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 & Buford, 2020). During the entire course of
the pandemic so far, data compiled by the non‐profit APM Research Lab (2020) has shown
that the crude death rate for Black Americans is more than double that for all other
racialized groups. When adjusted for age, the risk of death from COVID‐19 is as much
as nine times higher for African Americans than it is for whites (Bassett, Chen, &
Krieger, 2020).
This inequity—as appalling as it is—may still underestimate the problem, as data remain
woefully incomplete. Despite calls for comprehensive, nationwide data on COVID‐19
cases and deaths by race and socioeconomic status, the U.S. federal government has
no such system in place, and journalists and scholars have stepped in to collate disaggregated
data by race from a patchwork of state health departments. The need for better data
remains.
But data alone are not enough. We also need an explicit conceptual framework to know
what the numbers mean, shape the questions researchers ask, and direct attention to
appropriate public health and policy responses. In the absence of such a framework,
the legacy of racial‐genetic determinism in American medicine makes it likely that
excess Black death will be interpreted as intrinsic Black vulnerability—a pattern
that has already begun to emerge (Gravlee, 2020). Here I propose that the theory of
syndemics may be a useful framework for making sense of the unfolding pandemic and
directing future research on COVID‐19.
1
DEFINING SYNDEMICS
Merrill Singer and colleagues (Singer, 1994, 1996; Singer & Snipes, 1992) developed
the concept of syndemics in the early 1990s, in the context of research on the HIV
epidemic, which was then ravaging poor, Black, and other communities of color in urban
North America. Singer built on the long‐standing observation that communities most
impacted by new epidemics often are already facing other threats to their health.
In the case of HIV among marginalized people in the U.S., those threats included “a
set of closely interrelated endemic and epidemic conditions (eg, HIV, TB, STDs, hepatitis,
cirrhosis, infant mortality, drug abuse, suicide, homicide, etc.), all of which are
strongly influenced and sustained by a broader set of political‐economic and social
factors” (Singer, 1996). The crucial point, Singer argued, was that these conditions
did not merely co‐occur; the synergy among epidemics made each worse.
Syndemic theory, then, integrates two concepts: disease concentration and disease
interaction (Mendenhall & Singer, 2020; Tsai & Venkataramani, 2015). Disease concentration
refers to the co‐occurrence or clustering of multiple epidemics as a result of large‐scale,
political‐economic forces and adverse social conditions. Disease interaction refers
to the ways that overlapping epidemics exacerbate the health effects of adverse social
conditions, either through biological interactions between disease states or through
interactions between biological and social processes.
Neither disease concentration nor disease interaction is unique to syndemic thinking;
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 & Phelan, 1995), ecosocial theory (Krieger, 2001), and the concepts of
structural violence (Farmer, 2003) and structural vulnerability (Leatherman, 2005;
Quesada, Hart, & Bourgois, 2011). Indeed, more than half a century ago, Cassel (1964)
argued for the relevance of social‐science theory to epidemiology by highlighting
social processes that lead to the clustering of seemingly unrelated diseases (in his
case, tuberculosis and schizophrenia). However, like Cassel, most models of population
health frame the co‐occurrence of epidemics in terms of the cumulative burden of disease.
What the syndemic framework adds is the prediction that overlapping epidemics are
more than the sum of the parts. Both (a) biological interactions between epidemics
and (b) biosocial ones between epidemics and the social conditions that shape them
can result in more suffering and death than would be expected in models that treat
each disease in isolation.
The focus on disease interaction also has deep, historical roots, stretching back
at least to Scrimshaw, Taylor, and Gordon's (1959) work on synergism and antagonism
between nutrition and infection (see also Scrimshaw, 2003). Disease interaction is
usually described in terms of comorbidity and multimorbidity (van den Akker, Buntinx,
& Knottnerus, 1996). These concepts, which have gained wider currency in the context
of COVID‐19, draw attention to common etiological pathways across disease states and
to the complexity of care for patients with more than one chronic disease. Comorbidity
and multimorbidity are most salient in clinical medicine but are also relevant to
epidemiology and health services research (Valderas, Starfield, Sibbald, Salisbury,
& Roland, 2009). Even when invoked in epidemiology, however, the focus is on the distribution
of comorbid conditions (and predisposing social conditions or risk factors) at the
level of the individual (Barnett et al., 2012). If syndemic theory were concerned
only with biological interactions at the individual level (eg, for people who were
infected with both HIV and TB), it is not clear what value it would add beyond the
framework of multimorbidity. The promise of the theory lies in raising questions across
levels of analysis about interactions among clustered epidemics and the underlying
social conditions that drive them. This unique perspective is what makes syndemic
theory relevant to the COVID‐19 pandemic.
2
RELEVANCE TO COVID‐19
The core tenets of syndemic theory, then, are that:
large‐scale, political‐economic forces, which play out over generations, result in
deep‐seated social, economic, and power inequities;
these inequities shape the distribution of risks and resources for health, resulting
in the social and spatial clustering of epidemic diseases (disease concentration);
and
some overlapping epidemics have synergistic effects due to (a) biological interactions
between disease states or (b) interactions between biological processes and the social,
economic, and power inequities that shape the distribution of health to begin with
(disease interaction).
COVID‐19 has made these ideas feel urgent from the start. In early March, for example,
the New York Times highlighted the intersection of social factors that increase the
risk of infection in impoverished communities, such as housing density and reliance
on public transportation, and “disproportionately high rates of disease and illness”
that make infection more deadly (Eligon, 2020). Days later Time predicted that people
with low incomes—disproportionately Black, Indigenous, or other people of color—would
face higher exposure to the virus (because they are less likely to be able to work
from home, more likely to work in service sectors where contact with strangers is
routine, more likely to live in multi‐family apartment buildings) and had less access
to sick leave and medical care if they did become sick (Vesoulis, 2020). In mid‐May,
when the New York City Health Department first released data on COVID‐19 deaths by
ZIP code, the prediction had borne out: the highest death rates were in low‐income
neighborhoods with disproportionate numbers of Black and Latinx people (Schwirtz &
Cook, 2020).
The spatial concentration of COVID‐19 death manifests on a broader scale, too. In
early April, The Atlantic ran a story about the demographic distinctiveness of COVID‐19
mortality in the American South (Newkirk, 2020), suggesting that younger people were
dying there at higher rates than in other hard‐hit regions because of the legacy of
slavery and Jim Crow. The suspected pathway was a higher burden of chronic diseases
like hypertension and diabetes, which followed from social and political‐economic
factors such as poverty, limited government investment in health care, and mass incarceration,
among others.
1
These accounts by journalists and others paint a compelling picture. The challenge
for researchers is to incorporate such observations into a theory that generates testable
propositions about the links between systemic racism, chronic disease, and risk of
mortality from COVID‐19. That work has already begun. Social scientists and public
health researchers have drawn attention to the structural conditions that shape the
concentration of COVID‐19 in communities already facing higher burdens of poverty,
racial inequity, and disease (Khazanchi et al., 2020; Laster Pirtle, 2020; Williams
& Cooper, 2020). Medical scientists and clinicians have emphasized the interactions
among comorbid conditions that are overrepresented among COVID‐19 hospitalizations
and deaths—particularly hypertension (Pranata, Lim, Huang, Raharjo, & Lukito, 2020),
diabetes (Kreutz et al., 2020), and obesity (Akoumianakis & Filippatos, 2020). Syndemic
theory draws together both approaches, bridging the population‐ and individual‐level
perspectives of the social and medical sciences, and it adds new questions about possible
interactions between COVID‐19 and pre‐existing social inequities that may exacerbate
suffering from chronic diseases like hypertension and diabetes.
Figure 1 offers a tentative syndemic model to guide research in this area. The right
side of the model highlights the concentration of and possible interactions among
COVID‐19 and two chronic conditions that seem to pose particular risks for people
infected with SARS‐CoV‐2: hypertension and diabetes (Richardson et al., 2020; Yang
et al., 2020). We do not yet understand why these conditions make COVID‐19 more dangerous—or
even, for certain, if they do
2
—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, & Nabipour, 2020). Because these systems
are also involved in diabetes and hypertension, researchers are pursuing the hypothesis
that those conditions interact with COVID‐19 to make infection with SARS‐CoV‐2 more
deadly.
FIGURE 1
A tentative syndemic model of systemic racism, cardiometabolic disease, and COVID‐19
in the United States
Emerging evidence suggests that COVID‐19, in turn, may exacerbate the risk of cardiometabolic
disease. Rubino et al. (2020) propose that SARS‐CoV‐2 may have pleiotropic effects
on glucose metabolism that could complicate pre‐existing diabetes and lead to new
onset of diabetes in people with COVID‐19. Other coronaviruses, including the one
that caused the original severe acute respiratory syndrome (SARS‐CoV), are known to
have long‐term effects on cardiovascular health. People who survived SARS in 2002
to 2003 exhibited altered lipid metabolism 12 years later (Wu et al., 2017). It is
too early to know whether COVID‐19 will have similar effects, but it is possible that
people who recover from the new coronavirus may experience long‐lasting damage that
increases the risks associated with hypertension and heart disease.
As we learn more about COVID‐19 and its long‐term sequelae, Figure 1 provides a framework
to develop specific hypotheses about how it interacts with chronic conditions like
hypertension and diabetes. The simultaneous attention to disease interaction and disease
concentration keeps in the foreground that physiological dysregulation and possible
interactions between COVID‐19 and cardiometabolic disease are socially patterned.
Indeed, the same physiological systems that are the focus of interactions among hypertension,
diabetes, and COVID‐19 are also involved in the pathways that link neighborhood disadvantage,
racial discrimination, and poverty to racial inequities in hypertension and diabetes
(Cobb, Parker, & Thorpe, 2020; Dolezsar, McGrath, Herzig, & Miller, 2014; Dusendang
et al., 2019; Lei, Beach, & Simons, 2018; 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, & Kawachi,
2017, p. 978; 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 & Link, 2015; Schulz, Williams,
Israel, & Lempert, 2002; Williams & Mohammed, 2013) and on the role of health equity
in pandemic preparedness (Quinn & Kumar, 2014). Building on such work links syndemic
theory to allied strategies for explaining racial health inequities—before, during,
and likely after COVID‐19—and clarifies what syndemic thinking adds to interdisciplinary
efforts. The unique contribution of syndemic theory is the integrative focus on disease
concentration and disease interaction in the context of large‐scale, long‐term, political‐economic
forces.
Figure 1 identifies systemic racism (Feagin, 2006) as a fundamental cause of racial
inequities in disease concentration. This perspective sees the social patterning of
hypertension, diabetes, and now COVID‐19 as culminating from a system of racial oppression
that has developed and morphed over four centuries—from settler‐colonialism and chattel
slavery to race‐based residential segregation and mass incarceration. Systemic racism
constitutes a fundamental cause (Phelan & Link, 2015) in the sense that it shapes
the risk of risk through multiple, interchangeable pathways (see also Laster Pirtle,
2020). Some of those pathways lead to increased risk of diabetes, some to hypertension,
some to COVID‐19—and some to combinations of the three.
For example, race‐based residential segregation, a result of deliberate social policy
(Rothstein, 2017), has far‐reaching consequences for health. It shapes the social
and spatial distribution of both risks and resources, including the quality of schools,
employment opportunities, density and quality of housing, availability of healthy
food, exposure to pollution, threat of police violence, and access to quality health
care (Williams & Collins, 2001). These aspects of the social environment, in turn,
have implications for cardiometabolic conditions through unequal nutritional status,
inflammation, and physiological dysregulation (eg, Lei et al., 2018; 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,
& Cao, 2020). The racialized structure of American labor entails differential exposure
to COVID‐19 (Hawkins, 2020) and to occupational stressors related to hypertension
(Cuevas, Williams, & Albert, 2017). Mass incarceration unjustly impacts Black people
and communities, with consequences for both COVID‐19 and cardiometabolic disease.
Incarcerated people face both greater exposure to SARS‐CoV‐2 (Akiyama, Spaulding,
& Rich, 2020) and elevated risk of hypertension and heart disease (Wang et al., 2009),
and nonincarcerated Black people living in neighborhoods with high rates of incarceration
have higher rates of cardiometabolic disease, independent of individual‐ and neighborhood‐level
factors like poverty and rates of crime (Topel et al., 2018).
All population health frameworks draw attention to the social production of health
inequities. The value added by a syndemic perspective is that it also highlights how
biosocial interactions move in both directions. Not only do social inequities shape
the risk of COVID‐19; 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 & Wilson, 2020), and the economic fallout from COVID‐19
has magnified racial inequities in income and housing (Greene & McCargo, 2020). Likewise,
the online transition of K‐12 and university teaching threatens to widen racial inequities
in educational opportunities, given that federal policies subsidize internet access
in disproportionately white, rural contexts but not in cities where residents are
disproportionately Black and other people of color (Siefer & Callahan, 2020). Further,
in regions where COVID‐19 is concentrated, the strain on healthcare systems may compound
pre‐existing inequities in access to care (Williams & Rucker, 2000). Already we see
evidence of racial inequities in COVID‐19 treatment (Eligon & Burch, 2020), and we
know that discrimination in healthcare settings adversely affects management of chronic
conditions like diabetes (Peek, Wagner, Tang, Baker, & Chin, 2011).
Note that each of these scenarios—unemployment, income, housing, education, health
care—involves synergies between biological and social processes at the population
level. They hint at how overlapping epidemics may not merely co‐occur but rather interact
to make matters worse. Much of the media commentary has focused on how comorbidities
like hypertension and diabetes increase the risk of COVID‐19 becoming deadly. Syndemic
theory alerts us, in addition, to the possibility that the pandemic could intensify
racial inequities in the social and economic conditions that increase risk for hypertension
and diabetes to begin with, exacerbating the toll those diseases already take on Black
people and communities. The possibility of such synergistic effects—over the short
and long term—underscores the relevance of syndemic thinking.
3
CHALLENGES AND FUTURE DIRECTIONS
The concept of syndemics has a broader reach than most anthropological ideas. It gained
institutional backing from the U.S. Centers for Disease Control (Milstein, 2002);
was recently the focus of a special collection in one of the world's highest‐impact
journals (The Lancet, 2017); generates several dozen scientific articles every year
(Mendenhall & Singer, 2020); is widely taught across disciplines (Singer, 2009); and
is the basis of multiple interventions with real‐world impact on public health (eg,
Chakrapani, Kaur, Tsai, Newman, & Kumar, 2020). It is clearly an idea that matters.
Yet recent commentaries highlight shortcomings in the burgeoning literature about
syndemics. A key conceptual issue, which has methodological implications, is the distinction
between syndemics and overlapping epidemics that merely co‐occur or are mutually causal
(Tsai et al., 2017). The defining feature of a syndemic is disease interaction in
addition to disease concentration. That is, true syndemics have synergistic effects
that can be traced to biological interactions between disease processes (bio‐bio)
or between biological processes and social conditions that harm health (biosocial).
Such interactions, which need to be tested explicitly, are thought to exacerbate the
toll of epidemics through multiplicative, not just additive, effects.
Most studies that purport to be about syndemics do not provide evidence of such interactions.
In a recent scoping review, Singer, Bulled, and Ostrach (2020) identified 188 articles
about syndemics that were published during 2015 to 2019 and found that only 12% (23
articles) met the full definition of a syndemic, including evidence of disease interaction.
Tsai and colleagues (Tsai, 2018; Tsai & Venkataramani, 2015) identified the analytical
problems, and Mendenhall and Singer (2020) outlined research strategies that researchers
are beginning to adopt to measure synergistic effects. For now, however, the central
proposition of syndemic theory remains largely untested. COVID‐19 presents an urgent
case for specifying testable hypotheses about interactions with chronic cardiometabolic
diseases that exacerbate pre‐existing inequities. The model in Figure 1 is meant as
a framework for developing such hypotheses as we learn more about COVID‐19.
A related conceptual challenge, which again has methodological implications, concerns
the level of analysis at which interactions take place. Like other frameworks for
population health, syndemic theory is inherently multilevel. It proposes that large‐scale,
political‐economic forces, which often play out over centuries, have embodied consequences
for individual health (cf. Gravlee, 2009). This proposition makes syndemic theory
a logical fit for multilevel analyses, which incorporate population‐level and contextual
effects, but existing syndemic studies have measured only individual‐level factors
(Tsai, 2018). This focus may result, in part, from the emphasis on biological interactions
between disease states. After all, to borrow an example from Singer et al. (2020),
the pathogen‐pathogen interaction that makes co‐infection with HIV and Hepatitis C
more lethal than infection with Hepatitis C alone occurs in individual bodies. These
interactions matter, but they are also captured by the concepts of co‐ or multimorbidity.
The utility of syndemic theory is that it directs attention to possible interactions
not only between diseases (at the individual level) but also between epidemics (at
the population level), taking social context and political‐economic inequities into
account.
The tentative syndemic model of COVID‐19 I offer here addresses these challenges by
outlining causal pathways from large‐scale social forces to individual biology and
positing synergistic interactions at the individual and population level. The intersection
of systemic racism, chronic health inequities, and COVID‐19—apparent to journalists
and other commentators—puts the onus on researchers to refine and test the syndemic
model and develop public health and policy responses that account for potential synergistic
effects.
AUTHOR CONTRIBUTIONS
Clarence Gravlee: Conceptualization; writing‐original draft; writing‐review and editing.