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

检查种族歧视和睡眠对心血管功能的相互影响：实验方法

• 批准号: 10448354
• 负责人: Aric Andrew Prather
• 金额: $ 67.53万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
• 依托单位国家: 美国
• 财政年份: 2018
• 资助国家: 美国
• 起止时间: 2018-07-01 至 2024-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10448354
• 关键词: Address; Affect; Affective; African American population; American; Anger; Anxiety; Attention; Beds; Blood Pressure; Cardiovascular Diseases; Cardiovascular Physiology; Cardiovascular system; Clinical; Cognitive; Cross-Sectional Studies; Data; Discrimination; European; Experimental Designs; Exposure to; Feedback; Foundations; Goals; Heart Diseases; Hour; Hypertension; Impairment; Laboratories; Link; Literature; Measures; Mediator of activation protein; Morbidity - disease rate; Parasympathetic Nervous System; Participant; Pathway interactions; Perception; Peripheral; Physiological; Physiological Processes; Physiology; Polysomnography; Process; Race; Randomized; Reaction; Research Personnel; Series; Sleep; Sleep Deprivation; Sleep disturbances; Social Interaction; Socioeconomic Status; Standardization; Stimulus; Stroke; Testing; Time; Withdrawal; actigraphy; base; blood pressure elevation; blood pressure regulation; cardiovascular disorder risk; cardiovascular risk factor; coronary artery calcification; experience; experimental study; member; mortality; novel; perceived discrimination; poor sleep; prospective; racial discrimination; racial disparity; sleep onset; sleep quality; social; vigilance

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.

项目总结/摘要 非裔美国人（AAs）不成比例地负担着临床和亚临床心血管疾病 (CVD)与欧洲裔美国人相比，虽然种族歧视的经历 与AA中CVD发病率相关，包括白天和夜间高血压， 这些关联的机制尚不清楚。睡眠不好，如睡眠时间短， 睡眠连续性可能是一种新的途径;然而，这种可能性尚未经过严格的测试。而 研究发现，睡眠不佳在AA中更常见，可预测CVD发病率和死亡率。 种族歧视影响睡眠和假定的心血管通路是混合的。证据表明种族歧视 歧视和睡眠是来自横截面研究，研究人员在很大程度上忽略了 相互影响的可能性。虽然种族歧视的经历可能会损害夜间睡眠， 可能会增加一个人的倾向，解释和反应模糊的刺激作为歧视或威胁。只 实验设计可以证明种族歧视对睡眠的因果影响，反之亦然。的 这项建议的总体目标是系统地剖析种族歧视的相互影响， 睡眠对心血管功能的影响，包括血压调节，并确定关键机制， 歧视与睡眠之间的联系。 为了实现这一目标，我们提出了两个实验研究。在研究1中，我们将随机分配80名AA 和80个EA，无论是种族歧视使用我们的良好验证的种族为基础的社会排斥范式（即， 被外群成员拒绝）或同种族社会拒绝，以测试种族的因果影响。 辨别客观睡眠参数，使用多导睡眠描记仪和夜间心血管 包括夜间血压。在研究2中，我们将测试睡眠不足对睡眠质量的影响。 通过使用睡眠限制作为实验， 探针在这里，我们将80名AA随机分为部分睡眠限制条件（2晚，每晚4小时） 或在我们的睡眠实验室进行正常睡眠，然后进行一系列实验室任务，以评估一个人的倾向， 将模糊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 在种族间的相互作用，并注意警惕外群体成员。建议情感， 将检查认知和生理机制以及潜在的调节剂（例如，社会经济 状态和基于种族的抑制灵敏度）。这些研究将填补科学文献中的根本空白 并提供关键的因果和机械证据，以解决睡眠中的种族差异， 心血管风险

项目成果

Better together: Sleep, circadian genes, and immunity.

更好的结合：睡眠、昼夜节律基因和免疫力。

• DOI: 10.1016/j.bbi.2020.04.011
• 发表时间: 2020
• 期刊: Brain, behavior, and immunity
• 作者: Prather,AricA

"GrimAge," an epigenetic predictor of mortality, is accelerated in major depressive disorder.

“恶心”是一种死亡率的表观遗传预测指标，在重度抑郁症中加速了。

• DOI: 10.1038/s41398-021-01302-0
• 发表时间: 2021-04-06
• 期刊: Translational psychiatry
• 影响因子: 6.8
• 作者: Protsenko E;Yang R;Nier B;Reus V;Hammamieh R;Rampersaud R;Wu GWY;Hough CM;Epel E;Prather AA;Jett M;Gautam A;Mellon SH;Wolkowitz OM
• 通讯作者: Wolkowitz OM

HPA axis regulation and epigenetic programming of immune-related genes in chronically stressed and non-stressed mid-life women.

• DOI: 10.1016/j.bbi.2020.11.027
• 发表时间: 2021-03
• 期刊: Brain, behavior, and immunity
• 作者: Palma-Gudiel H;Prather AA;Lin J;Oxendine JD;Guintivano J;Xia K;Rubinow DR;Wolkowitz O;Epel ES;Zannas AS
• 通讯作者: Zannas AS