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.
African Americans are disproportionately affected by cardiovascular disease (CVD) and while experiences of racial discrimination are thought to contribute to their excess CVD risk, the mechanisms are unknown. Poor sleep, which is more common among African Americans, may be an important pathway but only experimental studies can demonstrate a causal link. The proposed experimental studies will provide the first evidence for the causal influence of racial discrimination on sleep and cardiovascular function as well as their reciprocal effects, thus providing the critical foundational data necessary for understanding racial disparities in cardiovascular disease.
