Carrington C. Merritt

Objective: Inflammation may be an integral physiological mechanism through which discrimination impacts cardiovascular health and contributes to racial health disparities. Limited research has examined psychosocial factors that protect against the negative effects of discrimination on inflammation. Perceived control is a promising possible protective factor, given that it has been shown to moderate the relationship between other psychosocial stressors and physiological outcomes. This study thus tested whether systemic inflammation mediated the link between discrimination and cardiovascular health and whether perceived control moderated this relationship. Methods: Data for this project included 347 non-Hispanic/Latinx Black adults (mean [standard deviation] age = 51.64 [11.24] years; 33% female) taken from the Midlife in the United States study. Perceived control and daily discrimination were assessed via self-report, and inflammation was measured via circulating levels of C-reactive protein (CRP), interleukin-6 (IL-6), fibrinogen, and tumor necrosis factor α. Cardiovascular health was measured by morbidity of cardiovascular conditions: heart disease, hypertension, and/or stroke. Results: CRP (indirect effect: b = 0.004, 95% confidence interval [CI] = 0.001–0.007) and fibrinogen (indirect effect: b = 0.002, 95% CI = 0.0003–0.005) mediated the link between discrimination and cardiovascular conditions. Perceived control moderated the relationship between discrimination and CRP (F(1, 293) = 4.58, ΔR ² = 0.013, b = −0.02, SE = 0.01, p = .033). CRP mediated the link between discrimination and cardiovascular conditions only for those who reported low levels of perceived control (Index = −0.003, 95% CI = −0.007 to −0.0001). Conclusion: Findings provide empirical evidence of inflammation as a mechanism linking discrimination to cardiovascular conditions among Black Americans. Additionally, perceived control may be protective. Findings could suggest beliefs about control as a potential intervention target to help reduce the negative effects of discrimination on cardiovascular health among Black Americans.

Black Americans are diagnosed with schizophrenia spectrum disorders at more than twice the rate of White individuals and experience significantly worse outcomes following diagnosis. Little research has examined specific factors that may contribute to worse functional outcomes among Black Americans diagnosed with schizophrenia. One approach to understanding why racial disparities emerge is to examine established predictors of functioning in this population: neurocognition, social cognition, and symptom severity. The present study aims to broaden existing literature on racial differences within these domains by (a) examining racial differences in functioning and these established predictors of functioning (i.e., neurocognition, social, and symptom severity) and (b) investigating whether cognition and symptom domains similarly predict functioning between Black and White Americans with schizophrenia. Sixty-six participants' baseline neurocognition, social cognition, symptom severity, and functioning were assessed. Black participants demonstrated lower neurocognition scores and higher levels of disorganized symptoms relative to White participants. No racial differences in functioning or social cognition were observed. Further, race did not moderate the relationship between any of these established predictors and functioning outcomes. The largely nonsignificant differences in known predictors of functioning highlight the need to explore further domains that may be more relevant for understanding racial disparities in schizophrenia. Considering that psychosocial treatments for schizophrenia spectrum disorders often focus on cognition, these results underscore the importance of identifying whether these domains or other treatment targets may be better in addressing racial disparities in functioning. Possible areas of exploration for future work (e.g., structural factors, racism-related stress) are discussed. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Racial disparities in health are a major public health problem in the United States, especially when comparing chronic disease morbidity and mortality for Black versus White Americans. These health disparities are primarily due to insidious anti-Black racism that permeates American history, current culture and institutions, and interpersonal interactions. But how does racism get under the skull and the skin to influence brain and bodily processes that impact the health of Black Americans? In the present article, we present a model describing the possible neural and inflammatory mechanisms linking racism and health. We hypothesize that racism influences neural activity and connectivity in the salience and default mode networks of the brain and disrupts interactions between these networks and the executive control network. This pattern of neural functioning in turn leads to greater sympathetic nervous system signaling, hypothalamic-pituitary-adrenal axis activation, and increased expression of genes involved in inflammation, ultimately leading to higher levels of proinflammatory cytokines in the body and brain. Over time, these neural and physiological responses can lead to chronic physical and mental health conditions, disrupt well-being, and cause premature mortality. Given that research in this area is underdeveloped to date, we emphasize opportunities for future research that are needed to build a comprehensive mechanistic understanding of the brain-body pathways linking anti-Black racism and health. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Roughly 20 years of functional magnetic resonance imaging (fMRI) studies have investigated the neural correlates underlying engagement in social cognition (e.g. empathy and emotion perception) about targets spanning various social categories (e.g. race and gender). Yet, findings from individual studies remain mixed. In the present quantitative functional neuroimaging meta-analysis, we summarized across 50 fMRI studies of social cognition to identify consistent differences in neural activation as a function of whether the target of social cognition was an in-group or out-group member. We investigated if such differences varied according to a specific social category (i.e. race) and specific social cognitive processes (i.e. empathy and emotion perception). We found that social cognition about in-group members was more reliably related to activity in brain regions associated with mentalizing (e.g. dorsomedial prefrontal cortex), whereas social cognition about out-group members was more reliably related to activity in regions associated with exogenous attention and salience (e.g. anterior insula). These findings replicated for studies specifically focused on the social category of race, and we further found intergroup differences in neural activation during empathy and emotion perception tasks. These results help shed light on the neural mechanisms underlying social cognition across group lines.