Professional Documents
Culture Documents
ABSTRACT The current debate over racial inequal- presents an opportunity to refine the critique of race in
ities in health is arguably the most important venue for three ways: 1) to reiterate why the race concept is incon-
advancing both scientific and public understanding of sistent with patterns of global human genetic diversity;
race, racism, and human biological variation. In the 2) to refocus attention on the complex, environmental
United States and elsewhere, there are well-defined influences on human biology at multiple levels of analy-
inequalities between racially defined groups for a range sis and across the lifecourse; and 3) to revise the claim
of biological outcomes—cardiovascular disease, diabetes, that race is a cultural construct and expand research on
stroke, certain cancers, low birth weight, preterm deliv- the sociocultural reality of race and racism. Drawing on
ery, and others. Among biomedical researchers, these recent developments in neighboring disciplines, I present
patterns are often taken as evidence of fundamental a model for explaining how racial inequality becomes
genetic differences between alleged races. However, a embodied—literally—in the biological well-being of
growing body of evidence establishes the primacy of racialized groups and individuals. This model requires a
social inequalities in the origin and persistence of racial shift in the way we articulate the critique of race as bad
health disparities. Here, I summarize this evidence and biology. Am J Phys Anthropol 139:47–57, 2009. V 2009 C
argue that the debate over racial inequalities in health Wiley-Liss, Inc.
A recent cover story in Scientific American posed a special issues to race; in each case, racial inequalities in
question that has gained new life: ‘‘Does race exist?’’ health were a major focus of debate (Nature Genetics,
(Bamshad and Olson, 2003). For decades, there seemed to 2004; American Journal of Public Health, 2005; Ameri-
be broad agreement among anthropologists and geneti- can Psychologist, 2005). Moreover, when research on
cists that the answer was ‘‘no,’’ but some observers sug- race and human variation makes the news, it often has
gest that the consensus is unraveling (e.g., Leroi, 2005). to do with race, medicine, and disease (e.g., Wade, 2002,
Indeed, in both the scientific literature and the popular 2004; Bakalar, 2007; Drexler, 2007). Thus, if anthropolo-
press, there is renewed debate over the magnitude and gists want to reconcile race for anyone other than our-
significance of genetic differences between racially defined selves, we have to engage the debate over racial inequal-
groups (Jorde and Wooding, 2004; Keita et al., 2004; ities in health.
Ossorio and Duster, 2005; Bakalar, 2007; Drexler, 2007). Third, the association between race and health
Yet much of the debate falters on the question—does exposes the inadequacy of the conventional critique of
race exist?—because it can be interpreted in different race in anthropology and other social sciences. Social sci-
ways. The implicit question is usually whether race entists often dismiss race as a cultural construct, not a
exists as a natural biological division of humankind. biological reality (e.g., Palmié, 2007; Shaw, 2007). How-
This question is important but incomplete. We should ever, this position requires more nuance. If race is not
also ask in what ways race exists as a sociocultural phe- biology, some may ask, why are there such clear differ-
nomenon that has force in people’s lives—one with bio- ences among racially defined groups in a range of biolog-
logical consequences. ical phenomena? This question highlights the need
In this article, I take up these questions in the context to move beyond ‘‘race-as-bad-biology’’ (Goodman, 1997,
of the current interdisciplinary debate over racial inequal- p 22) to explain how race becomes biology.
ities in health (Dressler et al., 2005a). This debate is im- There are two senses in which race becomes biology.
portant for three reasons. First, the magnitude of racial First, the sociocultural reality of race and racism has bi-
inequalities in health demands attention. In the United ological consequences for racially defined groups. Thus,
States, where debate over race is most intense, the risk of ironically, biology may provide some of the strongest
morbidity and mortality from every leading cause is pat- evidence for the persistence of race and racism as socio-
terned along racial lines (Keppel et al., 2002). The burden
of poor health is especially high for African Americans:
*Correspondence to: Clarence C. Gravlee, Department of Anthro-
Between 1945 and 1999, more than 4.3 million African pology, University of Florida, 1112 Turlington Hall, PO Box 117305,
Americans died prematurely, compared to their white Gainesville, FL 32611-7305, USA. E-mail: cgravlee@ufl.edu
counterparts (Levine et al., 2001). This inequality needs
to be explained and addressed. Received 16 May 2008; accepted 27 October 2008
Second, debate over race and health provides an im-
portant opportunity to advance scientific and public DOI 10.1002/ajpa.20983
understanding of race, racism, and human variation. In Published online 18 February 2009 in Wiley InterScience
recent years, several high-profile journals have devoted (www.interscience.wiley.com).
C 2009
V WILEY-LISS, INC.
48 C.C. GRAVLEE
the claim that race is inadequate to describe global (Risch, 2006, p 408). This misleading portrayal of the cri-
human genetic diversity. Second, it is critical to refocus tique sets the bar too low for proponents of racial classi-
attention on the complex, environmental influences on fication; to resuscitate race, all they must do is show
human biology. Third, it is necessary to revise the con- that they can reliably detect some genetic differentiation
ventional view of race as a cultural construct to stimu- between racially defined groups, but the critique of race
late new research on the sociocultural dimensions of does not imply that racial categories correspond to no
race and racism. I discuss each point in turn. genetic differentiation. On the contrary, the argument
that conventional racial classification accounts for only
5–10% of human genetic variation (Lewontin, 1972;
Brown and Armelagos, 2001) implies a level of genetic
Race = Human genetic variation differentiation that clustering algorithms ought to
The classic critique of race has focused on three detect. Evidence of genetic clustering, then, does not con-
claims. First, most human genetic variation is clinal, tradict the claim that most human genetic variation
such that there are seldom clear genetic boundaries occurs within rather than between traditional racial cat-
between populations (Livingstone, 1962; Serre and egories.
Pääbo, 2004; Barbujani and Belle, 2006). Second, most Third, recent studies confirm the claim that most
human genetic variation is nonconcordant, such that the human genetic variation is clinal. Several researchers
traits we use to distinguish races may have no value for have shown that genetic distance is strongly associated
predicting other aspects of biology (Goodman, 2000; with geographic distance between populations (Serre
Jorde and Wooding, 2004). Third, human genetic varia- and Pääbo, 2004; Manica et al., 2005; Handley et al.,
tion is widely shared across our species, with relatively 2007; Li et al., 2008). The association is even stronger if
little variation occurring between racially defined groups one takes in account probable migration routes between
(Lewontin, 1972; Long and Kittles, 2003). Our basic continents over human history. For example, Ramachan-
understanding of these patterns has not changed in 50 dran et al. (2005) show that geographic distances based
years, despite enormous improvements in our technical on likely migration paths explain 78% of the variation in
ability to describe human genetic variation (Weiss and genetic distances between populations. Other studies
Fullerton, 2005). show that geographic distance from East Africa explains
Yet some researchers still defend race as a useful 82–85% of the genetic diversity within populations
framework for describing human genetic variation—and (Prugnolle et al., 2005; Li et al., 2008). This pattern is
for identifying genetic influences on racial differences in consistent with a single origin of anatomically modern
disease (Risch et al., 2002; Gonzalez Burchard et al., humans in East Africa, followed by serial migrations to
2003; Bamshad et al., 2004). The defense of race relies other parts of the globe. Recent studies suggest that
on two related lines of evidence: 1) studies of worldwide both clines and clusters are part of the structure of
genetic variation show that individuals from the same human genetic variation, but clusters explain relatively
continent reliably cluster together (Rosenberg et al., little total variation (Handley et al., 2007).
2002; Bamshad et al., 2003; Shriver et al., 2004; Fourth, the claim that continental ancestry may help
Rosenberg et al., 2005), and 2) in the United States, to explain racial differences in disease (Salari et al.,
‘‘self-identified race/ethnicity’’ is a useful proxy for 2005; Risch, 2006; Tang et al., 2006) poses conceptual
genetic differentiation between groups that vary in conti- and methodological problems: First, estimates of genetic
nental ancestry (Tang et al., 2005). ancestry are generally based on noncoding DNA with
These findings have important implications for unknown functional effects on disease (Cooper et al.,
genetic epidemiology (Barnholtz-Sloan et al., 2008) and 2003). Second, many alleles associated with common,
population history (Tishkoff and Verrelli, 2003), but complex diseases are likely to be ancient and shared
they do not refute the key arguments against the race across continental clusters (Keita et al., 2004). Third,
concept. First, the claim that recent genetic studies nonconcordance implies that genetic clusters based on
‘‘have recapitulated the classical definition of races’’ neutral markers may differ from clusters based on sus-
(Risch et al., 2002, p 3) misrepresents the purpose of ceptibility alleles (Jorde and Wooding, 2004). Fourth, in
cluster analysis, which is to detect pattern in a given racially stratified societies like the United States, conti-
dataset, not determine the essential number of subdivi- nental ancestry is likely to be confounded with many
sions in our species. An example of this error is the environmental factors; consequently, reported associa-
common interpretation of Rosenberg et al. (2002) as evi- tions between genetic ancestry and disease may be medi-
dence that humans are divided into five genetic clusters ated through unmeasured environmental mechanisms
(e.g., Bamshad et al., 2004; Mountain and Risch, 2004; (Kaufman and Cooper, 2008). These considerations imply
Leroi, 2005; Tang et al., 2005). Evidence that humans that researchers should test specific hypotheses about the
can be divided into five clusters does not mean they are mechanisms linking ancestry and disease and remain cog-
naturally divided, as the classical definition of race nizant that complex disease involves the interaction of
would suggest. In fact, the number of clusters necessary many genetic and environmental influences.
to describe global genetic variation has been inconsis- To be clear, the critique of race is neither a denial of
tent; some studies report five (Rosenberg et al., 2002) human biodiversity, nor a claim that genes are irrelevant
and others seven (Corander et al., 2004; Li et al., 2008). to racial inequalities in health. Rather, the central argu-
Even when the number of clusters is consistent, their ment is that the race concept is inadequate for describ-
boundaries and composition are not [compare Corander ing the complex structure of human genetic variation.
et al., (2004) and Li et al., (2008)], and finer substruc- Clearly, there is geographic structure to human genetic
tures are obscured. variation. This structure is most consistent with a model
Second, current defenders of race position themselves of serial founder effects beginning with a single African
against a straw-man view that ‘‘racial and ethnic catego- origin of our species. Relatively low levels of genetic dif-
ries are purely social and devoid of genetic content’’ ferentiation across major barriers to gene flow (e.g.,
Biology = Genetics
The argument that race does not correspond to global
patterns of human genetic variation has come to domi-
nate the critique of race. Yet, as important as the genetic
evidence is, it understates the case against race. Indeed,
the emphasis on genetic evidence may undermine the
critique, because it tacitly accepts the primacy of genes
in describing and explaining human biological variation.
Thus, it is important to expand the critique of race by
rejecting naı̈ve reductionism and replacing it with a
more complex view of human biology that acknowledges
the interplay of organisms and environments over the
life course. Fig. 3. Conceptual model for the study of multilevel and de-
This goal may require a shift in the way we articulate velopmental influences on phenotype.
the critique of race. Often the critique is condensed to
the idea that ‘‘race is not biology.’’ Sometimes, this idea tial model is Krieger’s ecosocial theory for social epide-
appears in the context of more subtle arguments about miology (Krieger, 1994, 2001). To comprehend humans’
the complexity of human biology (e.g., Goodman, 2000), dual status as biological organisms and social beings,
but more often it stands alone as a ritual repudiation of Krieger proposes the construct of embodiment:
the race myth. Despite its popularity in scholarly circles,
this ritual has failed to sway public understanding of
race. As one observer put it, ‘‘Clearly for mainstream a concept referring to how we literally incorporate, biologically,
popular culture, the idea that race is not biology is still the material and social world in which we live, from conception to
‘surprising’ news’’ (Caminero-Santangelo, 2004, p 207). death; a corollary is that no aspect of our biology can be
The debate over racial inequalities in health brings understood absent knowledge of history and individual and
this problem into sharp relief. Epidemiologic evidence societal ways of living (Krieger, 2005, p 352).
shows that, in a very certain sense, race is biology. There
are, in fact, well-defined differences between racially
defined groups for a range of biological outcomes—cardi- There is an obvious affinity between embodiment and
ovascular disease, diabetes, renal failure, cancer, stroke, a century of anthropological research on human biology
and birth outcomes, to name a few. In the face of this in the context of culture. Indeed, Franz Boas might be
evidence, the refrain that race is not biology is impotent seen as a pioneer in the study of embodiment. His dem-
at best, counterproductive at worst. The challenge is to onstration that descendants of immigrants embodied the
move beyond the pat assertion that race is not biology to new American environment (Boas, 1912) established
explain how race becomes biology. plasticity as a central construct in human biology and
This shift in emphasis suggests that we may need to turned the tide against biological determinism in anthro-
devote as much attention to revising our conception of pology (Gravlee et al., 2003). Yet the construct of embodi-
biology as we do to our conception of race. Some observ- ment does work that plasticity alone does not. In particu-
ers may be uneasy with talk of biological differences lar, Krieger’s model reflects an emerging consensus that
among racially defined groups. They may worry—with the next wave of research needs to integrate 1) multiple
good cause—that such talk reinforces the perception of levels of analysis with 2) developmental and life-course
intrinsic, genetic differences between alleged races. This perspectives. The conceptual model in Figure 3 illus-
well-founded concern is important, because it reveals trates the approach, drawing on previous recommenda-
how deeply entrenched the twin assumptions of reduc- tions for research on the social patterning of health (e.g.,
tionism and genetic determinism are in our understand- Kaplan, 2004; Glass and McAtee, 2006; Diez Roux, 2007;
ing of race (Caspari, 2003) and biology in general Krieger, 2008).
(Lewontin, 2000). The idea that it is politically danger- A key feature of this model is that it situates pheno-
ous to discuss biological differences among racially type at the intersection of two axes. The first (horizontal)
defined groups makes sense only if we (or our audience) axis represents time. This axis may reflect life-course,
implicitly reduce biology to genetics and minimize or developmental processes at an individual level or histori-
ignore the causal influence of external, environmental cal change at a population level (Glass and McAtee,
factors on human biology. The tacit conflation of genes 2006). The second (vertical) axis represents the nested
and biology in the conventional critique of race unwit- hierarchy of causal influences on phenotypes, ranging
tingly perpetuates this form of reductionism. from the genome to global political economy and ecology.
Recent research on racial inequalities in health pro- The line depicting embodiment represents the direct and
vides a counterweight to reductionism and lends support indirect influences of sociocultural context at multiple
for renewed attention to phenotypic plasticity and a com- scales and levels (Krieger, 2008) on gene expression and
plex view of human biology as biocultural. One influen- biological functioning. Although the model draws on cur-
by other Puerto Ricans in everyday social interaction. In cle is based. Connie Mulligan offered helpful comments
a small epidemiologic survey, we compared blood pres- on my review of literature in population genetics.
sure to color, as defined by the local cultural model, and
to skin pigmentation, as measured by reflectometry. The
key finding was that both self-rated and culturally LITERATURE CITED
ascribed color—but not skin pigmentation—were associ- Acevedo-Garcia D. 2000. Residential segregation and the epide-
ated with blood pressure through an interaction with miology of infectious diseases. Soc Sci Med 51:1143–1161.
income and education (Gravlee and Dressler, 2005; Grav- Adair L, Dahly D. 2005. Developmental determinants of blood
lee et al., 2005). This finding suggests that empirical pressure in adults. Annu Rev Nutr 25:407–434.
research on how race is culturally constructed better American Journal of Public Health. 2005. Special issue on ‘‘race,
positions us to identify the biological consequences of genetics, and health disparities.’’ Am J Public Health 95.
cultural constructs like race in the United States or color American Psychologist. 2005. Special issue on ‘‘genes, race, and
in Puerto Rico. psychology in the genome era.’’ Am Psychol 60.
Anderson MR, Moscou S. 1998. Race and ethnicity in research
on infant mortality. Fam Med 30:224–227.
Bach PB, Schrag D, Brawley OW, Galaznik A, Yakren S, Begg
CONCLUSION CB. 2002. Survival of black and whites after a cancer diagno-
sis. JAMA 287:2106–2113.
Race has played a pivotal yet tortured role in the his- Bakalar N. 2007. Study points to genetics in disparities in pre-
tory of anthropology. In the nineteenth and early twenti- term births. New York Times, February 27, 2007, p F5.
eth century, anthropologists were central in legitimating Baker PT. 1997. The Raymond Pearl memorial lecture, 1996:
race as a framework for understanding human biological the eternal triangle—genes, phenotypes, and environment.
variation. By the mid-twentieth century, most anthropol- Am J Hum Biol 9:93–101.
ogists rejected race as biology, and the view of race as a Bamshad MJ, Olson SE. 2003. Does race exist? Sci Am 289:78–85.
Bamshad MJ, Wooding S, Salisbury BA, Stephens JC. 2004.
cultural construct came to dominate the social sciences.
Deconstructing the relationship between genetics and race.
However, the anthropological critique of race has had Nat Rev Genet 5:598–609.
only partial success. In particular, current debate over Bamshad MJ, Wooding S, Watkins WS, Ostler CT, Batzer MA,
racial inequalities in health exposes important weak- Jorde LB. 2003. Human population genetic structure and in-
nesses in the usual framing of the critique and points ference of group membership. Am J Hum Genet 72:578–589.
the way toward a more constructive approach to the Banton M. 1998. Racial theories, 2nd ed. Cambridge: Cambridge
links between race, biology, and culture. University Press.
The specific challenge is to explain how race becomes Barbujani G, Belle EMS. 2006. Genomic boundaries between
biology. Our response to this challenge must deal with human populations. Hum Hered 61:15–21.
two senses in which race becomes biology: Systemic rac- Barker DJP. 2004. The developmental origins of adult disease.
J Am Coll Nutr 23:588S–595S.
ism becomes embodied in the biology of racialized groups
Barnholtz-Sloan JS, McEvoy B, Shriver MD, Rebbeck TR. 2008.
and individuals, and embodied inequalities reinforce a Ancestry estimation and correction for population stratifica-
racialized understanding of human biology. To break this tion in molecular epidemiologic association studies. Cancer
cycle, I propose that the conventional critique of race Epidemiol Biomarkers Prev 17:471.
needs to be refined in three ways: 1) to clarify why Bell JF, Zimmerman FJ, Almgren GR, Mayer JD, Huebner CE.
recent genetic findings do not warrant a return to racial 2006. Birth outcomes among urban African-American women:
thinking, 2) to promote a more complex, biocultural view a multilevel analysis of the role of racial residential segrega-
of human biology, and 3) to revise the conceptualization tion. Soc Sci Med 63:3030–3045.
of race so that it becomes more than a mantra. Bhopal RS. 2007. Racism in health and health care in Europe:
These three claims inform a conceptual model for reality or mirage? Eur J Public Health 17:238–241.
Biffl WL, Myers A, Franciose RJ, Gonzalez RJ, Darnell D. 2001.
research on the multilevel and developmental influences
Is breast cancer in young Latinas a different disease? Am J
on racial inequalities in health. This model crosses old Surg 182:596–600.
fault lines and lays the groundwork for more productive Boas F. 1912. Changes in bodily form of descendants of immi-
collaboration between the social and biological sciences. grants. New York: Columbia University Press.
The model does not promote a focus on social and cul- Borrell LN, Jacobs DR Jr, Williams DR, Pletcher MJ, Houston
tural factors to the exclusion of genetic ones; rather, it TK, Kiefe CI. 2007. Self-reported racial discrimination and
implies that the embodiment of social inequality passes substance use in the Coronary Artery Risk Development in
through biological systems regulated by genes. It does Adults Study. Am J Epidemiol 166:1068–1079.
not deny human biological variation; rather, it claims Borrell LN, Kiefe CI, Williams DR, Diez-Roux AV, Gordon-
that the pattern and causes of human biological varia- Larsen P. 2006. Self-reported health, perceived racial discrim-
ination, and skin color in African Americans in the CARDIA
tion are more complex than the race concept allows. It study. Soc Sci Med 63:1415–1427.
does not claim that race is a myth; rather, it treats race Brace CL. 2005. ‘‘Race’’ is a four-letter word: the genesis of the
as deeply embedded in sociocultural systems. Research concept. New York: Oxford University Press.
on the biological consequences of race and racism can Braun L. 2006. Reifying human difference: the debate on genet-
help to reinvigorate the critique of race by offering a con- ics, race, and health. Int J Health Serv 36:557–573.
structive framework for explaining biological differences Braveman P, Tarimo E. 2002. Social inequalities in health
between racially defined groups. within countries: not only an issue for affluent nations. Soc
Sci Med 54:1621–1635.
Brockerhoff M, Hewett P. 2000. Inequality of child mortality
among ethnic groups in sub-Saharan Africa. Bull World
ACKNOWLEDGMENTS Health Organ 78:30–41.
Brondolo E, Libby DJ, Denton E-G, Thompson S, Beatty DL,
My thanks go to Heather Edgar and Keith Hunley for Schwartz J, Sweeney M, Tobin JN, Cassells A, Pickering TG,
organizing and inviting me to participate in the sympo- Gerin W. 2008. Racism and ambulatory blood pressure in a
sium at the University of New Mexico on which this arti- community sample. Psychosom Med 70:49–56.