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SECTION III
THE SEARCH FOR CAUSAL PATHWAYS



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Critical Perspectives on Racial and Ethnic Differences in Health in Late Life SECTION III THE SEARCH FOR CAUSAL PATHWAYS

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Critical Perspectives on Racial and Ethnic Differences in Health in Late Life 8 Genetic Factors in Ethnic Disparities in Health Richard S. Cooper I very early got the idea that what I was going to do was prove to the world the Negroes were just like other people.—W.E.B. DuBois Biology is being transformed by the advent of technology that allows us to define the molecular basis of genetic variation. Having pushed physics off the pedestal reserved for “big science,” biologists have sequenced the genomes of half a dozen organisms, altered the sequence in even more, and cataloged millions of the DNA variants found in humans. The technological capacity to read and manipulate genes has in turn generated speculation that our ability to solve health problems will be transformed in a similarly dramatic fashion. Acknowledging that we are in the early stages of this new era, the practical accomplishments of genetic medicine to date are much more modest, however. Although great success has been achieved with the rare monogenic disorders, for the common chronic illnesses that account for most of the death and disability in our society, genomics has yet to elucidate the pathophysiology in important ways or improve treatment (Cooper and Psaty, 2003; Khoury, 2000; Lander, 1996; Report of the Advisory Committee on Health Research, 2002). Describing the genetic underpinnings of common chronic diseases is a challenge of infinitely greater complexity than obtaining a sequence of nucleotides or finding single gene mutations. A quantum leap in biology will be required before the genes and the associated physiologic abnormalities that confer susceptibility to chronic disease can be understood. Given the intertwined effects of genes and environment on these conditions, the question remains as to whether or not important genetic causes can even be identified. Nonetheless, the exploration of the genome has accumulated unstoppable momentum and will profoundly alter our understanding of the

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Critical Perspectives on Racial and Ethnic Differences in Health in Late Life biological world, even if it does not transform the practice of medicine or public health. Genomics is connected to public health science through population genetics and epidemiology, and to the everyday practice of public health through race. An important goal of this discussion will be to try to disentangle genomics from race, based on the argument that they are categorically different ways of framing the epidemiologic questions. This is more than an intellectual challenge, however, because deeply held beliefs about the relative influence of nature and nurture on variation in disease patterns between populations bind the two together. After centuries of reliance on race as a surrogate for genes, the impulse has been to merely incorporate molecular data as new details, leaving the accepted framework in place. However, this solution can only be temporary. Among its many consequences, molecular genetics has made the current model of race obsolete and, in the long run, untenable. As a result, through no initiative of its own, public health suddenly has been presented with the opportunity to rethink one of its most intractable problems. Perhaps, one might argue, that will be the most important contribution of genetics to public health: Given our complete inability to devise effective solutions to racial inequalities in health, discarding what now passes for theory could be a salutary development. The two main dimensions of the race controversy can be discussed separately. First, the “ideological” concept of race informs popular discourse and shapes policy, with a parallel impact in public health. This version of race is defined by social and historical forces and is used to create and justify many of the divisions that exist among people of varying religious, ethnic, or geographic backgrounds. This concept assumes the existence of categories that have no scientific foundation—at least none based on molecular data. This concept has been challenged since Darwin (1981), yet it persists for ideological purposes (Cooper, 1984; Montagu, 1964; Root, 2001). Although everyone in public health needs to be reminded of the importance and illegitimacy of this notion, and those who have not yet heard the news need to be informed, there is little of substantive importance that is really new to add to this debate: We should begin by simply acknowledging that race in the world of politics, and all the nutritional, educational, and social influences it entrains, continues to be the determining influence on ethnic variation in health. A second use of race has assumed new relevance. As a label for regional populations, race has a long history in population genetics, and in this arena, important opportunities exist to revisit old questions on interethnic variation in health. At stake is whether or not we can move beyond the indirect methods applied in epidemiology or the generalizations built on estimation of genetic distance that have preoccupied population geneticists and anthropologists (Cavalli-Sforza, Menozzi, and Piazza, 1996; Relethford,

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Critical Perspectives on Racial and Ethnic Differences in Health in Late Life 1998). Specifically, it is now possible to ask a set of testable questions: Can the global variation in the human genome be aggregated into subunits, and do those units correspond to the categories we call race? Can we assess the relative magnitude of shared and nonshared genetic material among population groups? Is there variation in causal genetic polymorphisms that is associated with important differences in chronic disease risk? Is it possible to conceptualize the collective human genome as a whole, and express that concept in quantitative terms? Of course, complete answers to these questions are still well beyond our grasp. Some of the questions, like the aggregation of variants within population groups, are likely to be answered in the near future, while others, like the relative frequencies of causal variants for chronic diseases, may never be fully answered. Yet molecular genetics is changing the way we think about human variation, and it is crucial that this change has a positive impact on medicine and public health. Even though the noxious effects of racism—the social and economic consequences of the ideology—will only be eliminated through a political process, it remains the obligation of biological scientists to contribute to this eventual outcome by providing a clear description of the natural phenomena as we understand them. With an eye to history, it will be necessary, first and foremost, to ensure that the mistakes surrounding racial comparisons in the past are not repeated using molecular data. In its current usage among epidemiologists, who have provided most of what we know about interethnic variation in health, the “common sense” or popular meaning of race is accepted as a given, unsupported by biological evidence, and serves both as a construct that frames research questions and a premise on which explanations are based. This standard application of race has obvious limitations and has resulted in widespread misunderstanding about the potential of genes to influence health (Cooper, Kaufman, and Ward, 2003; Kaufman and Cooper, 1996; Krieger, Rowley, Herman, Avery, and Phillips, 1993). As in society at large, incorporation of these notions into the intellectual grammar of science can lead to racist practice (Cooper and Kaufman, 1998). Thus, one of the aims of this paper will be an attempt to explore the role of scientific racism within the discipline of public health, and examine how that shapes the discourse and the research agenda. ETHNIC DISPARITIES IN HEALTH STATUS The focus of this discussion will be on the broad medical syndromes that account for most of the disability and premature mortality in the U.S. population. The first problem that arises when examining the racial/ethnic health patterns is how best to organize the data. As is well known, the definitions used by government agencies are explicitly not based on biologi-

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Critical Perspectives on Racial and Ethnic Differences in Health in Late Life cal categories (Cooper, 1994; Hahn, 1992; Lott, 1993); instead this system was developed to meet the political obligations of the Census. The designation of “black,” “white,” “American Indian,” and “Asian” are considered races, while “Hispanic” is a language or cultural grouping, and the conglomerate category of “Asian/Pacific Islanders/American Indian” is often used to collapse data from many smaller race groups. There is no way to map these categories directly onto genetic subpopulations, although there is some broad correspondence between the racial/ethnic labels and the continent of origin of the ancestral populations. With the availability of vital statistics on both Hispanics and Asian/ Pacific Islanders, we now have a reasonably clear description of the patterns of common disease in the U.S. racial/ethnic groups (Table 8-1). Health status will be discussed in more detail in other sections of this volume, the more limited purpose here is to frame the specific question that needs to be addressed by a genetic analysis. The first and most striking feature is the heterogeneity that exists among the groups. The most prevalent notion of minority health status in the United States is built on the “deficiency model,” that is, an expectation of poorer outcomes for groups other than whites. Dismissed in the past as artifactual, the relative advantage enjoyed by Hispanics, despite similar education and income to blacks, is now undeniable. Characterized as the “Hispanic paradox,” an active research agenda exists TABLE 8-1 Health Status Measures in Racial/Ethnic Groups in the United States, 1998 Cause of Death Age-Adjusted Death Rates* White Black Hispanic Asian All causes 450.4 690.9 432.8 264.6 Heart disease 121.9 183.3 84.2 67.4 Coronary heart disease 79.2 92.5 54.7 42.9 Stroke 23.3 41.4 19.0 22.7 Cancer 121.0 161.2 76.1 74.8 COPD 21.9 17.7 8.5 7.4 Pneumonia/influenza 12.7 17.4 9.8 10.3 Liver disease/cirrhosis 7.1 8.0 11.7 2.4 Diabetes mellitus 12.0 28.8 18.4 8.7 HIV infection 2.6 20.6 6.2 0.8 External causes 46.7 68.8 44.7 24.4 Infant Mortality per 1,000 6.0 13.6 5.8 5.5 Life expectancy (years from birth) 77.3 71.3 >80? >80? *Per 100,000. SOURCE: National Center for Health Statistics (2000).

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Critical Perspectives on Racial and Ethnic Differences in Health in Late Life in epidemiology to explain this counterintuitive finding (Markides and Coreil, 1986). Unreported “shoebox” burials were said to contribute to low infant mortality, while a healthy migrant effect and the return of sick elderly to their country of origin accounted for low adult mortality (James, 1993; Markides and Coreil, 1986). A number of cohort studies now document low age-specific death rates in Hispanics, primarily Mexican Americans, which cannot be ascribed to these biases (Wei et al., 1996). This relative advantage is not universal, however; in many Hispanic communities, obesity and diabetes occur at much greater frequencies than among whites (Diehl and Stern, 1989; Harris et al., 1998). On the other hand, black Americans experience higher rates of all the major causes of death except chronic obstructive pulmonary disease and liver disease (Table 8-1). The excess rates of cardiovascular disease (CVD) have long been recognized as being secondary to the high prevalence of hypertension (Cooper, 1993). Despite high rates of hypertension, coronary heart disease mortality was lower among blacks than whites over the past half century, and it was once widely held that blacks were constitutionally resistant to atherosclerosis (Johnson and Payne, 1984). Rates of coronary heart disease in blacks now exceed whites (Cooper et al., 2001). Asian Americans experience remarkably lower death rates, particularly from CVD (Liao, McGee, and Cooper, 1999). Type II diabetes had been less common in blacks in the first half of the 20th century; it now occurs twice as often among blacks as among whites (Harris et al., 1998; Stamler et al., 1979). Death rates from common malignant neoplasms are highest among black Americans (Table 8-2). The black excess is found in all the common forms of cancer except myeloma, and the differences are particularly marked in the younger age groups. Potential genetic influences are given considerable attention in studies of prostate cancer, where blacks have an incidence twice that of whites (National Center for Health Statistics [NCHS], 2000; TABLE 8-2 Death Rates from Malignant Neoplasms in Racial/Ethnic Groups in the United States, 1998 Racial/Ethnic Group Total* Lung Breast Men Women Men Women Women White 146 106 49.4 27.4 19.0 Black 208 129 70.8 27.2 26.2 American Indian/ Alaskan Native 96 74 33.9 16.5 10.8 Asian/Pacific Islander 91 63 24.6 11.2 9.3 Hispanic 93 64 21.4 8.3 12.5 *Per 100,000. SOURCE: National Center for Health Statistics (2000).

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Critical Perspectives on Racial and Ethnic Differences in Health in Late Life Robbins, Whittemore, and Thom, 2000). Lung cancer has attracted less speculation, despite a black to white mortality rate ratio of 1.0:1.4; overall, blacks smoke less than whites, so the etiologic forces at work are obscure (NCHS, 2000). Breast cancer mortality is higher in blacks than whites, and at a younger age the excess is twofold; the long-awaited downturn in mortality that began in 1992 has been observed only in whites. Known mutations at the BRCA loci account for a substantial proportion of breast cancer cases only among women of Jewish ancestry. Deaths from diabetes and liver disease are higher among Hispanics than whites, although total mortality is lower and life expectancy among Hispanics is thought to exceed 80 (Table 8-1). All-cause mortality for Asians is remarkably low—only 38 percent of the rate among blacks. The risk of dying from HIV is 2.4 times higher in Hispanics than whites, but 8 times higher in blacks. Infant mortality is lower in Hispanics and Asians than whites, but more than twice as high in blacks; the persistently higher rates among blacks are driven in large measure by prematurity and low birthweight (Kleinman and Kessel, 1987). The prevalence of diabetes is currently 14 percent among Mexican Americans, 12 percent among blacks, and 7 percent among whites (Harris et al., 1998). In general, other measures of health status are consistent with this overall picture. Self-reported health is rated lowest by blacks and Native Americans, followed in order by Hispanics, whites, and Asian/Pacific Islanders (McGee, Liao, Cao, and Cooper, 1999). These differences tend to be accentuated with increasing age (McGee, Liao, Cao, and Cooper, 1999). Similar patterns exist for disability (Liao, McGee, Cao, and Cooper, 1998). Higher incidence of Alzheimer’s disease has been reported among African Americans, independent of the prevalence of APOE-4 by some investigators (Tang et al., 1998), but not others (Bohnstedt, Fox, and Kohatsu, 1994). Growing sophistication in descriptive epidemiology, particularly related to CVD and diabetes, has made it possible to model the relationship between risk factor exposures and subsequent disability and disease rates. Measurement of smoking habits, blood pressure, and cholesterol in young adulthood has been shown to predict directly the quality of life and health care experience of persons over 65 (Daviglus et al., 1998). In broad strokes, therefore, health among the elderly can be linked to surveillance data on known exposures. Against this increasingly well-defined epidemiologic background, we are observing growing inequality by social class and geographic region, as well as race/ethnicity (Cooper et al., 2001; Pappas, Queen, Hadden, and Fisher, 1993). Thus, while coronary heart disease rates have been declining at a rate of about 3 percent a year among whites nationwide, CVD mortality has turned upward among blacks in Mississippi (Jones et al., 2000). Blacks in communities located in the center of large cities have also experienced declining health; life expectancy for black men in Atlanta,

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Critical Perspectives on Racial and Ethnic Differences in Health in Late Life Baltimore, St. Louis, Los Angeles, and several other cities was less than 60 years in 1992 (Good, 1998). The contrasts in disease patterns among U.S. racial and ethnic groups are obviously much more complex than can be described in this brief overview. The relevant question for this discussion is how the influence of genetics on variation in health outcomes among U.S. racial/ethnic groups might be recognized. The syndromes that have attracted the most attention are hypertension, asthma, dementia, low birthweight, renal disease, obesity/diabetes, and prostate cancer among blacks and, to a lesser extent, diabetes in Hispanics and Native Americans; in each instance the markedly elevated incidence ratios, with whites as the reference group, have fueled speculation about potential genetic predisposition. The magnitude and consistency of the ethnic differentials, such as in relation to hypertension and prostate cancer, lends credence to these arguments, although the potential environmental contribution is universally acknowledged. A focus on specific syndromes can be misleading, however. It is essential to remember that the health disadvantage extends across a range of key public health measures. Although the hypothesis of genetic predisposition may seem plausible taken one disease at a time, when faced with the pattern as a whole, the probability that the black disadvantage is primarily genetic becomes remote. Rather than postulating a genetic cause for each condition, a more parsimonious explanation would suggest a common-source exposure to a disease-promoting environment. Likewise, a universal characteristic of the syndromes that vary across ethnic groups, with the exception of prostate cancer, is a strong social class gradient. Most of these syndromes have also shown marked secular trends in recent decades, and the prevalence changes across generations among migrants (Collins, Wu, and David, 2002). Stated in its complementary form, the entire basis for the genetic predisposition hypothesis lies in the contrasts in disease rates between historically defined racial/ethnic populations living in the same country. Clearly a strong set of assumptions regarding equal levels of exposure to environmental factors is required to sustain this hypothesis. Although it is subject to many of the same caveats, a different test of the racial predisposition hypothesis is provided by comparisons of genetically related populations in contrasting social settings. All forms of CVD, including hypertension, are low in West Africa, and the levels are equal to U.S. whites in the Caribbean (Cooper et al., 1997a). The evolution of hypertension risk occurs in parallel with changes in known risk factors (Figure 8-1) (Cooper et al., 1997a). The blood pressure gap between blacks and whites is narrow in Cuba (Ordunez-Garcia, Espinosa-Brito, Cooper, Kaufman, and Nieto, 1998) and between blacks and persons of Indian descent in Trinidad (Miller, Maude, and Beckles, 1996). Blacks in Brazil have more hypertension than whites, but the differential is also smaller than in the

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Critical Perspectives on Racial and Ethnic Differences in Health in Late Life FIGURE 8-1 Hypertension prevalence and body mass index in populations of the African diaspora. United States (Cooper and Rotimi, 1994; Sichieri, Oliveira, and Pereira, 2001). Obesity and diabetes are infrequent in Africa and among Native American groups not living in U.S. reservations (Cooper et al., 1997b; Esparza et al., 2000; King and Rewers, 1991). Diabetes is less common among blacks than whites in Brazil (Franco, 1992). Asthma and dementia are less common in Africa than among U.S. blacks (Hendrie et al., 1995; Litonjua, Carey, Weiss, and Gold, 1999). The rate of prostate cancer in blacks outside the United States is not yet reliably known, although high rates have been reported from Jamaica (Glover et al., 1986). Foreign-born women of African descent have children whose birthweight on average is close to whites (David and Collins, 1997; Friedman et al., 1993), and the disparity only emerges after a period of residence in the United States (Collins et al., 2002). Life expectancy in Jamaica and Barbados is longer than among U.S. blacks, where the estimated income is 1/30th to 1/5th as high. Although this pattern is still logically consistent with a predisposition inherent in blacks that is unmasked by environmental stimuli in the United States, it demonstrates that genes are not the determining factor in any of

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Critical Perspectives on Racial and Ethnic Differences in Health in Late Life these examples. To avoid misunderstanding on this point, however, it must be acknowledged that among members of populations that share a common environment, genetic susceptibility can play a crucial role in determining who develops a particular illness; the issue addressed here has been the variation in aggregate health status among groups across time and place. In summary, the broad pattern of racial/ethnic variation in disease occurrence seen in the United States has formed the basis for strong arguments in favor of genetic predisposing factors among blacks and, to a lesser extent, Hispanics and Native Americans. However, the competing hypothesis that the root cause is embedded in the historical and social circumstances peculiar to each of these groups is more consistent with the data (Chaturverdi, 2001). Furthermore, the probability that genes account for the general pattern of health disadvantage is untenable and it must follow that the claims made, for example, by investigators studying diabetes, renal failure, hypertension, and prostate cancer regarding genetic predisposition cannot all be true based on this joint probability. Likewise, the presence of a strong environmental hypothesis, based on the overall pattern, creates a prior assumption against genetic predisposition for any given disease. But these arguments are simply logical inferences; the possibility that genes make an important contribution to interethnic variation of a major disease cannot be dismissed. The contemporary standard will require molecular evidence in order to resolve the question of the relative balance of genes versus environment. Nonetheless, as in all other branches of science, the rules require that the null hypothesis is the only legitimate starting point; the burden of proof should fall on those who claim the genetic, not social, content of race is causal. THE CONTRIBUTION OF GENETIC EPIDEMIOLOGY TO UNDERSTANDING ETHNIC DISPARITIES The search for nongenetic explanations of racial/ethnic variation has occupied epidemiologists for many years, and this experience has important implications for the study of genetic factors. Traditionally, epidemiology has placed emphasis on studies that use the individual as the unit of measurement. When group variation is of interest, it is modeled as the average of the individuals, rather than through any emergent or higher order properties. Alternatively, a second approach uses ecological analyses and attempts to analyze social and economic forces that impinge on groups, taking as the unit of analysis a community or population subgroup. Although risk factor epidemiology at the individual level has enjoyed enormous success, its limitations as a tool to understand variations in population health have also been recognized (Koopman, 1996). However, the conceptual framework for ecologic studies is less well established, and the proposition that economic inequality and institutionalized racism, for example, should be considered causes of

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Critical Perspectives on Racial and Ethnic Differences in Health in Late Life FIGURE 8-4 Frequency distribution of haplotypes in the RAS genes in whites and blacks. has not been demonstrated yet. Africans share virtually all the common variants found in humanity and should represent the genetic “central tendency” of our species. The image of the genome that suggests itself based on this story is a time-lapse photograph of the sun—a globular whole, fringed with a corona that spurts outward and collapses to the center again. Studies of population variation in health status will continue to be constrained if deterministic theories like the “thrifty gene” are applied whenever a disease emerges at a higher prevalence in a new ethnic group. The properties of the genome that make it a single unit shared across all regional populations would be a more appropriate premise for comparative analyses. CONCLUSIONS The study of genes and variation in the health of populations continues to struggle under two constraints imposed by social reality—one that influences how we frame the questions and the other that determines how people are arranged in the hierarchy. Our notion of race suggests certain answers, thereby prejudicing the questions, and the arrangement of people

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Critical Perspectives on Racial and Ethnic Differences in Health in Late Life by race and class structures the environmental exposures, and, by extension, many aspects of health status. Although both constructs—race and inequality—confront us as products of the natural world, they are in fact reflecting an image of what we have made. That image has become nearly impossible to decipher where race and inequality merge. Stripping away its claims to a natural origin, what is race? A name we call ourselves, sein finn, as they say in Irish—we ourselves—or a name for the Other? Until very recently the study of race had never been a possibility for science, despite the depths of its penetration into biology. We now have reason to believe that era is about to end as empirical questions begin to dominate the research agenda. Does race have any meaning beyond geography and history? Does the genome of our species aggregate into subunits? Does it even branch into trees? If we see it as a whole, will it look like the sun? These questions, which can be answered only with molecular data, are now at least “askable.” But scientific questions are not asked in a vacuum. Although it can legitimately be argued that in some instances the results of experimentation describe the shape of nature, questions are patently a human construct, made from materials already available to us in the social environment. Given the potency of race as a cultural idea and its influence on scientific thinking, there is reason for concern about where the attempts to discover the genetic determinants of health and disease will take us. An analogy to history may help frame this dilemma. In questioning the “memory-storage” model of history, attention has been drawn to the variable chance with which events are recorded and archived and how narratives about these events reflect the understanding of the present (Trouillot, 1995). Differential claims on the archive, and differential chances of being the hero of the narrative, are determined by differentials in power. A record of uneven quality, subjected to the filter of ideology, does not yield a description of the past, but rather a context within which we interpret the events of today. Although not a myth, because history makes a different set of claims on reality, the narratives of the past are never true or objective. In that sense, there is no “pastness,” only an understanding of what shaped the present. Genetics, like history, queries the past, attempting to use the record left in the genome to understand how evolution and population dynamics created the current pattern of variation. Although the course of human history—wars, famine, migration, conquest, and slavery—biases and complicates the record, the ability to know all the sequence variation means that the geneticist’s archive is far more egalitarian and complete than is the historian’s. One need only consider the story of Thomas Jefferson’s family to appreciate the gap between what is recorded in history books and what is recorded in our genome (Ellis, 1998; Foster et al., 1998). If in fact the genetic history of our species is essentially complete and unbiased, the

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Critical Perspectives on Racial and Ethnic Differences in Health in Late Life opportunities for objective description are limitless, constrained only by the questions we are asking. We can, in a sense, no longer blame our sources, but only ourselves. But of course, after a moment’s reflection, we know this is a false hope; the questions we ask are determined by the history of our consciousness, itself created from the narrative written by those in power today from an inconsistent record of the past. We are returned to the original problem—biological and social history can never be divorced. Biological scientists like to think that they work in an intellectual space uncontaminated by superstition and prejudice and therefore resist the rhetoric of context. But race is a true chimera—part geography, part history, part genes—and neither the idea nor the practice can be understood as anything other than the fantastic creation of the human mind. There is no use of race that isolates the biological from the social. The study of genes and ethnic variation in health occupies contested territory, where genotype is hidden within phenotype and the biologic is molded by the social. Race attempts to distill and simplify this dialectical process into a linear pattern of cause and effect, obfuscating everything. We are looking to population genetics to give structure to this debate, using empirical observation as the scaffold. Can it relieve us entirely of the concept of race? Races exist only in distinction to each other; “whiteness” is defined by “blackness,” and each is endowed with a distinct essence. If in fact there is no “other,” then there is no essential difference, and the notion becomes empty of meaning. As on so many other occasions, however, these optimistic pronouncements will have no authority, or, at the very least, they will come too late in Western history. We live in a world where every construct is racialized—citizenship, personal identity, neighborhood, health—and it is unlikely that the evidence of genetics will be sufficient to counterbalance the enormous weight of social ideology. But within the narrow discipline of genetic epidemiology, is it too much to ask that essentialist notions, which molecular data are now demonstrating to be mere superstition, should no longer hold sway? ENDNOTE 1.   Refers to Rtinal Information Network. Information can be found at www.sph.uth.tmc.edu/Retnet/home.htm. REFERENCES Altmuller, J., Palmer, L.J., Fischer, G., Scherb, H., and Wjst, M. (2001). Genomewide scans of complex human disease: True linkage is hard to find. American Journal of Human Genetics, 69, 936-950.

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