or normal sleep in our sleep laboratory followed by a series of laboratory tasks to assess one's tendency to perceive ambiguous stimuli as discriminatory, magnitude of sympathetic activation/parasympathetic withdrawal during inter-racial interactions, and attentional vigilance toward outgroup members. Proposed affective, cognitive, and physiological mechanisms will be examined as will potential moderators (e.g., socioeconomic status and race-based rejection sensitivity). These studies will fill fundamental gap in the scientific literature and provide the critical causal and mechanistic evidence necessary to address racial disparities in sleep and cardiovascular risk.