Nancy Krieger is associate professor of society, human development, and health at Harvard University. She has published numerous articles on social inequalities in health and has recently edited Embodying Inequality: Epidemiologic Perspectives.
If “race” is the answer, then what is the question? In this era of the human genome and visions of 21st century science, one sure candidate is: “why are there racial/ethnic disparities in health?”
Or, more specifically, why is it that currently the average life expectancy of black Americans is 5.5 years less than that of white Americans (77.9 vs 72.4 years), their risk of being born low birthweight is 1.9 times higher, and their mortality for all causes, heart disease, and cancer is 1.3 times higher and for diabetes 2 times higher, plus nearly 6 times higher for homicide, and 8.6 times higher for deaths due to HIV/AIDS? (Table 1). Or why are American Indians and Alaska Natives and Hispanics at least 1.5 to 1.9 times more likely to die of diabetes compared to white Americans, and at twice the risk for homicide?
Related, why have racial/ethnic disparities in health been so persistent, even as health in the US has overall improved during the 20th century for all racial/ethnic groups? In 1950, for example, life expectancy at birth among the US white population was 69.1 years compared to 60.8 years among the black population, a gap of 8.3 years; in 1900, the respective figures were 47.6 years versus 33.0 years, a gap of 14.6 years.1 (p. 143)
For the better part of US history, the conventional answer to why racial/ethnic health disparities exist has been: because the “races” are innately different—and whites are inherently superior.2-7 From this perspective, any biological differences observed between the “races”—whether in appearance or health status—necessarily reflected inborn and unalterable differences; by implication, health disparities and social inequality were a fact of nature. Thus, during the 1830s and 1840s, in a time of fast rising debates about both slavery and the removal of American Indians, leading US physicians and scientists endorsed the widespread idea that the different “races” of humanity constituted different species and argued that “racial” differences in disease rates and mortality were proof of underlying difference.2-7
Not that everyone agreed. Leading US abolitionists and physicians, black and white alike, including both Dr. James McCune Smith (1811-1865) and Dr. James S. Rock (1825-1866), two of the country’s first credentialed African American physicians, challenged convention by arguing that the poorer health of the black compared to white population resulted not from innate inferiority, but rather from a phenomenon rarely if ever discussed in sanctified science: that of white privilege, enforced via slavery in the South and legal racial discrimination in the North.6-9 The Choctaw and Cherokee Nations, forcibly evicted from their homelands after the US Congress passed the Indian Removal Act in 1830, likewise understood their health was being decimated by not only territorial but also cultural dispossession.7,10,11 Concerns about health consequences of racism clearly are not new; to suggest otherwise is to misstate the historical record.
Translated to contemporary terms, the arguments about causes of racial/ethnic health disparities have remained essentially the same, albeit updated by advances in the biological, population health, and social sciences. On the one side is the causal emphasis on genetic differences between the “races,” which are posited to be biologically distinct groups distinguished by measurable differences in gene frequency and hence genetically predisposed to differential disease risk.12-15 On the other is the causal emphasis on social inequality, whereby disparities in health status reflect the impact of past and present racial discrimination and contingent racial/ethnic disparities in socioeconomic resources, premised on the view that “races” are a social construct with real biological consequences.5-7,16-19
One recent salvo in these debates is a New York Times op-ed piece entitled “A Family Tree in Every Gene,” written by Armand Marie Leroi, an evolutionary biologist. This article argued that: “it is genetic variants common to one group or another that defines race, that race is a vital shorthand that enables people to speak sensibly about genetic rather than cultural or political differences” and that “discussion of race offers benefits: it would remove disjunction in which government and public embrace categories that most scholars and scientists say do not exist; it would improve medical care and treatment, as different races are prone to different illnesses; it could lead to further study of why certain races have specific characteristics; finally, it gives reason to protect most obscure and marginalized people.” 20,21
These are strong—and contested—claims. And, as in prior epochs, what matters is not only what is asserted but what is omitted. In particular, one especially striking feature of the Leroi op-ed is its singular lack of attention to not only the sordid 20th century history of scientific racism and eugenics, including the Holocaust,22,23 but also to the fast-growing body of research demonstrating how social and economic deprivation harms health.7,16,17,24-29 Similarly, in the recent special supplement of Nature Genetics on “Genetics for the Human Race,” not one of the articles, when discussing possible “non-genetic” factors (a rather all-embracing construct) that might contribute to racial/ethnic health disparities, cited any of the contemporary research on how racial discrimination harms health (e.g.,7,16,17,31,32).
Racism, biology, and health: clarifying the connections—an ecosocial perspective
What is the evidence that causes of racial/ethnic disparities in health cannot meaningfully be reduced to a question of gene frequency? Two frequently used lines of argument concern: (a) the overwhelmingly greater genetic variability within compared to between so-called “racial groups,” 18,19,33-35 and (b) major changes in disease rates in a short period of time, e.g., the recent rapid rise of obesity, hypertension, and diabetes among populations of West African descent living in the UK, the Caribbean, and the US, as well as in West Africa, which can be explained only by changes in gene expression, not gene frequency.36-39
But to keep the argument at the level of gene frequency obscures much of what is at issue. Here, helpful insights may be obtained from the discipline of social epidemiology, a domain of inquiry “distinguished by its insistence on explicitly investigating social determinants of population distributions of health, disease, and well-being, rather than treating such determinants as mere background to biomedical phenomena.” 40 (p. 263) A starting point is the theoretical framework of ecosocial theory, a multilevel epidemiologic theory of disease distribution concerned with links between society and biology and focused on understanding how current and changing patterns of social inequalities in health and disease are fundamentally shaped by societal conditions.24,40-43 At issue are how people, as both biological organisms and social beings, literally embody—via processes which necessarily involve gene expression—the dynamic social, material, and ecological contexts into which we are born, develop, interact, and endeavor to live meaningful lives, thereby raising key questions about agency and accountability for health inequities.24,40-43 The contrast is to pervasive etiologic hypotheses concerned mainly with decontextualized and disembodied “behaviors” and “exposures” interacting with equally decontextualized and disembodied “genes.”
From an ecosocial perspective, an important first step is to define what is meant by racism and to conceptualize how it can harm health.7,31 Briefly stated, racism refers to institutional and individual practices that create and reinforce oppressive systems of race relations and their contingent racial definitions, whereby dominant groups define themselves and others through the possession of arbitrary physical characteristics, such as skin color, and adversely restrict, by judgment and action, the lives of those against whom they discriminate, and benefit from so doing.31,44-46 Health consequences can thus be conceptualized as biologic expressions of race relations,31-47 referring to how harmful physical, biological, and social exposures, plus people’s responses to these exposures, are ultimately embodied and manifested in racial/ethnic disparities in somatic and mental health, with these exposures including: economic and social deprivation, toxic substances and hazardous conditions, social trauma, targeted marketing of harmful commodities, and inadequate and degrading medical care. Conversely, the arbitrary biological traits conventionally used to delineate “races” may be conceptualized as racialized expressions of biology.31,47 In both cases, biology and society matter, but in profoundly different ways: the first concerns the impact of society on biology, the second, its impact on the interpretation of biological phenomena.
By clearly distinguishing between and emphasizing the importance of taking into account both racism and biology, these two constructs make clear that we can never study human biology in the abstract. Exemplifying that we instead study people in context is Sapolsky’s cautionary tale: in the early 20th century, researchers’ chief source of human adrenal glands (an endocrine organ that secretes cortisol in response to stress) was from cadavers of the poor. Forgetting, however, the impact of poverty on biology, these researchers took as “normal” the size of the actually abnormally large adrenal glands among the poor (long since hypertrophied due to excess secretion of cortisol, reflecting the greater stress of impoverished persons), such that the wealthy were misdiagnosed and wrongly treated for adrenal deficiency disorders. Simplistic divisions of the social and biologic will not suffice. The interpretations we offer of observed average differences in health status across socially-delimited groups reflects our theoretical frameworks, not ineluctable facts of nature.
Consider, then, two additional lines of evidence routinely ignored by the “gene frequency” approach to explaining racial/ethnic health disparities. The first concerns socioeconomic gradients in health within racial/ethnic groups, the second the impact of racial discrimination on health.
The evidence that health varies by socioeconomic position within all US racial/ethnic groups—and strongly contributes to racial/ethnic disparities in health—is substantial and longstanding.5-7,16,17,24-29,50-52 To give but one example, consider the findings of our recently completed Public Health Disparities Geocoding Project, designed to overcome the absence of socioeconomic data in most US public health surveillance systems by augmenting them with data on the socioeconomic conditions of the neighborhoods (census tracts) in which people live.53-58 In this study, we found evidence of important socioeconomic gradients in all US racial/ethnic groups for outcomes ranging from low birthweight and childhood lead poisoning to sexually transmitted infections to cancer incidence to all-cause, premature, and cause-specific mortality, as illustrated in Table 2.
Exemplifying the patterns we discerned is the case of premature mortality (death before age 65). Using data from Massachusetts in 1989-1991, we found that marked socioeconomic disparities in premature mortality within each racial/ethnic-gender group, such that persons living in the most impoverished census tracts (in which 20% or more of the population lived below the US poverty line, thereby constituting a federal poverty area) compared to the least impoverished census tracts (in which less than 5% of the population lived below the poverty line) were anywhere from 1.8 to 4.3 times more likely to die prematurely (Table 2). We likewise reported, for the first time for any US state, the proportion of deaths that would have been prevented if persons living in the most impoverished census tracts had the same risk of dying early as those living in the least impoverished census tracts. For the total population, this proportion equaled nearly one-quarter of all premature deaths; among women, this fraction ranged from 13% (white women) to 100% (American Indian women), and among men, from 23% (white men) to 69% (black men). Thus, a large portion of premature deaths could be averted, in every racial/ethnic group, if everyone had the same low risk of dying early as their counterparts living in the least impoverished census tracts.
Our data also revealed that whereas almost half the white women and men lived in census tracts with <5% of persons below poverty, fully half the black and Hispanic population lived in census tracts with 20% or more below poverty. Adjusting for solely the single relatively crude measure of census tract poverty reduced the overall age-adjusted 2-fold black excess risk of premature mortality by 50%, down to a 40 to 50% excess, a remarkable reduction for just one “risk factor”—and not an effect that can be chalked up to “gene frequencies.” Had more detailed socioeconomic data been available, e.g., on socioeconomic position from conception to death, it is highly plausible that we could have explained even more of the excess.24-29,50-52
Yet, even had we obtained the most complete socioeconomic data possible, it could still be hypothesized that we would see residual racial/ethnic disparities, precisely because of additional non-economic dimensions of racial discrimination that play out within and across socioeconomic strata. Only recently has epidemiologic research begun to address this issue.7,16,17,24,31,32
Turning then to the alternative hypothesis that racial discrimination can harm health directly, in another study we explicitly tested the hypothesis that self-reported experiences of racial discrimination contribute to black/white disparities in risk of low birth weight (<2500 g), chiefly through the pathway of preterm delivery (<37 weeks gestation). To date, the two-fold greater risk of low birthweight among black infants has not been explained by the major conventional risk factors—and it has only been since the early 1990s that researchers have begun to consider, explicitly, whether racial discrimination—rather than “race”—accounts for this difference, likely via the mechanism of the chronic strain of everyday racism affecting neuroendocrine function relevant to hormonal cues for the onset of delivery.60,61 Importantly, both preterm delivery and low birthweight greatly increase risk of infant mortality and adult cardiovascular disease.24,25,59-61 Among the handful of studies starting to test aspects of this hypothesis,62-65 ours was the first to quantify the extent to which observed black/white birth disparities could be explained by self-reported experiences of racial discrimination.
Using data from the CARDIA cohort, a national 4-city US longitudinal study of cardiovascular risk factors among young adults, along with a recently validated instrument regarding self-reports of racial discrimination,67-69 we were able to show that, first, overall black women were 2.5 times more likely than white women to have a preterm delivery (Table 3). If we then controlled for the self-reported experiences of racial discrimination alone, and also the other factors known to increase risk of preterm delivery (income, education, smoking, alcohol, depression) alone, each helped explain the higher risk of preterm delivery among the black women. Adding both sets of factors completely accounted for the black/white difference, and in this model, women who reported racial discrimination in 3 or more situations were at 3.1 times the risk of preterm delivery compared to women who reported no racial discrimination. Previously, myriad studies adjusting for conventional risk factors have failed to account for black/white disparities in risk of preterm delivery. By considering the impact of racial discrimination on health, we could, for the first time, account for the black excess risk for preterm delivery.
In summary, as these two examples suggest, explanations of racial/ethnic disparities in health that ignore the impact of socioeconomic deprivation and racial discrimination are woefully incomplete and scientifically inadequate. All the more stunning, then, that the primary reason, according to Leroi, to reinstate “race” as a biological category is that “it would remove disjunction in which government and public embrace categories that most scholars and scientists say do not exist.” By this astounding illogic, the more popular doctrine of creationism should trump scientific theories of evolution,70,71 including when it comes to explaining the biological diversity Leroi holds so dear. At a time when US science museums are refraining from showing movies alluding to evolutionary theory for fear of offending religious beliefs,72,73 it is scientifically irresponsible to pander to anti-scientific beliefs about “race” or to suggest the equation “race” = “genes” will by itself lead to health improvements. A scientifically responsible position on addressing racial/ethnic disparities in health would instead entail frank recognition of the social reality of popular and scientific racism and the harms they wreak on human health.
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|Selected health outcomes, US population by race/ethnicity, 2002.1(pp.120,143,147,148)|
|Population counts (cases and denominators), rate ratio (RR) and 95% confidence interval (CI), test for trend, and population attributable fraction (PAF), by census tract (CT) poverty level, for the total population and by race/ethnicity and gender: Massachusetts (MA) and Rhode Island (RI), circa 1990.53|
|Risk of preterm delivery comparing births among black (n = 152) to 200 white (n = 200) women in the CARDIA study, 1992-1995.59|