Du Bois meets Darwin

While “race is a social construction” has become a mantra in the U.S., contemporary racial formation theory and critiques of biological race concepts (BRCs) have yet to demonstrate this truism. This deadlock is most confounding in research on racist health inequities and human genetics. Attempts to understand the relationships between race and differential health outcomes reproduce in lieu of disrupting racism and racialization. While some argue that race should be phased out of human genetics, others contend that the race variable is needed to highlight the effects of racism. With these issues in mind, I ask, “How do we study race without socially reproducing racism?” In this dissertation project, I argue that the root of the problem is the use of ahistorical definitions and theories that separate race from racism and Euro-colonialism. Without critical historiography, scholars use incorrect information to understand how external conditions shape and produce the environments that racialized peoples live in. This problem extends to how geneticists model and describe contemporary patterns of human genetic variation. Consequently, scientific critiques of BRCs abandon the historical information needed to demonstrate the social construction of race/ism and the evolutionary thinking required to interpret human genetics. Utilizing a Du Boisian historiography, I analyze dynamic events or sites of the social construction of race/ism to show how race is a product of racism, what I call race/ism. Race/ism is an issue of power, not phenotype. Created by and for Euro-imperialism, race/ism is a socio-political system that co-opts, marks, and groups people to regulate the reproduction and inheritance of “population-specific modes of colonial domination through time” (Wolfe 2016:10). Using these insights, I analyze genetic and sociodemographic data collected in the Midwest region of the U.S. to isolate distinct variables often used as “race proxies” in genetics research: self-identified race/ethnicity, internalized response to externalized racialization, and genetic ancestry. Each race proxy captures the dynamic interactions of racialization, or rather, the doing of race/ism, structured by effective human actions and social milieux. I use genotype, phenotype, and sociodemographic data to explore the relationships between race/ism, blood pressure, and candidate polymorphisms associated with hypertension. I’m interested in the presence of gene by environment interactions (GEI) because they both refute reductionism and demonstrate complex relationships between genetics, biology, and society. Through modeling race/ism as an ecological phenomenon that shapes the conditions in which people live and die, I present an evo-ecosocial theory of disease distribution for understanding the biological consequences of race/ism.LimitedAuthor requested closed access (OA after 2yrs) in Vireo ETD syste