The end of Richard Towne’sTreatise of the Diseasesmost Frequent in the West Indies (1726) takes up the description of “diseases to which the blacks are no strangers, but as far as I am informed they are utterly unknown in Europe.” Given that these afflictions seemed to be limited to a single race, one might imagine that Towne had in mind some innate cause for this difference in susceptibilities. To the contrary, however, an essentialist biology mattered little for his explanation: “Those Blacks are the more subject to it,” he wrote of “the Elefantiasis under the circumstances it occurs in the West Indies,” “who after severe acute fevers, long continued intermittents, or other tedious illnesses, are either much exposed to the inclemency of Rainy seasons, and the cold penetrating Dew of the evenings, or are constrained to subsist upon bad diet and undigestible unwholesome food.” In other words, the causes of the diseases were previous maladies, poor accommodations, and a wretched diet.” As if to make clear how little race mattered to his medicine, Towne observed that Europeans who lived like the enslaved population of the islands were just as liable to the Elefantiasis as those of African descent: “Sometimes white people, whose unhappy circumstances have reduced them to hardships but little inferior to what the Blacks are obliged to undergo, have given us proof that this disease is not limited to one colour.” Compare this multiplicity of plausible causes in a non-racialised account of disease to the paucity of causal explanations in one of the few eighteenth century medical writings to center racial difference. In 1756, the South Carolingian physician John Lining put forward a description of what he termed “the American yellow fever.” This “dreadful malady” attacked almost everyone, yet it spared one group: “There is something very singular in the constitution of the Negroes,” wrote Lining, “which renders them not liable to this fever…I never knew one instance of this fever amongst them.” ‘Constitutional singularity’ would be the only cause Lining would marshal to explain this peculiar racial discrepancy in susceptibility to the disease. The vagueness and lack of detail in causal accounts of disease for racialists, compared with the multiple and explicit causes of non-racialists is my focus here. Among the reasons that race was invoked so uncommonly as a cause in eighteenth century medicine, I argue, was because, in general, race was an explanandum in the period, not an explanans. That is, naturalistic arguments in the early modern period were far more concerned with the cause of race than with race as a cause. This was even more true in medicine, where Neo-Hippocratic explanations, which invoked the power of “Airs, Waters, and Places” as well as habituation to the climate, could explain why some populations were struck and others spared without invoking essential differences. In the eighteenth century, race was a solution in search of a problem, and the problems it found were few.

Precision medicine offers a precious opportunity to change clinical practice and disrupt medicine’s reliance on crude racial, ethnic, or ancestral categories by focusing on an individual’s unique genetic, environmental, and lifestyle characteristics. However, precision medicine and the genomic studies that are its cornerstone have thus far failed to account for human diversity. This failure is made clearer when looking at multiracial individuals who encapsulate a mosaic of different genetic ancestries. This presentation argues that precision medicine is failing multiracial individuals and relies on the same forms of crude categorization it seeks to unsettle. I provide examples of where multiracial individuals are being failed in genomic research, research translation, and public health. Until the scientific community creates inclusive solutions for multiracial individuals in medical genomics, precision medicine will continue to fall short in its aims. I conclude by offering a way more just and equitable path forwards for precision medicine.

South Africa has some of the most genetically diverse and the most genetically admixed human population groups on the planet. This is due to South Africa’s peculiar history, both social and biological. Nevertheless, people in the country are divided into four ‘population groups’ by which official agencies mean ‘demographic groups’ designed to correspond to Apartheid racial categories. These categories are “Black African,” “Coloured,” “Indian/Asian,” and “White”. Although there may be strong normative reasons for us to continue to use racial classifications in monitoring and reporting on issues of equity and health inequalities, here I argue that the use of racial classifications in health is such a blunt and imprecise instrument as to be dangerously misleading except when assessing the health consequences of racism. The racial or demographic population groups to which people in South Africa are sorted are so internally diverse as to constitute many distinct biological population groups whose variation is relevant to therapeutic interventions in different ways. These biological differences between race groups and most especially within race groups is important for the (lack of) predictive ability of race in medicine despite the broad correlation of health outcomes with race in South Africa. Each race group also comprises of different ethnic and cultural groups whose differences in environmental exposures have independent health consequences. This makes race of quite limited use in properly incorporating in analysis other social determinants of health that are not necessarily tied to racism. I argue that both the internal biological variation of race groups in South Africa and the differences in their environmental exposures makes the use of racial classifications inappropriate in clinical and biomedical settings. The only exception to this rule is the use of racial categories in tracking progress on equity and the elimination of racial inequalities.

Much of the literature on the nature and limits of using race as a scientific variable in medicine focuses primarily on United States (US) racial categories. This focus on the US is seemingly justified by ‘contextualism’ - the assumption that we must limit discussion of race and its deployment to a specific national context because “there is no transnationally valid ontology of race” (Ludwig, 2019), race does not travel across geographic or national contexts. Thus, American scholars are justified in restricting their arguments to a US ontology of race, and scholars in Brazil, the United Kingdom, India, and South Africa ought to similarly restrict their arguments (ibid.). We draw on two case studies of race-based correction in health measurement to illuminate the ways in which there are global continuities and discontinuities with the ways in which race enters into medicine. We argue that although the explanations for racial difference and their underlying racial ontologies differ across national contexts, nevertheless, a tension exists because the correction factor itself is made to travel across these contexts. This has the potential to pose unique ethical and political challenges. The first case study we draw upon is that of the history of how spirometric measurement became racialised in South Africa (SA). The spirometer is a test that doctors use to measure lung capacity for the diagnosis and treatment of respiratory disease. The spirometer is controversial because a ‘race correction’ factor is directly programmed into many commercially-available spirometers. In the US, spirometers either ‘correct’ the lung capacity of individual patients labelled ‘Black’ by 10-15%, for example, or use population-specific norms (Braun, 2015). First, 3 during Apartheid, South African researchers used American data in an effort to bolster their database of purported innate racial differences in lung function between white and Black South Africans. Second, historically, South African clinicians adopted US standards of race correction in their spirometers. Despite alternative explanations of racial difference in lung function, and a more biosocial conception of race in SA, clinicians and researchers relied on American standards of correction. The second case study we draw upon is that of Body Mass Index (BMI) thresholds. The ‘Y-Y paradox’ was proposed by two endocrinologists who juxtaposed their own (identical) BMIs with their differing levels of body fat (9.1% for the British researcher compared with 21.2% for the Indian researcher). This ‘paradox’ has been expanded on, forming the broader notion of the ‘thin-fat Indian’: a body which is thin morphologically but metabolically “obese”. This has led to changes in public health policy (notably, a lowering of the BMI threshold for clinical surveillance or intervention) both for the Indian population and for South Asian diaspora in places such as the United Kingdom (UK). Although the explanations for differing rates of metabolic illness frequently differ between India and the UK, the racial or ethnic groups that are taken to be the target of intervention differ, and, plausibly, the underlying racial ontologies differ, the lowered BMI threshold continues to be in place in these disparate settings.