Racism is seen at the genomic and cellular level, and it qualifies as a health risk factor.
Human biology perceives psychological and physical stressors alike. Exercise and public speaking both excite a stress response, for example. Stress is favorable in the short term as it trains the body’s tolerance for stress. But there’s always a biological limit. The problem arises when baseline stress levels become chronically high, such as in the case of major depression or metabolic disorders. Why? Because chronic stress cripples the body in many different ways, slowly but surely. One known psychological chronic stressor is being racially discriminated.
Telomeres are DNA sequences situated at both ends of a chromosome. Each time a cell replicates, its telomeres shorten. Once telomeres length becomes critically short, the cell dies or becomes senescent. Thus, telomere length correlates with chronological age. It also reflects the cumulative wear-and-tear — or aging — at the cellular or immunological level. As follows, quicker telomeres shortening, which can be blunted with healthy lifestyle choices, expedites age-related diseases.
A 2017 cross-sectional study of 595 older African Americans found that high experiences of racism predict shorter telomeres. This effect is independent of other confounds such as overall health, sociodemographics, stress, or mental health. That same year, another study on 550 blacks in the United States also corroborates the findings on racism and shorter telomere length.
A 2020 study by the American Psychological Association (APA) is the first longitudinal research on 391 middle-aged African Americans. Results showed that the more one endures racism, the quicker the telomeres shrink at a 10-year follow-up. “Our study supports previous findings suggesting that leukocyte telomere length is sensitive to racial discrimination and that it may be one pathway through which racism-related factors contribute to increased disease risk and accelerated declines in health among African Americans,” the authors concluded.
For each life domain in which racism occurred, telomeres shortened by 19 base pairs — equivalent to nearly one year of lifespan — more than usual.
What is the acceleration rate precisely? The 2020 study measured six life domains : (1) at school, (2) at work, (3) getting a house, (4) getting a job, (5) getting medical care, and (6) in public settings. For each life domain in which racism occurred, telomeres shortened by 19 base pairs more than usual at the 10-year follow up. For reference, the annual loss of telomeres is 20–30 base pairs, based on a 2013 systematic review of 129 studies. Hence, the 19 base pairs the study calculated equates to nearly one year of accelerated aging. And this is for one life domain. The effect is additive.
Cellular Stress and Inflammation
In a 2019 study, “Experienced discrimination and racial differences in leukocyte gene expression,” researchers analyzed the blood DNA of 23 White and 48 Black people with equal socioeconomic status. Yet, compared to White, the Black’s genomic profile displayed increased pro-inflammatory and stress-responsive cellular activities. Further bioinformatics analyses revealed that racism accounts for more than 50% of these genomic variations.
They also found striking similarities between the Black’s genomic profile and a previously characterized profile called Conserved Transcriptional Response to Adversity (CTRA). Those facing adversity, such as loneliness, caregiver stress, and poverty, usually have the CTRA genomic profile. CTRA genomic profile is even observed in mice experiencing social defeat and low social rank.
What does the CTRA genomic profile look like? It is a subtle but prolonged fight-or-flight response, akin to low-grade chronic stress. Pro-inflammatory and stress signaling pathways are always switched on, followed by blunted antiviral response and antibody production.
Racism affects people at the genomic level — akin to loneliness, poverty, and caregiver burden — spurring inflammation and stress while debilitating immune functions.
“We’ve seen this [CTRA genomic profile] before in chronic loneliness, poverty, PTSD, and other types of adversity, but until now, nobody had looked at the effects of discrimination,” says Steven Cole, Professor of Medicine, Psychiatry and Biobehavioral Sciences at the University of California, who led the 2019 study. “If those genes remain active for an extended period of time, that can promote heart attacks, neurodegenerative diseases, and metastatic cancer.”
As the antiviral and antibody responses weakened in the CTRA genomic profile, researchers have also proposed that it might be one reason why Blacks have been disproportionately affected by Covid-19. Their review paper, “The fire this time: The stress of racism, inflammation and COVID-19,” is published in Brain, Behavior, and Immunity.
A Health Risk Factor
It is not only Covid-19. “For most of the 15 leading causes of death including heart disease, cancer, stroke, diabetes, kidney disease, hypertension, liver cirrhosis and homicide, African Americans (or blacks) have higher death rates than whites,” David R. Williams, Professor of Public Health, African and African American Studies, and Sociology at Harvard University, wrote in a 2010 review, citing data from the CDC. How?
- Victims of racism had accelerated telomere shortening equivalent to a one-year shorter lifespan for each life domain racism occurs.
- Victims of racism have increased pro-inflammatory and stress-responsive signaling pathways, akin to biological reflections of loneliness, poverty, and caregiver burden.
- Victims of racism have lowered immunity characterized by weaker antiviral and antibody defenses.
As racism provokes cellular aging, inflammation, and stress, it should qualify as a risk factor for chronic or age-related diseases. Or even Covid-19 mortality for that matter. “I believe racism and discrimination should be treated as a health risk factor — just like smoking,” The Conversation reported. “It is toxic to health by damaging the natural defenses our bodies use to fight off infection and disease.”
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