Race has been an important category in medicine, despite scientists coming to a consensus that race makes a poor scientific concept (Rotimi, 2004; Tishkoff & Kidd, 2004; Wilson et al, 2001). It has been found that humans, regardless of race, share 99.9% of their genetic makeup. The variants that occur in the remaining 0.01% are shared between whole populations (Weigmann, 2006). Furthermore, critics of racial classification argue that race is not real, but just an illusion, and that it is meaningless in science (Root, 2003). In this literature review, I will summarize how race is used as a proxy for drug response as well as how race is used as a proxy for susceptibility to some diseases.
BiDil: A Racialized Pharmaceutical
Well-intentioned scientists have steered that race might function a proxy for drug response. many studies have indicated that patients of differing racial and ethnic groups metabolise drugs differently because of variations in their genetics (Wood, 2001). Other scientists have refuted, stating that the observed racial differences in drug metabolism are not accurate or remarkable enough to make them clinically useful in directing the choice of drugs (Holden, 2003).In short, BiDil is a combination drug consisting of two vasodilators, hydralazine hydrochloride and isosorbide dinitrate, that was patented by cardiologists Jay Cohn and Peter Carson in 1989 for congestive heart failure. During the first clinical trial in 1997, the drug was rejected because it failed to show sufficient evidence of effectiveness in a multiracial population. The data of the clinical trial was re-examined along racial lines by NitroMed, and a new clinical trial was put in place. BiDil was then tested on 1050 men and women who self-identified as African American, and the results showed a 43% decrease in mortality and a 39% reduction of risk of first hospitalization against placebo. The FDA then approved the drug, after three more clinical trials that showed a “dramatic effectiveness” of BiDil in black patients, as a supplement to standard therapy for the treatment of heart failure in black patients (Krimsky, 2012).
Though BiDil reinscribes racial taxonomies, either through geographical ancestry or indigenous populations, into science, it has been doing this without credible genetics. For instance, no genetic markers were used to acquire a population samples in the clinic trial for BiDil. Moreover, there are no racial genes, no clear genomic divide between any of society’s socially constructed racial categories, and no stable cluster of medically relevant genes that is necessarily linked with ancestry or skin colour. BiDil’s success with self-identified black people could have been a statistical accident or there could be, as yet, some unknown factor that accounted for it. There were many criticisms towards BiDil regarding the use of race as a proxy for genotype in the clinical trial. Since race is poorly defined and self-identified racial identity is neither consistent or well grounded, then any science that is acquired from it will not be accurate. This comes after follow-up interviews in the 1970s by the US Bureau of the Census, to assess the consistency of self-reporting, which discovered that 34% of respondents changed their racial or ethnic identity within 2 years. Ironically, it was a science-based agency that approved BiDil for a racial group, despite all the reasons why race has no part to play in science. Nonetheless, the idea behind BiDil has not been disputed – because vasodilators can be an effective supplementary therapy in reducing heart attacks for some people with congestive heart failure who do not produce enough nitric oxide. However, neither socially constructed nor self-identified concepts of “race” can serve as a proxy for an unknown or poorly defined biological marker that provides a causal connection to or strong association with a drug’s effectiveness (Krimsky, 2012).
Sickle Cell Anemia: A Race Specific Disease
Race could even function as a proxy for vulnerability to certain maladies (Wang, 2004). This unpredictable, wrecking disease moved toward becoming credited to the black body because of its development in science during a time of high racial transformation and the political battles pursued in connection to it. Medicine, much like all aspects of life, carried racialized undertones specifically when it came to black individuals, following the involvement of natural science in the creation of race in the mid-nineteenth century. Eventually, black people were seen as disease carriers by the beginning of the twentieth century, and were associated with prominent diseases such as tuberculosis and syphilis (Wailoo, 2001). Their defenselessness to sickness was believed to be a result of their numbness, superstition, and unpreventable physical and mental mediocrity (Tapper, 1999). Sickle Cell Anemia’s relation to blackness was a mix of its introduction in medication and how attention was caught around the illness: first as a way to demonstrate black mediocrity and later in the black power movement as an approach to create solidarity awareness to the condition of blacks in the U.S.
The first documented case of the disease was in 1910 by James B. Herrick. He entitled it “sickle cell anemia” (Herrick, 1910/2001). In his article, Herrick portrays the instance of Walter Clement Noel, an immigrant from Grenada going to dental school in Chicago who obtained a strange set of symptoms. Herrick at that point incorporates a depiction of those symptoms, investigation of bodily, proposed treatment course, patient history and physical assessment. In the latter two segments, he describes Noel as an “intelligent negro” and “a young man of typical negro facies” (Herrick, 1910/2001). In 1911, Benjamin Earl Washburn documented the second case. In his article, he describes Ellen Anthony as a “fairly well developed negro woman, with facies characteristic of her race”, similarly taking note of her race (Washburn, 1911). In 1915, the third case was documented in scientific literature by Jerome E. Cook and Jerome Meyer who described their female patient as a “very light mulatto”, illustrating the recognition of a problem with black and white binary. Upon this discovery, one would think that it would complicate the connection of Sickle Cell Anemia to race, but the opposite held true; Cook and Meyer continued to compare their case to that of Herrick and Washburn. They then listed the similiarities between the cases with “all three of the patients were of negro blood”(Cook and Meyer, 1915). Cook and Meyer additionally understood the conceivable connection to inheritance, unavoidably beginning an association between blackness, sickle cell, and genetics. Less than ten years after Cook and Meyer’s article, other articles illuminating and grouping the disease began to surface. Despite unmistakably highlighting the mixed nature of early patients’ heritage, Verne R. Mason (1922) still observed their ‘blackness’ as a critical connection between the patients.
During the following twenty years, the association between Sickle Cell Anemia and blackness was embedded in the scientific community. In cases of the disease occurring in someone who appeared to be another race, there was an assumption that there was racial mixing in that person’s ancestry (Tapper, 1999). In situations where the connection to a black ancestry was not evident, there was continuous denial that the individual had sickle cell since sickle cell just happened in blacks (Tapper, 1999). Because sickle cell has multiple origins, and the unsubstantiated method of categorizing people based on highly variable phenotypic “race characteristics”, it is highly likely that individuals who could be categorized as white were an allele carrier or had the disease. Regardless, to concede the fact that racial classifications were quite shallow and not characteristic of significant inner markers, one would need to deal with the idea that there is no pure white race (Tapper, 1999). That end would have been hard to envision for somebody who had grown up with colossal racial partiality. It would likewise have been bothersome on the grounds that it would have worn down a portion of the power and privilege that whiteness gives. As a result, rather than relaxing the polarity between whites and blacks, science searched for better approaches for finding contamination of the white race by blacks (Tapper, 1999). This push in turn gave rise to more studies on the origins of Sickle Cell Anemia.
Race, though not biologically based, has substantial and influential consequences both socially and politically, and therefore must still be addressed in those domains. Rather than an emphasis on race and distinction, as Dorothy Roberts contends, genetics could concentrate on discovering more about our similarities, for example, how the genes themselves work. This could prompt a change in perspective in how racial contrasts are tended to in science; and this move is fundamental for current inequality to be viewed as important to address on a huge scale.
- Rotimi CN (2004) Are medical and nonmedical uses of large-scale genomic markers conflating genetics and ‘race’? Nat Genet 36 (Suppl): S43–S47
- Weigmann, K. (2006). Racial medicine: here to stay?. EMBO reports, [online] 7(3), pp.246-249. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1456889/pdf/7400654.pdf.
- Root, M. (2003). The Use of Race in Medicine as a Proxy for Genetic Differences. Philosophy of Science, 70(5), 1173-1183. doi:10.1086/377398
- Wood, A. (2001). Racial Differences in the Response to Drugs — Pointers to Genetic Differences. New England Journal Of Medicine, 344(18), 1394-1396. doi: 10.1056/nejm200105033441811
- Holden, C. (2003). Race and Medicine. Science, 302(5645), 594-596. doi: 10.1126/science.302.5645.594
- Krimsky, S. (2012). The short life of a race drug. The Lancet, 379(9811), 114-115. doi: 10.1016/s0140-6736(12)60052-x
- Wang, Lu-in. (2004). Race as Proxy: Situational Racism and Self-Fulfilling Stereotypes. DePaul Law Review, Vol. 53, p. 1013, 2004 ; U. of Pittsburgh Legal Studies Research. Available at SSRN: https://ssrn.com/abstract=1367888
- Wailoo, K. (2001). Dying in the city of the blues :Sickle cell anemia and the politics of race and health. Chapel Hill: University of North Carolina Press.
- Tapper, M. (1999). In the blood :Sickle cell anemia and the politics of race. Philadelphia: University of Pennsylvania Press.
- Herrick, J. B. (2001). Peculiar elongated and sickle-shaped red blood corpuscles in a case of severe anemia. 1910. The Yale Journal of Biology and Medicine, 74(3), 179-184.
- Kwateng, Margaret. (2014). ‘Repackaging Racism: The Role of Sickle Cell Anemia in the Construction of Race as Biological’ (2014). Senior Capstone Projects. Paper 331.
- Cook, J.E. & Meyer, J. (1915). Severe anemia with remarkable elongated and sickle-shaped red blood cells and chronic leg ulcers. Archives of Internal Medicine, 16, 644–651.
- Washburn, R.E. (1911). Peculiar elongated and sickle-shaped red blood
- corpuscles in a case of severe anemia. Virginia Medical SemiMonthly, 15, 490–493.
- Mason, V.R. (1922). Sickle cell anemia. Journal of the American Medical Association, 79, 1318–1320.
- Roberts, D. E. (2011). Fatal invention :How science, politics, and big business re-create race in the twenty-first century. New York: New Press.