Systemic racism, chronic health inequities, andCOVID‐19: A syndemic in the making?

For a brief moment, in the early days of COVID-19, some reports heralded the new coronavirus, SARS-CoV-2, as a “great equalizer.” It is unlikely that any anthropologist, human biologist, historian, or public health scientist found this idea tempting. Pandemics always follow the fault lines of society—exposing and often magnifying power inequities that shape population health even in normal times (Wade, 2020). Soon, that stark reality became clear to all. By early April, evidence began to emerge in the United States—first in Milwaukee, then in Detroit, eventually everywhere data were disaggregated by race—that mortality from COVID-19 was disproportionately affecting Black people and communities (Johnson Singer the synergy among epidemics made each worse. Syndemic theory, then, integrates two concepts: disease concentration and disease interaction (Mendenhall Tsai the uniqueness lies in their integration. Attention to disease concentration is a common feature of most frameworks for population health, including fundamental cause theory (Link Quesada, Hart, Laster Pirtle, 2020; Williams Yang et al., 2020). We do not yet understand why these conditions make COVID-19 more dangerous—or even, for certain, if they do2—but suspected pathways for disease interactions include the renin-angiotensin system (Kreutz et al., 2020), the endothelium (Sardu et al., 2020), and inflammatory dysregulation (Mahmudpour, Roozbeh, Keshavarz, Farrokhi, Dolezsar, McGrath, Herzig, Dusendang et al., 2019; Lei, Beach, Panza et al., 2019; Simons et al., 2018). It is plausible, therefore, that the COVID-19 pandemic in the U.S. involves both kinds of interactions put forward by syndemic theory: (a) biological interactions between overlapping diseases (ie, diabetes, hypertension, and COVID-19) and (b) biosocial ones between noxious social conditions and the biological processes involved in progression of SARS-CoV-2 infection to COVID-19 risk. The left side of Figure 1 specifies some of the noxious social conditions. It delineates systemic racism as a set of policies and structures that spawn toxic environments and identifies behavioral and physiological pathways that mediate the social and spatial concentration of disease. Here the model departs from other conceptual diagrams of syndemic interactions, which often focus only on overlapping epidemics, “without reference to the social forces conditioning exposure” (Tsai, Mendenhall, Trostle, see also Singer, 1996). The reason for this departure is that lack of specificity about how large-scale, political-economic forces translate to individual biology impedes progress in testing the theory. My goal in specifying the conditions that shape exposure across multiple levels of analysis is to stimulate further development of testable propositions and research questions that advance the state of syndemic theory beyond a useful heuristic. Pursuing that goal does not require new theory. Figure 1 draws on widely tested and supported models for research on racism and health (Phelan Schulz, Williams, Israel, Williams Morenoff et al., 2007). Some of these pathways (eg, inflammation) may also increase susceptibility to COVID-19, while other aspects of residential segregation may increase exposure, rather than susceptibility, to the novel coronavirus in the first place (eg, density of housing or inability to follow social-distancing guidelines leading to higher viral load). Still other pathways have both COVID-19 and cardiometabolic disease as endpoints. For example, air pollution increases the risk of hypertension and diabetes (Coogan et al., 2012) and has been proposed as a risk factor for COVID-19 (Zhu, Xie, Huang, COVID-19 is also likely to exacerbate social inequities, further harming health. For example, devastating job losses during the pandemic have disproportionately affected Black Americans (Gould Tsai & Venkataramani, 2015) the and and Singer (2020) research strategies that researchers are to to For however, the of syndemic theory COVID-19 an urgent case for specifying testable hypotheses about interactions with chronic cardiometabolic diseases that exacerbate pre-existing inequities. The model in Figure 1 is as a framework for such hypotheses as we learn more about COVID-19. related conceptual which has the level of analysis at which interactions other frameworks for population health, syndemic theory is It that large-scale, political-economic which often over have consequences for individual health 2009). This makes syndemic theory a for which incorporate and effects, but syndemic have only individual-level factors (Tsai, 2018). This focus may in from the on biological interactions between disease to an from Singer et al. the interaction that makes with HIV and more than infection with alone in individual These interactions but they are also by the concepts of or multimorbidity. The of syndemic theory is that it attention to possible interactions not only between diseases the individual but also between epidemics the population social context and political-economic inequities into The tentative syndemic model of COVID-19 I these by pathways from social forces to individual biology and interactions at the individual and population level. The intersection of systemic racism, chronic health inequities, and to journalists and other the on researchers to and the syndemic model and develop public health and policy that for I for the to the Cassel for the and an for to early work by and on the entire I in medical for work some of these ideas in and