Infectious Disease, Susceptibility, and Race

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Infectious Disease, Susceptibility, and Race

“VIRGIN SOIL” EPIDEMICS

TUBERCULOSIS, RACE, AND EXTINCTION

RACE, GENETICS, AND SUSCEPTIBILITY

BIBLIOGRAPHY

Disparities in health status, whether measured by infant mortality, life expectancy, or rates of disease, have always existed between different groups. They have been especially stark during epidemics. HIV (human immunodeficiency virus), for instance, exhibits marked disparities between developing and developed countries and between different populations within developing countries. How can these disparities be explained?

Some observers have argued that disparities in disease and mortality reflect disparities in socioeconomic conditions, with impoverished populations being most vulnerable to a wide range of diseases. Others have argued that the disparities reflect biological differences between groups that have different genetic susceptibilities to infectious disease. Genetic explanations have been especially popular in the many cases in which health disparities have existed among racial and ethnic groups.

Two diseases, smallpox and tuberculosis, demonstrate this well. During epidemics of smallpox in the sixteenth and seventeenth centuries, and during epidemics of tuberculosis in the nineteenth and twentieth centuries, doctors and other observers debated the extent to which substantial disparities in mortality could be attributed to assumed biological differences between racial groups. These cases each suggest that biological differences between “races” might be less important determinants of disease than variations in social and economic conditions.

“VIRGIN SOIL” EPIDEMICS

Since ancient times, physicians have been aware that disease is distributed unevenly. Different people living in different places suffer from different diseases, or from different rates of the same diseases. In one of the most influential texts of ancient Greece, On Airs, Waters, and Places, the author traced disease to the source and quality of drinking water, the direction and intensity of the prevailing winds, and the topography of the land. Yet the susceptibility to disease went deeper than these environmental conditions. Because people who lived in a specific place became adapted to the local environment, environmental differences became embodied as biological differences (but not necessarily heritable differences) between different groups. Athenians who moved to Alexandria would have found themselves in a climate to which they were not adapted. They would therefore have been more vulnerable to the local diseases of Alexandria. In this way, ancient authors traced variations in rates of disease, in part, to biological differences between people.

Patterns in the distribution of disease among different peoples and places became more obvious and more relevant during the European voyages of exploration and colonization in the sixteenth and seventeenth centuries. As Europeans initiated sustained contact with foreign populations in Africa, Asia, and the Americas, they encountered new diseases and spread their own diseases throughout the world. Smallpox, measles, malaria, and many others spread from Europe and Africa to the Americas. Syphilis spread from America to Europe and then throughout the world. This exchange of diseases had devastating consequences, particularly for the indigenous inhabitants of the Americas. The population of Hispaniola, the first group subjected to Spanish Conquest, foretold the fate of other areas: The Arawak population fell from roughly 400,000 in 1496 to 125 in 1570. As the historian Alfred Crosby has shown, every encounter brought disease and decimation—to Mexico and Peru in the sixteenth century, to New France and New England in the seventeenth century, and throughout North America and the Pacific Islands in the eighteenth and nineteenth centuries. American and Pacific populations typically declined by 90 percent in the first century after contact, falling victim to smallpox, measles, influenza, and countless other epidemics.

The new encounters between people and disease inspired substantial speculation about the distribution of disease and the causes of susceptibility. Colonists produced a diverse range of explanations for the prevalence of disease among American Indians, including religion, diet, environmental conditions, and hygiene. Early colonists, at least in New England, did not see the mortality disparity in racial terms nor did they assume that there were intrinsic differences between European and Indian bodies. Instead, as Philip Vincent, who led English forces in the Pequot War, put it in 1637, “we have the same matter, the same mould. Only art and grace have given us that perfection which they yet want, but may perhaps be as capable thereof as we” (Jones 2003, p. 38). However, the disparities in health status became more and more striking over time. Colonists described epidemics that devastated American Indians but had no effect on the Europeans who lived among them. European populations grew steadily even as Native populations declined. As Joyce Chaplin has argued, these observations led more and more colonists in the seventeenth and eighteenth centuries to suspect that there were intrinsic differences between Europeans, Native Americans, and Africans. Within their starkly Eurocentric worldview, Europeans saw themselves as both more civilized and more resistant to disease.

Historians and medical researchers have debated for centuries why American Indians had such high mortality from epidemics. Many have favored explanations based in evolutionary theory and natural selection. According to the popular “virgin soil” theory of epidemics, European and Asian populations suffered a high burden of infectious disease throughout their history. As a result, they developed a genetic resistance to smallpox, measles, and many other infections. Because these diseases did not exist in the Americas before Christopher Columbus, the indigenous population never developed similar resistance. Alfred Crosby and Jared Diamond have argued that this differential susceptibility explains the outcome of the encounter: American Indians were doomed because they lacked genetic resistance to a wide range of Eurasian pathogens.

However, the theory of virgin soil epidemics has had many critics. Despite intensive study, medical researchers have not found any substantial evidence that different races have different genetic susceptibilities to smallpox, measles, or other acute viral infections. At the same time, Linda Newson, Stephen Kunitz, and other historians have shown that environmental conditions and social factors played a decisive role in shaping the outcome of encounters between Europeans and Native Americans. Many American populations barely eked out a subsistence living before the European arrival, with life expectancies as low as twenty to twenty-five years. When European colonizers disrupted patterns of subsistence and exposed Indians to warfare, slavery, and dislocation, the populations suffered terribly. The severity of the mortality varied between different groups, often depending on the intensity and intrusiveness of European contact. This suggests that American Indian populations were not born vulnerable to European pathogens. Instead, they may have been made vulnerable by the chaos of colonization and conquest.

TUBERCULOSIS, RACE, AND EXTINCTION

During the nineteenth century, tuberculosis replaced smallpox as the dominant cause of mortality in Europe and the United States. Smallpox declined for a variety of reasons, including the spread of vaccination and the emergence of a less virulent strain of smallpox. The rise of tuberculosis is more complex, with urbanization, overcrowding, working conditions in factories, and malnutrition all contributing. By the late nineteenth century, tuberculosis caused roughly 20 percent of all deaths in Europe and the United States. The impact was even more dire on some populations. Randall Packard has shown how Africans working in South African mines in the first half of the twentieth century suffered terribly from tuberculosis, even after it had receded among the white population of South Africa. Medical researchers at the time wondered whether the Africans were a “virgin soil” for tuberculosis. Packard argued instead that the epidemic arose from the poverty, malnutrition, and physical stress experienced by the black laborers.

In North America the most afflicted populations were American Indians who had been confined on reservations. Tuberculosis caused more than half of all deaths on the Sioux reservations in the Dakotas. Observers continued to emphasize environmental conditions, tracing tuberculosis to overcrowded housing, poor hygiene, and inadequate food. Racial theories, however, became more common. By the mid-nineteenth century, many scientists believed either that the races had been created separately or that they had diverged thoroughly from their common creation. In either case, there was no reason to think that the different races were equivalent. As a result, many scholars in the United States and Europe believed that whites were superior to both American Indians and blacks. This belief led to a widely held conclusion: Indians and blacks, unable to compete with whites, would inevitably go extinct. The burden of tuberculosis among the Native population was seen as proof of their eventual fate.

These theories of racial susceptibility to tuberculosis had many subtleties. White Protestants were not always seen as the most superior race. Just as American Indians were believed to be susceptible because they had only recently encountered tuberculosis, Jews were seen as particularly resistant because they had long lived in urban ghettos where tuberculosis had thrived. However, as the historian Alan Kraut has shown, Jewish doctors did not welcome this theory. Instead, they argued that there was no particular connection between Jews and tuberculosis. The disease simply assailed everyone who lived in suitable conditions.

During the twentieth century, tuberculosis receded from the United States and Europe but remained endemic in many other countries. By 2000, one-third of the world’s population (two billion people) were infected. More than two million people died each year. It became clear over the twentieth century that socioeconomic factors have an enormous impact on tuberculosis. In many populations, everyone would become infected, but only those weakened by physical stress or malnutrition would die. This was seen clearly during wartime conditions, when famines, fatigue, and dislocation greatly increased tuberculosis mortality. Such observations led the microbiologist and author René Dubos to christen tuberculosis a “social disease.” Any population, when weakened by poverty and malnutrition, can become devastatingly susceptible to tuberculosis.

Despite clear evidence of the importance of socioeconomic factors, researchers continued to seek and find evidence of genetic factors that influence susceptibility to tuberculosis. In the 1990s William Stead, Richard Bellamy, Adrian V.S. Hill, and other researchers identified a series of genetic variants that increased both the risk of infection with the bacteria that causes tuberculosis and the risk of active disease once infected. In 2006, Philip Liu and his collaborators showed a link between melanin concentration in skin (i.e., darkness of skin) and susceptibility to tuberculosis. It is possible that variations in the frequency of susceptibility genes between different populations contribute to the observed variations in the frequency of tuberculosis in different racial and ethnic groups. The discovery of new susceptibility genes became more common as the Human Genome Project and the International HapMap Project facilitated high-volume genomic analysis. The new genetic data, taken with the existing evidence of the importance of socioeconomic conditions, forced researchers to continue to debate the contribution of genetic and environmental factors to disease susceptibility and health disparities.

RACE, GENETICS, AND SUSCEPTIBILITY

Discussions of race and susceptibility to disease have not been limited to virgin soil epidemics and tuberculosis. Instead, racial disparities in disease incidence and mortality rates have been described for most diseases. Diabetes has been most prevalent among the Pima Indians, a problem attributed to the mismatch between scarce ancestral food supplies and the overabundance of modern life. Sickle-cell disease is largely a problem for people of African ancestry, a legacy of evolution in malarial environments. Tay-Sachs disease occurs almost exclusively among Ashkenazi Jews, a product, it has been speculated, of their long exposure to tuberculosis. Countless other “racial” diseases and susceptibilities have been described. This research benefited from increasingly fine-grained analyses of human genetics. Although it has become clear that humans are remarkably homogeneous genetically (much more so than fruit flies or dogs), there is enough variation between humans for genetic subpopulations to be identified. As Noah Rosenberg’s analysis has shown, these genetically defined populations correlate well with conventional racial categories. These various lines of research are seen by some to support the conclusion that race is both biologically real and medically significant.

However, as happened with both virgin soil epidemics and theories of tuberculosis susceptibility, questions emerged about the significance of genetic differences between racial and ethnic groups. Even if a disease is distributed along racial lines, genetic differences between races might not be the cause. Race in the United States is correlated with education, living conditions, and socioeconomic status, each of which influences disease outcomes. The limitations of racial theories, and the discomfort with them, can be clearly seen in the case of HIV. From the earliest years of the epidemic, HIV/AIDS has exhibited striking disparities in morbidity and mortality. Few scientists or historians, however, have argued that the disparities between South Africans and Europeans, or between urban minorities and suburban whites, existed because the afflicted populations were genetically susceptible to HIV. Instead, the social contingency of HIV on a local and global scale has long been recognized.

Ironically, as more and more genetic data emerge to explain observed racial disparities in health status, the overall argument about the importance of genetics becomes harder and harder to sustain. For instance, disparities between American Indians and the general population of the United States have been described for acute infections, such as smallpox and measles; chronic infections, especially tuberculosis and trachoma; and for the endemic ailments of modern society, including heart disease, diabetes, alcoholism, and depression. A different, but equally diverse, set of disparities exists for African Americans. The persistence of disparities across changing disease environments is actually a powerful argument against the belief that disparities reflect the genetic susceptibilities of different racial groups. Instead, the disparities could arise from disparities of wealth and power that exist between different racial and ethnic groups.

Disparities in disease incidence and mortality rates among different racial and ethnic groups have existed for millennia. However, the causes of these disparities remain unclear. Many researchers have argued that biological differences between racial groups, especially variations in disease susceptibility genes, are the cause of the differential susceptibility. Others have rejected these claims and argued instead that environmental conditions and socioeconomic factors have a greater influence on patterns of disease. Until the questions are resolved, researchers, clinicians, and policymakers need to recognize the complexity of race and the many other factors that interact to produce patterns of disease and mortality.

SEE ALSO Diabetes; Diseases, Racial; Genetic Variation among Populations; Health Disparities between Indians and Non-Indians; Heritability; HIV and AIDS; Human Genetics; Sickle Cell Anemia; Tay-Sachs and “Jewish” Diseases.

BIBLIOGRAPHY

Bellamy, Richard, et al. 1998. “Variations in the NRAMP1 Gene and Susceptibility to Tuberculosis in West Africans.” New England Journal of Medicine 338: 640–644.

Chaplin, Joyce E. 2001. Subject Matter: Technology, the Body, and Science on the Anglo-American Frontier, 1500–1676. Cambridge, MA: Harvard University Press.

Crosby, Alfred W. 1972. The Columbian Exchange: Biological and Cultural Consequences of 1492. Westport, CT: Greenwood.

Diamond, Jared. 1997. Guns, Germs, and Steel: The Fates of Human Societies. New York: W.W. Norton.

Dubos, René, and Jean Dubos. 1987 (1952). The White Plague: Tuberculosis, Man, and Society. New Brunswick, NJ: Rutgers University Press.

Jones, David S. 2003. “Virgin Soils Revisited.” William and Mary Quarterly 60: 703–742.

_____. Rationalizing Epidemics: Meanings and Uses of American Indian Mortality since 1600. Cambridge, MA: Harvard University Press.

Kraut, Alan M. 1994. Silent Travelers: Germs, Genes, and the “Immigrant Menace.” Baltimore, MD: Johns Hopkins University Press.

Kunitz, Stephen J. 1994. Disease and Social Diversity: The European Impact on the Health of Non-Europeans. New York: Oxford University Press.

Liu, Philip T., et al. 2006. “Toll-Like Receptor Triggering of a Vitamin D-Mediated Human Antimicrobial Response.” Science 311: 1770–1773.

Newson, Linda A. 1985. “Indian Population Patterns in Colonial Spanish America.” Latin American Research Review 20 (3): 41–74.

Packard, Randall M. 1989. White Plague, Black Labor: Tuberculosis and the Political Economy of Health and Disease in South Africa. Berkeley: University of California Press.

Rosenberg, Noah A., Jonathan K. Pritchard, James L. Weber, et al. “Genetic Structure of Human Populations.” Science 298 (5602): 2381–2385.

Stead, William W., John W. Senner, William T. Reddick, and John P. Lofgren. 1990. “Racial Differences in Susceptibility to Infection by Mycobacterium tuberculosis.” New England Journal of Medicine 322: 422–427.

David S. Jones