Abstract
(type = abstract)
In this dissertation, I examine how race has been molecularized through the hormone tes-tosterone and the impact that this process has had on the construction of racial disparities in prostate cancer between black and white men. While testosterone is widely conceptual-ized as a molecular marker of masculinity by both scientific and popular accounts, femi-nist science studies scholars have documented how these claims are both misleading and dangerous. Building from this foundational work, this project explores how testosterone has been both gendered and racialized by scientists over the course of the 20th-century. More specifically, biomedical researchers claim that racial differences in testosterone help explain racial disparities in prostate cancer between black and white men. This discourse endorses the theory that higher levels of testosterone, which has historically been a marker used to designate prostate cancer risk, must differ between black and white men and thus explain the persistence of prostate cancer disparities between these two groups.
To examine the validity of these racialized claims, I use insights from science & technology studies, critical race theory, and social network analysis to critically evaluate the triangular linkages between testosterone, race, and prostate cancer in biomedical re-search. In my first analytic chapter, I examine the relationship between testosterone and race. To do this, I conduct a content analysis of 147 studies that evaluate population dif-ferences in testosterone. I find that, despite widespread claims that testosterone varies be-tween racial groups, the literature provides scant evidence to support these assertions. To demonstrate how population differences are enacted and reproduced, I use social net-work analysis to visualize a citation network of these data and trace how the racialization of testosterone circulates through scientific research. I identify three mechanisms – ambi-guity, absence and data recycling – to help explain how racial difference testing has con-tributed to preserving the cultural myth of testosterone as a molecular marker of racialized masculinity.
Second, I evaluate the linkage between race and prostate cancer, looking to un-derstand how racial disparities in this disease are constructed. Biomedical and epidemio-logical researchers widely claim that African American men suffer from prostate cancer at two to three times the rate of white Americans. However, a critical review of this litera-ture finds that racial disparities in prostate cancer-specific mortality are largely explained by socioeconomic differences between the two groups. While scientists do discuss the ef-fects of socioeconomic inequalities in their work, researchers also suggest that black men’s more “aggressive biologies,” propelled by testosterone and other biological differ-ences, help explain why this group is more likely to experience earlier onset of disease, faster growing tumors and worse overall survival. These racialized claims shape group-differentiated patterns in the use of prostate-specific antigen screening, racially-specific treatment guidelines, and variability in the distribution of hormone-based pharmaceuticals and surgical interventions. Ultimately, I argue that biomedical researchers’ focus on ex-plaining prostate cancer through racial differences in biology (i.e. testosterone) ultimately leads to the misallocation of funding away from addressing the structural causes that drive these disparities in the first place.
In the final analytic chapter, I investigate the linkage between testosterone and prostate cancer to see how this association has changed over time. By examining changes in scientific consensus over time, I demonstrate that the association between testosterone and prostate cancer has undergone a radical paradigm shift over the past 25 years. While high levels of testosterone were considered a robust indicator of prostate cancer risk for more than seven decades, most biomedical experts now argue that clinically low levels of testosterone may, in fact, be a more accurate risk factor for diagnosing this disease. Alt-hough prostate cancer researchers have moved towards consensus, this paradigm shift has not carried over to impact all domains of research in the same way. For example, today’s most widely used clinical guidelines on testosterone replacement therapies explicitly ad-vise clinicians not to prescribe testosterone to African American men because of their in-creased risk of prostate cancer. These guidelines are not only predicated on the assump-tion that black and white men have different testosterone levels, but also on the antiquat-ed theory that higher levels of testosterone contribute to prostate carcinogenesis, which unjustly withholds testosterone therapies from black men. In response to these findings, I call for the Endocrine Society to reassess their guidelines to reflect a more equitable poli-cy on testosterone replacement therapies, which relies on the best available evidence on the topic.
Together, these chapters demonstrate that molecularization and racialization are co-constitutive processes that shape the contours of today’s biomedical markets, includ-ing the “gold-standards” of evidence-based medicine and access to hormone-based phar-maceuticals for black and white men across the United States. In the conclusion, I discuss how my work speaks to scholars working in science & technology studies as well as the literatures on the medicalization and pharmaceuticalization of race. Furthermore, I outline how my work affects biomedical research on testosterone. Most notably, I argue that those responsible for constructing the Endocrine Society’s clinical guidelines on testos-terone replacement therapies need to revise their recommendations to remove race as a ba-sis for withholding pharmaceuticals from black consumers. While it is crucial to recognize and assess the potential risks of hormone-based pharmaceuticals, using race as a basis for (not) disseminating medical treatment perpetuates the legacy of scientific racism and un-justly bars important resources from patients who may benefit from the use of testos-terone replacement therapies.