Section 4: Looking Ahead

Epigenetics: One Intersection of Biology with Sociopolitical Determinants of Health

Despite the many ways in which new scientific developments like precision medicine threaten to entrench biological racism, new fields such as epigenetics, developmental origins, and life course research are contributing to our understanding of how racism, not race, has biological effects on the body. Epigenetics and other biopsychosocial fields are pulling together biology, psychology, and upstream determinants of health to answer how racism “gets under the skin,” showing how the social and structural determinants of health (mediated or created by racism) can literally embed themselves in our cells.

Research in the developmental origins of disease has shown that the first one thousand days after conception (up to age two) is a critical period in which the developing fetus and child’s cells are most susceptible to outside influences. During this period, the fetus grows from one cell to trillions, so any early changes in these cells will be replicated and reproduced for the entirety of one’s life. Thus, exposures in the uterine environment and early childhood environment can either be protective or increase the risk of developing chronic diseases in adulthood. Literature shows, for example, that low childhood socioeconomic status both increases the physiological response to stressors and increases the reactivity to social support.[1] That is, growing up poor can both increase the body’s stress response and increase the body’s ability to calm down or resists those responses in the presence of social support. Furthermore, certain exposures during this critical or sensitive period have been shown to increase the risk of type 2 diabetes, stroke, heart disease, some cancers, impaired cognitive function, and mental health issues.

The exposures posited to increase chronic disease risk in adults include environmental exposures, such as toxins and pesticides, but also “normal” or endogenous exposures produced by the mother and transmitted to the fetus in utero.[2] Although the majority of literature has focused on the effects of cortisol, the stress hormone that acts as a danger signal for the growing fetus, there is also a role of environmental racism (a form of structural racism) that increases exogenous exposures. These articles posit that the more stress a mother is under during pregnancy (including overt physical and mental, as well as more subtle or everyday stressors, such as racist microaggressions), the more cortisol reaches the cells of the fetus. This is also referred to as the mother’s “allostatic load,” or amount of biochemical response to stress.

Over time, a constantly high allostatic load can cause the stress response to stay on permanently. High allostatic load impacts neuroendocrine, cardiovascular, immune, and metabolic systems, in turn contributing to various forms of damage, including cardiovascular disease, neurological atrophy, psychiatric symptoms, mortality, mobility limitations, cognitive decline, and functional impairments.[3] The fetus interprets high levels of cortisol in utero as a signal that the postnatal environment will be stressful, and reprograms the developing stress response systems to stay on high alert with a short fuse, as well as inhibit the growth of some organs. This predisposes the child to increased stress-related biological damage and increases the risk of adult chronic diseases. Most importantly, as shown in section 1, the mother’s stress can be due to racist social and structural determinants of health, such as white supremacy and inequities in neighborhoods, rather than some biological aspect of their race.

A number of studies further document how racism is stressful. For example, one study at Duke University found that Black students had higher levels of salivary cortisol after learning about a violent racist crime on campus.[4] Another study showed how the mere anticipation of prejudice is associated with poor physiological and cardiovascular responses.[5] Amani Nuru-Jeter, a social epidemiologist at the University of California, Berkeley, further found that chronic stress from frequent racist encounters is associated with chronic low-grade inflammation.[6] This literature illustrates the biological pathway through which racism leads to increased risk of adult chronic diseases.

Epigenetics, a related but slightly different field, shows similar biological causal pathways for health disparities by embedding racism’s effects under the skin. One of the major threads of current epigenetics research focuses on the body’s varied responses to stress and how these epigenetic responses, rather than inherent genetic causes, lead to racial health disparities.[7] Genetics refers to the static genes inherited from a person’s biological parents, but, as noted elsewhere, these genes do not create or explain race nor many other salient physical characteristics. Epigenetics, however, are changes in the way those inherited genes are turned on or off. In other words, these are the dynamic volume controls that tell genes to amplify certain proteins while muting others, despite the same initial signal from the static genes. Epigenetics provides one mechanism by which our health and our body is dynamically created in real time by the environment inside us and outside us. More specifically, “weathering” is a term used by epigeneticists to describe how constant stressors increase allostatic load and create biochemical and cellular level by-products that wear down the body’s normal ability to regulate itself over time. Weathering may help explain racial health disparities by proposing a mechanism for the physical wear and tear of chronic stress caused by all levels of racism.[8] The effects of epigenetic weathering are further exacerbated by structural factors including inequitable access to quality health care.

Darlene Francis and related researchers have shown that epigenetic mechanisms could be a key mediating process by which the social and structural determinants of health become incorporated into biochemical changes.[9] This has implications for both risk and resilience to disease processes. Human development research demonstrates that many of these processes occur during the postnatal “critical period.” Epigenetic changes can be harmful, protective, or both. Other research shows implications for epigenetic changes as a link between early life (e.g., maternal stress during pregnancy) and adult health disparities along racialized lines for conditions such as hypertension, diabetes, stroke, and coronary heart disease.[10] Kuzawa and Sweet note that epigenetics help explain how the effects of social-environmental exposures combine with plasticity of phenotypes (i.e., physical traits determined by genetics) in response to those environmental exposures. Most importantly, Kuzawa and Sweet make the explicit link between racism and epigenetics. Social and structural effects of racism lead to environments that affect many aspects of bodies of color.

Dr. Francis interprets this as a call to action: “If we hypothesize that racial discrimination is capable of directly altering the epigenomic profiles of genes that are important to the stress response, we can then predict that targeting and ameliorating discrimination and racism should have an equally direct, potent, and protective effect on the stress-axis epigenome.”[11] Her paper “Conceptualizing Child Health Disparities: A Role for Developmental Neurogenomics” demonstrates that the social, structural, and psychological worlds in which a child is living can influence the sensitivity of a child’s stress axis during the critical period. Developmental neurogenomics, which is a hybrid of sorts between developmental origins and epigenetics research, posits a biological plasticity in early developmental life that moves away from characterizing health disparities as purely biological, purely environmental, or psychological. Instead, the effects of racism are experienced somatically as a product of immediate environment, genes, and sociopolitical context.

Epigenetics and related research provide the language and a framework for the intersection of critical race theory and biology, which should be used across clinics and research labs. It begins to elucidate how the sociopolitical effects of racism are quite literally changing the building blocks of biochemical life. This allows critical race theorists and clinicians alike to show how socially constructed race categories and racist society cause intergenerational harm on the cellular level. In other words, “critical philosophy of race should also be critical physiology of race” and vice versa.[12] These fields of research show most clearly that as clinicians and researchers, we cannot engage in health without understanding both biology and critical race theory.

It is crucial to recognize that research in epigenetics and developmental origins complements but does not replace the understanding of social and structural determinants of health. Exposures at every level, from cortisol in utero up through mass incarceration, environmental racism, and white supremacy, contribute to biological risk. Thus, it is necessary and critical to clearly articulate that epigenetics does not constitute scientific evidence that Black and brown bodies are permanently damaged or broken. We as clinicians and researchers need to be loudly unequivocal that epigenetics is one line of promising research into how the many levels of racism cause biological harm, and that race is not a risk factor for disease.

This understanding of epigenetics calls on clinicians and medical educators to learn critical race theory, to become active in investigating social and structural determinants of health, and to equip themselves with the language and tools to identify racism, not race, as a cause of racial health disparities.

As medical students, we have seen that such physicians and health-care professionals are thus compelled to not only treat the medical concerns but also the structural ills in society. Our training in both medicine and critical race theory has taught us that race has no business in clinical guidelines and that the use of race in clinical guidelines is just one symptom of much larger systems of oppression. Further, the conflation of race with biology has real, negative consequences when it is incorporated into clinical practice. We are not the first to say this. Yet we seek to be physician-activists who change it. Therefore, we call on our colleagues and our educators to discontinue the use of race in guidelines as one step toward equity. We call on students, physicians, and educators to use the power of medicine to help create an equitable world in which racism no longer causes biopsychosocial harms for this generation and the ones to come.