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Stress-related diseases (SRDs) are a group of conditions comprising of some of the most impactful and life-threatening diseases, ranging from cardiovascular disease and stroke to Alzheimer’s disease. While we possess an understanding of the various pathologies of many diseases, we must concede to the reality that environmental factors significantly impact pathogenesis and progression. Studies of racial differences within diagnostic groups have started to explicitly suggest that race itself is not a risk factor but, instead, may merely serve as a proxy measure of environmental stress in the form of racism (Williams & Ovbiagele, 2020). Unsurprisingly, this stress in the form of racial discrimination is strongly associated with the chronic inflammation implicated in the development and advancement of these SRDs (Cuevas et al., 2020). In a world that has been rattled and simultaneously motivated to action by COVID-19 and egregious acts against Black people, it is critical that we understand the long-term effects of the racism pandemic on the health of its targets.

Data from Johns Hopkins suggests that the COVID-19 infection rate among Black communities is more than three times that of white communities (Thebault et al., 2020). In Chicago alone, a city in which Black people constitute 30% of the population, roughly 50% of COVID-19 infections and 70% of COVID-19 deaths have involved Black people (Yancy, 2020). Cytokine storms and premature immunosenescence, particularly in the context of vascular risk factors, increase the likelihood of subsequent neurodegenerative diseases (Lennon, 2020). Black people consistently demonstrate significantly greater likelihood of developing vascular diseases, accounting for nearly 45% of vascular-related deaths while constituting less than one-quarter of the U.S. population (Ajilore & Thames, 2020). These health disparities have existed over the course of history, yet the most recent occurrences have brought them to light.

Psychological impacts of present-day racism are not to be neglected, as their associations with biological alterations within limbic and cortical regions are far from innocuous. Serotonergic alterations through depression, which can occur through not only racism but also social distancing, are associated with Alzheimer’s disease pathogenesis and its rate of progression (Chakraborty et al., 2019). The hypothalamic-pituitary-adrenal (HPA) axis is adversely impacted by chronic stressors, such that it ceases to operate at an evolutionarily appropriate level. As the central stress response system, the HPA axis is partially responsible for the body’s ability to respond to stress in the form of racism and airborne pathogens, to name just a couple. The innate inflammatory responses needed to overcome these obstacles to well-being are essentially thwarted in the context of chronic stress and racism, resulting in systemic problems such as hypertension, diabetes, asthma and other medical comorbidities (Ajilore & Thames, 2020) in the context of psychosocial and politicoeconomic stressors.

From a research perspective, some continue to suggest that racism is not the variable that results in biological alterations and subsequent disease but, instead, a component of racial differences that are of a biological nature. Even if this were true, we know that heavily biological factors such as apolipoprotein E (APOE) genotype moderates the relationship between psychological trauma and future symptomatology (Lyons et al., 2013). APOE is heavily implicated in neurodegenerative processes and health outcomes, with the APOE4 allele being carried at a greater frequency by Black people than their white counterparts (Barnes & Bennett, 2015). However, virtually everything that informs our makeup is contrived by one’s culture. For example, educational disadvantage is one significant difference between Black and white people. In a study of more than 12,000 adult participants, this disadvantage directly mediated C-reactive protein (CRP) changes and indirectly impacted depressive symptoms (Zahodne et al., 2019). As the common index for systemic inflammation and a known biomarker for cardiovascular disease, CRP changed as a result of the educational disadvantage experienced by Black people compared to their white counterparts. Higher inflammation burden is not isolated to educational differences across racial groups. CRP and lifetime exposure to discrimination are independently associated with inflammation burden while controlling for education and other demographic variables (Ong & Williams, 2019), with Black people consistently demonstrating worse health outcomes than white people. Discrimination effects are not limited to the individual being targeted or attenuated by distance, as bystanders can vicariously experience negative outcomes. Generation to generation, the damages against the eldest can impact the most vulnerable children. Distress levels resulting from these acts have been found to be similar between direct victims and bystanders and, furthermore, have exceeded distress scores related to natural disasters and other life-threatening experiences (Janson, 2004). This points to a severely harmful societal problem that targets those most vulnerable.

Biology is neither an impermeable membrane of fate nor an unmalleable component of human life. There is no need to conflate the various types of trauma to recognize that the forms originating from the external world negatively impact, and are impacted by, one’s unique and ever-changing genotype. It is only through an understanding of biology and SRDs that we can fully grasp racial disparities and the occurrence of racism within health care. The substantial ramifications of race and racism on health are so commonplace and deeply ingrained in our society that they should be palpable to those who examine them. If we are to reduce or eliminate the racial disparities that now serve as the centerpiece of 2020, we must confront the reality that the very health of those impacted by racism is precariously awaiting our finely tuned attention and action.

About the Author

Jack C. Lennon is a clinical psychology PsyD candidate at Adler University in Chicago, Illinois. He conducts neuropsychological assessment for the purposes of differential diagnosis and risk stratification for a wide range of neurologic and psychiatric conditions. He is interested in the cognitive and neuropsychiatric sequelae of mood disorders in the context of neuromedical conditions. This extends to trauma and suicidal behaviors in aging brains. He is a board member of Journal of Alzheimer's Disease and reviews for several scientific journals across psychiatry and neuroscience.


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