No abstract

Historically and contemporarily, Black Americans have been compelled to use effortful coping styles characterized by high behavioral and emotional restraint in the face of systematic racism. Lynch and colleagues have previously conceptualized a class of regulatory strategies—overcontrolled coping—characterized by emotional suppression, hypervigilance for threat, and high distress tolerance, which bear close analogy to coping styles frequently used among individuals facing chronic racial stress. However, given the inherent culture of racism in the United States, engaging in highly controlled coping strategies is often necessitated and adaptive, at least in the short term. Thus, for Black Americans this class of coping strategies is conceptualized as culturally compelled coping rather than overcontrolled coping. In the current article, I offer a critical examination of the literature and introduce a novel theoretical model—culturally compelled coping—that culturally translates selected components of Lynch’s model. Cultural translation refers to considering how the meaning, function, and consequences of using overcontrolled coping strategies changes when considering how Black Americans exist and cope within a culture of systematic racism. Importantly, this model may offer broad implications for future research and treatment by contextualizing emotion regulation as a central mechanism, partially answering how racism “gets under the skin” and affects the health of Black Americans.

Objective Decades of research suggest that there may be important ethnic differences in the hemodynamic mechanisms that co-determine arterial blood pressure, the primary diagnostic index of hypertension. In general, studies have observed that, compared with European Americans (EAs), African Americans (AAs) exhibit higher total peripheral resistance (TPR), an important summative index of peripheral vascular constriction. In contrast, EAs have been reliably shown to exhibit greater cardiac output (CO), which is directly linked to left ventricle and overall cardiac blood flow. We have previously proposed that elevated basal TPR, in particular, represents one component of the cardiovascular conundrum, characterized, paradoxically, by elevated resting heart rate variability among AAs relative to EAs. The present meta-analysis and systematic review of the literature sought to extend this previous work by establishing the magnitude of the empirically implied ethnic differences in resting TPR and CO. Methods A search of the literature yielded 140 abstracts on differences in TPR between AAs and EAs; 40 were included. Sample sizes, means, and standard deviations for baseline TPR with samples that included EAs and AAs were collected, and Hedges g was computed. Results Findings indicated that AAs had higher baseline TPR than did EAs (Hedges g = 0.307, SE = 0.043, confidence interval= 0.224 to 0.391, p < .001). In addition, EAs had higher resting CO than did AAs (Hedges g = −0.214, SE = 0.056, confidence interval = −0.324 to −0.104, p < .001). Conclusions We discuss the present findings in the context of the role of elevated TPR in the deleterious effects of high blood pressure specifically for AAs.