Brain-Body Pathways Linking Racism and Health

Abstract

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.

“But all of our phrasing—race relations, racial chasm, racial justice, racial profiling, white privilege, even white supremacy—serves to obscure that racism is a visceral experience, that it dislodges brains, blocks airways, rips muscle, extracts organs, cracks bones, breaks teeth. You must never look away from this. You must always remember that the sociology, the history, the economics, the graphs, the charts, the regressions all land, with great violence, upon the body.”

Ta-Nehisi Coates, Between the World and Me

There are long standing and persistent racial health disparities in the United States. Disparities are particularly pronounced when comparing the health and well-being of Black Americans to that of White Americans. Specifically, Black Americans have significantly higher risk of asthma, diabetes, hypertension, kidney disease, obesity, and pancreatic disease compared to White Americans (Centers for Disease Control and Prevention, 2019). Black Americans also have a shorter life expectancy and more than twice the infant and maternal mortality rate relative to White Americans (Driscoll & Ely, 2020; Hoyert, 2019). These health inequities are a public health crisis that must be addressed to facilitate economic, social, and health justice for all.

The fundamental cause of Black/White racial disparities in health is racism. Despite a long history of racial biological essentialism, race is a social construct and not a coherent biological category (Phelan & Link, 2015; Smedley & Smedley, 2005). It follows that health disparities between Black and White people are not due to inherent biological or genetic differences by race, but rather, differences in racist treatment encountered by Black individuals (Braveman & Parker Dominguez, 2021). Racism is encountered at nearly every level of society—from institutions to everyday social interactions—and its insidiousness leaves an impact on the brains and bodies of Black Americans. And, like other forms of chronic stress (Dunkel Schetter et al., 2013), experiencing racism leads to poor health. Below, we briefly outline different subtypes of racism encountered by Black Americans and others from oppressed groups.

The most pervasive form of racism is structural or institutional racism. Structural racism is racism that permeates U.S. laws and institutional policies such that dominant social groups (e.g., White Americans) are advantaged and oppressed groups, including Black Americans, are disadvantaged (Jones, 2000; Williams et al., 2019). Structural racism is, in part, maintained by cultural racism, or the belief that the cultural products (e.g., music, language, preferences) of the dominant group are superior to the cultural products of oppressed groups (Cogburn, 2019; Williams et al., 2019). Such ideas of superiority and inferiority can become a form of internalized racism, where members of oppressed groups may begin to internalize and accept stereotypes about their own group (Sosoo et al., 2020; Speight, 2007; Williams & Mohammed, 2013). As a consequence of these societal conditions, the majority of Americans engage in interpersonal racism (Galvan et al., 2022), whether implicit and unintentional or explicit and intentional, toward members of oppressed racial groups (Dovidio et al., 2002; Jones, 2000). Interpersonal racism can also result in vicarious racism, where members of oppressed groups experience racism indirectly through witnessing the racism encountered by their racial in-group members (e.g., hearing stories, watching footage; Chae et al., 2021; Heard-Garris et al., 2018; Sosoo et al., 2022). Together, each of these subtypes of racism can influence the health of the constituents living within that society, particularly those from oppressed groups such as Black Americans (Nazroo et al., 2020).

Given that racial disparities in health exist and are largely due to these pervasive types of racism in our society, scholars have asked: What are the mechanisms, or pathways, through which racism leads to poor health? The present article focuses primarily on the neural and inflammatory processes that contribute to links between racism and health, given the importance of brain–body pathways in linking social processes to disease (McEwen & Gianaros, 2010). However, it is important to acknowledge that the mechanisms linking racism and health are multidetermined and multifaceted (see Table 1, for an overview of multiple mechanisms that play a role in linking racism and health). For example, systemic racism and anti-Black discriminatory behavior limit opportunities for economic mobility of Black Americans, and ultimately result in health disparities at the intersection of race and socioeconomic position, including in education and in the workplace (Braveman et al., 2022). Further, historical and current housing segregation (e.g., redlining) has resulted in disparities in exposure to environmental toxins like lead and cadmium (Masri et al., 2021), which increases risk for heavy metal poisoning and other negative health outcomes. Systemic racism also constrains Black individuals’ opportunities for engaging in positive, health-protective behaviors, given a lack of access to recreational green spaces for exercise, inadequate access to affordable, nutritious food, and an absence of quiet conditions conducive to restful sleep (Billings et al., 2019; Li & Yuan, 2022; Nardone et al., 2021). Finally, Black individuals often encounter systemic and interpersonal racism during interactions with the health care system and health care providers, which prevents them from receiving preventative care and high-quality treatment (Hausmann et al., 2008; Powell et al., 2019). Thus, there are many mechanisms within the historical and current economic, social, and built environments that contribute to racial health inequities. A full mapping of these mechanisms needs interdisciplinary research that acknowledges the multiple levels, from institutions to individuals, through which racism can influence health.

Table 1.

Overview of Multiple Mechanisms Linking Racism and Health

Domain	Examples	References
Socioeconomic	Poverty Education Wealth Bias in hiring Bias in housing	Kimmel et al., 2016 Fiscella & Williams, 2004 Pollack et al., 2013 Quillian et al., 2017 Auspurg et al., 2018
Healthcare	Healthcare access Bias in medicine Medical mistrust Delays in preventative care	Yearby, 2018 Dovidio et al., 2016 McClaran et al., 2022 Powell et al., 2019
Criminal Justice	Incarceration Discrimination in police stops Discrimination in sentencing	Wildeman & Wang, 2017 Simoiu et al., 2017 Kutateladze & Andiloro, 2014
Behavior/Environment	Food insecurity/poor diet Limited physical activity Sleep quality Heavy metals poisoning Air pollution exposure Access to greenspaces	Bowen et al., 2021 Hawes et al., 2019 Fuller-Rowell et al., 2016 Masri et al., 2021 Brandt et al., 2020 Nardone et al., 2021
Cognition/Affect	Vigilance Rumination John Henryism Superwoman schema	Lewis et al., 2019 Dondanville et al., 2022 Bennett et al., 2004 Perez et al., 2022
Development	Racial socialization Weathering Allostatic load Cognitive impairment/dementia	Neblett et al., 2010 Simons et al., 2021 Miller et al., 2021 Glymour & Manly, 2008

Note. Although the present article focuses on the possible neural and inflammatory pathways through which racism may influence health, there are multiple mechanisms that have been shown to contribute to racism-based health disparities. Neurophysiological processes are just one piece of this mechanistic puzzle. This table attempts to highlight some of the additional mechanisms not covered in detail in the current model and points to additional research that may be of interest to readers. Of note, many of the mechanisms presented here interact with and influence one another and should be thought of as synergistic processes that can come together to set Black individuals on trajectories toward disease and early mortality.

Against the backdrop of this complexity, the present article seeks to add a relatively new piece to the puzzle by considering the neural and immunological processes that may be affected by racism and lead to racial health inequities for Black Americans. Incorporating brain–body pathways into research on racism and health is important for (at least) three key reasons. First, the brain is the primary organ responsible for initially identifying, appraising, and regulating responses to stressors, including racism (McEwen, 2007). As such, a mechanistic model seeking to map the pathways between racism and health should consider how the brain responds to racism in the moment, as well as how brain functioning is affected by chronic exposure to racism. Second, mounting evidence suggests that inflammation is a key physiological mechanism that plays a role in linking racism and health, given burgeoning literature showing that differences in inflammation account for at least some Black/White health disparities (Jenny et al., 2019; Kiely et al., 2022; Kamin Mukaz et al., 2020; Wang et al., 2016), and that inflammation mediates associations between stress (including discrimination) and health outcomes for Black individuals (McClendon et al., 2021). Third, as the quote by Ta-Nehisi Coates at the start of this article so eloquently observes, racism “lands with great violence upon the body,” as evidenced in part by the extensive health disparities suffered by Black individuals. We hope that ultimately, research systematically documenting that bodily violence through rigorous scientific evidence will motivate policymakers and the public to understand and work to address the racism that is the fundamental cause of racial health disparities in American society.

In light of the importance of understanding the neural and inflammatory mechanisms linking racism and health, the primary goal of the present article is to present a model (see Figure 1) that we hope will drive future research in this area. Our model is grounded in rich traditions of research that have examined the biopsychosocial mechanisms linking racism and health (Brondolo et al., 2009; Clark et al., 1999; Lewis et al., 2019; Neblett, 2019; Williams & Mohammed, 2013), and builds on this work to bring cutting-edge research from neuroimaging and psychoneuroimmunology to the table (for related models incorporating neurophysiological pathways, see also Berger & Sarnyai, 2015; Harrell et al., 2011; Lockwood et al., 2018). We focus on the role of large-scale brain networks in processing and responding to racism, and how activity and connectivity of those networks lead to physiological responses (particularly inflammation) that, over time, can lead to poor health. Our model is grounded in the current literature on the neural and inflammatory impacts of racism, though that literature is underdeveloped. We thus emphasize future research that is needed to test, refine, and improve the model proposed here. Though we focus primarily on anti-Black racism in the present article, we note that many other oppressed groups also suffer from discrimination-related health disparities and that more work is needed to establish if similar or different brain–body pathways contribute to health disparities for other groups (Hatzenbuehler, 2014; King et al., 2009; Ruiz et al., 2018; Yip et al., 2021).

Figure 1.

Hypothesized Neural and Physiological Mechanisms Linking Racism and Health

Note. We hypothesize that multiple forms of racism (e.g., structural racism in the workplace and housing, interpersonal racism, vicarious racism), as well as protective factors (e.g., social support from family, activism and civic engagement) shape brain networks and physiological systems to lead to chronic disease and early mortality for Black Americans. Specifically, racism may lead to greater activity in and connectivity within the allostatic–interoceptive network (AIN; red circles on brain graph image), which consists of regions of the salience network, the default mode network, and subcortical regions. We also speculate that racism leads to differences in functional connectivity between the AIN and executive control network (ECN; blue circles on brain graph image). This pattern of brain activity/connectivity in the face of racism then leads to activation of physiological systems involved in responding to stress, including the sympathetic nervous system (SNS) and hypothalamic–pituitary–adrenal (HPA) axis. Specifically, racism can also lead to activation of the HPA axis, including release of adrenocorticotrophic hormone (ACTH), which can stimulate the adrenal gland to produce cortisol. Cortisol can then bind to glucocorticoid (GC) receptors on the surface of immune cells (i.e., leukocytes), which can also influence gene expression within immune cells. Encountering racism is also hypothesized to lead to activation of SNS neural fibers, which can cause the release of norepinephrine and (via stimulation of the adrenal gland), epinephrine. These catecholamines can then bind to beta-adrenergic (BAr) receptors on the surface of immune cells (i.e., leukocytes), which can lead to increased expression of inflammatory immune response genes and greater production of proinflammatory cytokines. Greater inflammation is then implicated in the etiology and pathophysiology of chronic disease and psychopathology. Further, physiological outputs such as cortisol and proinflammatory cytokines can feed back to the brain via afferent vagus nerve signaling to influence neural structure and function, creating a vicious cycle. Structural racism in the workplace image by macrovector on Freepik. Interpersonal racism image by pikisuperstar on Freepik. Protective factors image by Freepik. Adapated from “Social Safety Theory: A Biologically Based Evolutionary Perspective on Life Stress, Health, and Behavior,” by G. M. Slavich, 2020, Annual Review of Clinical Psychology, 16(1), p. 274 (https://doi.org/10.1146/annurev-clinpsy-032816-045159). Copyright by Annual Reviews. Adapted with permission.

Effects of Racism on Brain Function

To understand how racism might influence brain function, we must first consider some basic principles about how the brain is organized and shaped by its environment. One important consideration here is the relationship between brain structure and brain function. Brain structure, which is often studied through the use of magnetic resonance imaging (MRI) and diffusion tensor imaging, examines the size and shape (e.g., volume, thickness) of gray matter structures in the brain and/or the size, density, and structure of white matter fibers (e.g., fractional anisotropy). A few recent studies have examined associations between racism and brain structure, with some studies finding that greater exposure to racism is related to smaller volume of some gray matter regions (e.g., hippocampus; Hatzenbuehler et al., 2022) and disruptions to white matter microstructure (Fani et al., 2022). These studies provide important insight into associations between racism and the structural properties of the brain. However, it is important to note that there is not a one-to-one relationship between brain structure and brain function, at least as measured with MRI scans (Batista- García-Ramó & Fernández-Verdecia, 2018; Suárez et al., 2020). As such, we cannot infer that just because someone who has experienced more racism has a smaller hippocampus (a region important for episodic memory), that their hippocampus necessarily functions less efficiently and/or that they will perform worse on a memory test. Thus, it is important to also consider associations between racism and brain function, which is a more proximal predictor of physiological activation, as well as social, cognitive, and affective experience, than structural properties of the brain alone (Suárez et al., 2020).

One modern neuroscientific perspective suggests that a fundamental property of a well-functioning brain is the maintenance of allostasis (Katsumi et al., 2022; Sterling, 2012). Allostasis is the process by which the brain makes predictions about future energy demands to efficiently regulate energy in the body. The brain does this in part by preparing to satisfy energy needs before they are necessary. For example, as an individual prepares to start running, the brain preemptively begins to redistribute energy from organs that can spare oxygen (i.e., stomach) to striate muscles that need more resources to facilitate running (Barrett et al., 2016). But how does the brain know that it needs to prepare the body to run, even before the individual begins running? The brain is exceptional at utilizing information from prior experiences to make predictions about the best, most efficient way to engage with the environment in each moment. Thus, the brain is constantly monitoring the external environment for cues to use as predictions for how to most effectively mobilize physiological processes to meet anticipated energy demands while also considering the current physiological state of the body.

Given this view that the brain is a predictive organ that uses information from the external and internal environments to efficiently manage metabolic resources, we can consider how repeated exposure to many similar prior experiences might change the predictions made by the brain, which would shape the neurobiological and physiological processes that support those predictions. For example, chronic exposure to negative social contexts, including those characterized by high levels of racism (Payne & Hannay, 2021), may cause the brain and body to regulate energy in ways that are optimized for that specific context (McEwen & Gianaros, 2011). For the brains and bodies of Black individuals, prior experiences of racism might change how the brain manages resources in preparation for encountering potentially threatening or ambiguous social situations. For example, the brain may need to increase cognitive resources and attention to navigate ambiguous or stressful social interactions appropriately (e.g., facilitated by the executive control neural network), while also carefully considering both one’s own thoughts, feelings, and behaviors and those of an interaction partner so as to navigate the interaction as smoothly as possible (e.g., facilitated by the default mode neural network), and simultaneously attending to internal physiological changes that might provide cues to if one should prepare to fight or flee a social interaction (e.g., facilitated by the salience and allostatic–interoceptive neural networks; Muscatell et al., 2021). Over time, this frequent preparation in response to racism may shift the brain to maintain increases in certain neural and physiological resources at “default” (Brosschot et al., 2018) to most efficiently prepare to engage in racist social interactions and to cope with their aftereffects (Meyer, 2019).

What brain regions or networks are most likely to shift their functioning in response to experiences of racism? In line with other models of the impact of racism on brain functioning (Berger & Sarnyai, 2015), we propose that three intrinsic brain networks, the salience network, the default mode network, and the executive control network, are involved in processing, responding to, and coping with racism, and that chronic exposure to racism likely alters the functioning of these networks. The salience network, composed primarily of anterior cingulate cortex (ACC) and bilateral anterior insula, is thought to guide affective feelings, perceptions, and behavior based on internal shifts in physiological activation or when salient stimuli are detected in the environment (Barrett & Satpute, 2013; Lindquist & Barrett, 2012). The default mode network, comprised of the medial prefrontal cortex (mPFC), medial temporal lobe (i.e., hippocampus, entorhinal cortex), posterior cingulate cortex/precuneus, and bilateral superior temporal sulcus, is primarily responsible for generating representations of the self, others, and past and future experiences (Raichle, 2015). The interactions between the salience and default mode networks, together with subcortical regions such as the amygdala and striatum, have been theorized to make up a broader network called the allostatic interoceptive network (AIN), which may be involved in maintaining allostasis (Kleckner et al., 2017). The executive control network, comprising the bilateral dorsolateral prefrontal cortex (dlPFC), inferior parietal lobe, inferior parietal sulcus, precuneus, and middle cingulate cortex, is thought to be responsible for monitoring the activity of other functional networks as well as supporting working memory and cognitive control (Niendam et al., 2012).

To date, very little research has examined how the brain responds to and is shaped by experiences of racism. This is a major gap in our knowledge that neuroscientists must strive to fill moving forward. The little work that has been done in this area provides preliminary support for our hypothesis that the salience, default mode, and executive control networks are involved with processing and are affected by racism. For example, one study showed that Black young adults who demonstrated higher levels of distress after being socially excluded by White individuals exhibited greater activity in regions of the salience network (i.e., dorsal ACC, anterior insula), and less activity in executive control network regions (i.e., dlPFC), compared to those who experienced less distress (Masten et al., 2011). Further, experiencing more racial discrimination has been associated with greater amygdala activity at rest (Clark et al., 2018), as well as greater amygdala activity in response to pictures of White individuals displaying neutral facial expressions (Greer et al., 2012). Given the amygdala’s role as a key node of the salience network, these data suggest that experiences of racism may shape the extent to which the salience network is active by default and in response to potentially threatening or distressing social cues. This is consistent with the generalized unsafety theory of stress (Brosschot et al., 2017, 2018), which argues that, for people from disadvantaged backgrounds, the brain and body operate in a constant state of “unsafety” characterized by vigilance and chronic activation of neural and physiological stress systems. These findings are also consistent with research on other types of social stress (e.g., social rejection, social evaluation), which finds greater activity in regions of the salience network (e.g., ACC, insula) in response to socially stressful experiences (see Berretz et al., 2021; Muscatell et al., 2021, for a review).

While very little work has examined associations between racism and neural functioning, an intriguing set of new studies is converging to suggest that racism may also shape functional connections between networks of the brain. This is important, as recent neuroscientific evidence shows that the brain is organized into several intrinsic networks and that emotions, cognitions, behavior, and other mental phenomena arise from the functional connections between these networks, rather than activation of singular regions (Cohen & D’Esposito, 2016; Park & Friston, 2013). As such, examining how racism influences not just brain activity but also connections between brain networks is an important undertaking. Initial research in this area has shown that greater exposure to racism is associated with functional connectivity between the amygdala and other regions of the salience network, including the anterior insula, dorsal ACC, caudate, putamen, and thalamus, as well as connectivity between the amygdala and regions of the default mode network, including mPFC (Clark et al., 2018; Webb et al., 2022). Similarly, discrimination has been associated with enhanced connectivity between the insula, another key hub of the salience and allostatic–interoceptive networks, and posterior regions of the default mode network, including the precuneus (Webb et al., 2022) and intracalcarine cortex (Han et al., 2021). Finally, while not about racism per se, some prior work on the neural predictors of physiological responses to social evaluative stress shows that greater functional connectivity between the amygdala and the dorsal medial prefrontal cortex (dmPFC), regions of the salience and default mode networks, respectively, is associated with enhanced inflammatory reactivity to social evaluation (Muscatell et al., 2015). Together, these results suggest that exposure to racial discrimination may be related to increased functional connectivity among regions that comprise the salience network, as well as greater coupling of regions of the salience and default mode networks. This shift in brain functioning in the face of racism may help an individual to act adaptively in a socially threatening context.

Finally, we hypothesize that racism also shifts activity in the executive control network and functional connectivity between the executive control network and the salience and default mode networks. This hypothesis is mostly speculative, as very little neuroimaging research has examined associations between racism and brain activity and connectivity in response to tasks that require executive control (e.g., working memory, response inhibition, task switching). Future research should investigate this, as a well-functioning executive control network is important for a variety of health-relevant processes, including emotion regulation, behavior maintenance and/or behavior change, and self-regulation (Lowe et al., 2019; Morawetz et al., 2020). To date, the one known study that investigated associations between racial discrimination and brain functioning during an attentional control task found that greater racial discrimination was associated with more activity in regions within the default mode network (e.g., ventral medial prefrontal cortex [vmPFC], superior temporal sulcus) and the executive control network (e.g., dlPFC, occipital cortex) when engaging with threatening stimuli in an attentional control task (Fani et al., 2021). Given the dearth of research in this area and yet the importance of activity in and connectivity between the executive control network and other brain networks (Alvarez et al., 2022), future research that documents the associations between racism and functioning of this network is needed.

In sum, we propose (see Figure 1) that the salience and default mode networks, together with the executive control network, are integral to processing, responding to, and coping with the aftereffects of racism, and that chronic exposure to racism likely alters the functioning of these networks. To date, these hypotheses are speculative, in part because there is an extremely limited neuroimaging literature that has investigated links between racism and neural functioning. However, given the importance of these networks for responding to other types of social stressors that share features with racism (e.g., socioeconomic deprivation, negative social evaluation, social rejection; Muscatell et al., 2021), it is plausible that similar networks would undergird responses to racism. We also note that all of the limited neuroimaging research on the neural consequences of racism that has been conducted to date has focused on interpersonal racism, despite the important role that structural, cultural, internalized, and vicarious racism also play in health. As such, future research should also examine how exposure to these other types of racism influences brain function. For example, although speculative, we hypothesize that vicarious racism (i.e., secondhand viewing of racist encounters, such as videos of violent interactions with law enforcement) could lead to alterations in executive control network function at rest and/or during challenging cognitive tasks following exposure. We are currently testing this hypothesis in a study in our laboratory. As another example, it is possible that internalized racism could be associated with diminished activity in reward-related brain networks during the viewing of cultural products from the minoritized group (Maxwell et al., 2015). These examples illustrate how different types of racism may influence brain function in networks beyond those focused on in the present model. We note these ideas are purely speculative given the dearth of research in this area, but we hope they spawn future research that investigates how different types of racism may be processed by and influence the functioning of the brain.

Effects of Racism on Physiology

How might the associations between racism and neural activity and connectivity hypothesized here ultimately lead to poor health for Black Americans? The salience, default mode, and executive control networks play a role in initiating and regulating physiological processes that can, if activated repeatedly over time in the face of stress, lead to physiological dysregulation and set the stage for chronic disease (McEwen, 2012; see Figure 1). For example, subcortical regions thought to be involved in the allostatic–interoceptive network (e.g., amygdala, periaqueductal gray, nucleus of the solitary tract) project to brainstem regions (e.g., hypothalamus) that are responsible for mobilizing the sympathetic nervous system (SNS) and the hypothalamic–pituitary–adrenal (HPA) axis, two physiological systems that are consistently activated in the face of stress (Muscatell & Eisenberger, 2012). Specifically, activation of the SNS leads to the release of the catecholamines epinephrine and norepinephrine, which can bind to beta-adrenergic receptors throughout the body, including on the surface of immune cells (i.e., leukocytes), leading to increased expression of genes involved in inflammation (Irwin & Cole, 2011; MacCormack et al., 2021). Further, activation of the HPA axis ultimately leads to the production of glucocorticoids such as cortisol, a metabolic hormone that can also regulate the expression of genes in immune cells (Miller et al., 2008). While in the short term, cortisol has anti-inflammatory properties, chronic stress has been linked with glucocorticoid resistance, or the tendency for immune cells to no longer be sensitive to the anti-inflammatory effects of cortisol (Miller et al., 2014). Over time, chronic activation of the SNS and HPA can lead to heightened levels of circulating proinflammatory cytokines in the body, and elevated levels of inflammation are associated with the development of many chronic physical diseases and psychopathology (Bennett et al., 2018).

Given the major role that SNS and HPA axis play in responding to stress, much prior work has investigated the acute effects of racism on activity of these physiological systems. Indeed, laboratory studies have demonstrated pronounced cortisol reactivity in response to experimental manipulations of racism, including in response to anticipating interactions with a prejudiced cross-race/ethnicity partner (Sawyer et al., 2012), viewing or overhearing racially discriminatory content (Huynh et al., 2017; Weinstein et al., 2013), and experiencing social rejection by a presumed prejudiced evaluator (Townsend et al., 2014). Prior work has also demonstrated that racism-related stress may evoke a pernicious cardiovascular reactivity pattern characterized by elevated SNS activity and diminished parasympathetic nervous system activity (Sawyer et al., 2012). Laboratory studies in this domain have shown changes in autonomic nervous system activity as a function of reported or manipulated experiences of discrimination among racial/ethnic minorities, including higher blood pressure (Sawyer et al., 2012), diminished heart rate variability recovery following experiences of racism-related stress (Hoggard et al., 2015; Wagner et al., 2015), and elevated heart rate (Mendes et al., 2008; Sawyer et al., 2012). Thus, a robust literature shows that experiencing racism is associated with increases in SNS and HPA axis activity, which, if prolonged or repeated, could ultimately lead to multisystem physiological dysregulation (i.e., “allostatic load”) and chronic disease (McEwen & Seeman, 1999; Ong et al., 2017).

Ultimately, SNS and HPA axis activation likely largely influence health through their effects on inflammatory processes (Miller et al., 2009). However, to date, no known research has examined if an acute experience of racism leads to increases in inflammation; current ongoing work in our laboratory is investigating this question. Despite this lack of experimental evidence for links between racism and inflammation, cross-sectional studies have shown that greater perceived discrimination is associated with higher levels of markers of systemic inflammation (Cuevas et al., 2020). A few studies have also demonstrated a longitudinal association between racism and inflammation. For example, greater perceived discrimination has been associated with higher levels of C-reactive protein (CRP), a marker of inflammation (Lewis et al., 2010), and a composite score indexed by multiple inflammatory biomarkers (Ong et al., 2017). Furthermore, Boen (2020) found that Black–White disparities in CRP were mediated by participants’ reported levels of everyday and major lifetime discrimination, as well as by participants’ cumulative stress burden (Boen, 2020). Together, this work suggests that racism may lead to increases in inflammation, though future experimental research in this area is needed to establish causality.

To summarize, we hypothesize based on prior literature, that experiencing racism leads to activation of the SNS and the HPA axis, both of which can lead to expression of proinflammatory genes and the production of proinflammatory cytokines. These racism-induced increases in inflammation can lead to the development of chronic disease and psychopathology (Slavich, 2020), and may also feed back to the brain to cause greater reactivity to social threats and diminished responses to rewards (Eisenberger et al., 2017). There are major opportunities for future work in this area, including integrating neuroimaging and physiological measures (Eisenbarth et al., 2016; Muscatell et al., 2015) to examine the neural predictors of SNS, HPA, and inflammatory responses to racism, as well as work that moves beyond individual experiences of racism toward documenting the impacts of structural, vicarious, and area-level racism on physiological functioning.

Concluding Comments

While most of the present article focuses on the deleterious effects of racism on neural and inflammatory processes, it is also important to recognize the strengths of Black Americans, including various resilience and protective factors that may break the link between racism and health. Some factors that have been shown to buffer the effects of racism on various health outcomes include racial socialization, racial identity, spirituality, and sociopolitical activism (Hayward & Krause, 2015; Ingram & Wallace, 2019; Jones & Neblett, 2016; Neblett et al., 2008, 2013). A few studies have even explored protective factors that may influence physiological responses to racism. For example, individuals who felt more positively about being Black (i.e., the private regard dimension of racial identity) demonstrated reduced autonomic reactivity in response to listening to scenarios describing blatantly racist social interactions (Neblett & Roberts, 2013). Brody et al. (2015) found that the association between higher racial discrimination and elevated levels of inflammation was not significant among adolescents reporting more positive racial identities (i.e., higher racial centrality). Further, the use of spiritual coping in response to recalling racist experiences was associated with decreased diastolic blood pressure reactivity (Cooper et al., 2014). This smattering of findings suggests there are a variety of factors that enable Black Americans to be resilient against the physiological toll of racism. To our knowledge, no known work has examined protective factors that modulate neural responses to racism. More research is needed to document the strengths of Black individuals, families, and communities that may mitigate the neural and inflammatory impacts of racism. However, Black individuals should not be left to defend themselves from racism with individual resiliency alone; it is necessary to address racism at a societal level in order to mitigate long-standing racial inequities in health.

In the present article, we have outlined a model for understanding the neural and inflammatory mechanisms through which racism may impact health of Black Americans. We hope that having a shared conceptual model to use as a potential roadmap for exploring the relationships between racism and neural and physiological processes will be used to advance rigorous research on the psychoneuroimmunological mechanisms contributing to racial health disparities. Moreover, it is our hope that the advancement of research in this area will not only spur other scholars, but also policymakers and lay people alike, to understand and act against the pervasive racism in our society that perpetually harms Black Americans.

Public Significance Statement:

Health disparities due to racism are a major public health problem in the United States. Here, we present a model outlining the possible neural and inflammatory pathways linking racism to health for Black Americans. Understanding how racism influences the brain and body is an important next step for research in this area.