Kuzawa C.W., Sweet E. 2009. Epigenetics and the Embodiment of Race: Developmental Origins of US Racial Disparities in Cardiovascular Health. American Journal of Human Biology. 21(1): 2-15.
In this article Kuzawa and Sweet attempt to test explanatory power of the epigenetic and embodiment model of the racial health disparity with respect to cardiovascular disease in African Americans. Kuzawa and Sweet argue that the embodiment of social and material environments throughout developmental and epigenetic processes help explain the persistence of biological cardiovascular disease disparities. Through this model of embodiment, Kuzawa and Sweet analyze how social and economic inequalities experienced by African Americans put them at higher risks for low birth rate, diabetes, cardiovascular disease, as well as other forms of heart disease. The importance of early environments and adult health is reviewed in regards to showcasing how pre- and post-natal environments with respect to nutritional and psychological stress posing as dangers to the development and overall well-being of the zygote, fetus, and growing child. These researchers also discuss how these stressors have trans-generational impacts, where the epigenetic influences of the many stressors from racism increase the disease risk for cardiovascular disease increases for coming generations. Kuzawa and Sweet also discuss the number of different biological pathways through which epigenetic changes can occur which includes but is not limited to: (1) a change in the growth of tissue and/or an organ that can be reflected in its size or the number of cells, (2) changes in the chromatin that scaffolds the DNA within chromosomes resulting in changes in gene expression, where the “epigenome” is a result of the genome interacting with the intersecting constraints of the environment. Kuzawa and Sweet demonstrate how racial health disparities are a consequence of environmentally responsive phenotypic plasticity, showcasing the acute and chronic effects of social-environmental exposures.
Thayer, Z.M., Kuzawa, C.W. 2011. Biological memories of past environments: Epigenetic pathways to health disparities. Epigenetics. 6(7): 798-803.
In this article Thayer and Kuzawa investigate the explanatory power of epigenetics in understanding how social inequality influences human health and biology. Thayer & Kuzawa point out how research has shown that social status within a society has a greater impact on health disparities than genetic ancestry and common geographic origin. Research has demonstrated that those at the lowest social statuses are the sickest. It is well established that social and economic inequality influences health and disease but the biological mechanisms through which oppression ‘gets under the skin’ is not completely understood. In this research article Thayer and Kuzawa review how social and economic inequality can influence epigenetic expression and health through nutritional stress, psychosocial stress, and environmental toxicants. Nutritional stress in prenatal environments and childhood drastically impacts the health of adults, research has shown that the food insecurity of an individual’s grandparents can increase their risk for cardiovascular disease and diabetes related death. Psychosocial health and environmental toxins have also been shown to impact health and the impact ripples across generations. Thayer and Kuzawa show that as researchers we need to aim to not simply reduce stress but also improve the health of marginalized populations at risk. The sociopolitical and economic environment is crucial in influencing the health and wellbeing of groups of un-empowered populations.
Sullivan, S. 2013. Inheriting Racist Disparities in Health: Epigenetics and the Transgenerational Effects of White Racism. Critical Philosophy of Race. 1(2): 190-218.
In this research article Sullivan reviews how people of color can embody the deleterious effects of White racism. Sullivan utilizes epigenetics are the main praxis through which she demonstrates how racial health disparities is part of the evidence that demonstrates the impact of social forces like racism has transgenerational biological consequences. Sullivan makes this argument by providing an argument for the importance of studying the epigenetic effects of racism through looking at health disparities in preterm birth rates, investigating prenatal care for African American women as one place to investigate epigenetics and racial health disparities. Sullivan reviews the socio-historical perspective of racism and how public health scholarship has approached the topic. Sullivan demonstrates the divide within public health scholarship where many critical scholars have demonstrated how racism is a public health problem while others who subscribed to bio-medicalized perspective are still searching for genetically based causes for racial differences through biological deterministic models. Sullivan argues that epigenetics and the embodiment of social inequality demonstrates that we need to develop new ways to think about and understand human biology and genetics showcasing the holistic intersectionality of the impacts that ecosocial and political environments have on health. Sullivan reviews how white racism impacts where African Americans tend to live, what they tend to eat, the reality of their socioeconomic situatedness, and parenting styles for instance and how these factors are part of an overall framework where stressors are continuously impacting the phenotypic expression and adaptation of African Americans to deleterious ecosocial, political, and economic conditions. Sullivan then continues the discussion by addressing the impact that social inequality has on the zygotes of disenfranchised African Americans, where epigenetic effects of systemic, individual, institutional racism all get passed on to the grandchildren of the un-empowered. Sullivan concludes that it is important for researchers to understand how social environments inhabited by one’s ancestors can constitute the person that one is today, and this can occur physiologically via inherited hormonal and chemical markers that influence the expression of one’s genes.