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Do genes explain diabetes health disparities between ethnic groups?
Social taxonomies are not based on biology.
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For years, scientists have been looking for the genetic contributions to type 2 diabetes. Since the 1970’s, the high incidence and prevalence rates led researchers to begin their hunt for genes among those peoples most affected by the disease, namely Native Americans, Mexican Americans and other ethnic minority groups. The presumed relative genetic homogeneity of these groups seemed the perfect opportunity to crack the genetic code for this emerging epidemic.
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Over the decades, the scientific imagination and investments have created one of the most widely held beliefs about type 2 diabetes; to wit, that it is a genetic condition for which ethnic groups are susceptible. Scientists, clinicians and lay people alike attest to the fact that type 2 diabetes runs in families, that belonging to one of these groups is a risk factor, and that genes, therefore, explain the filial and group-wide inheritance patterns.
The question is not whether ethnic minorities are more susceptible than other groups. The question is whether we can infer genetic susceptibility if what is meant by “ethnic and racial minority” corresponds to sociocultural factors alone.
In spite of decades of trying, the actual genetic contributions for diabetes that explains the disease disparities between peoples of Northern European ancestry and Native American, African American, and Hispanic/Latino peoples remain elusive and likely do not exist. This apparent heterodoxy is less outlandish than it appears.
The crux of the matter is not whether genes are important. Rather, the issue is will genes ever explain all but a small fraction of the global prevalence of disparities between those groups most affected by diabetes?
To be sure, the eventual genetic contributions to diabetes are likely to be found as the human genome gets split in to ever finer-grained bits, as data sets are improved and new more powerful computational tools are developed.
Further, studies within individual groups and families may certainly reveal genes particular to their group. However, even these particular genetic findings cannot explain the differential risks between groups, because that is not what they purport to explain.
Chief among the reasons that suspected diabetes genes found within ethnically or racially labeled groups cannot explain the recent rise of diabetes is that genotypes are stable while the social worlds of affected peoples are not. How can ancient genes explain a 40-year-old epidemiological pattern? More to the point, genes cannot explain health disparities between human groups because the correspondence between social taxonomies and human biology is a fallacy.
This is deeper than the experimental search for correspondence between self-reports and specific markers. In the nonexperimental world of DNA collection, the ascertainment of ethnicity or race is a profoundly social enterprise anchored in contemporary history.
Race was a concept developed in the 17th and 18th centuries as a means to explain observable differences between missionaries, gentleman explorers and scientists and those people into whose worlds these mostly European labelers visited.
At the time, five races of man morphed into dozens and back into half as many again as the validity of these newly discovered “races” were debated and better measurements derived to place people in proper taxonomic order. Even though scientists of the day carefully wielded their calipers and morphologic matrices to map the richly diverse others into “races of man,” that taxonomic order was not based upon biology.
It turned out then, as now, that these measurements correspond best to the imaginations of the scientists and not the presumably defining and stable features being measured. Furthermore, features that were presumed to define human groups were found to change even within one generation.
The labels themselves also changed. Mongoloid became Asian became Native or Indigenous, and Indian became “other” as the taxonomic systems were reworked to fit contemporary social problems. More than a lack of standardization, however, the measuring of human variation suffered from changes in the labels used for the same individual at the time of birth and death and other taxonomic instabilities. Further, groups once thought “nonwhite” were soon incorporated into the “white” category (eg, Irish and Italians in the early 20th century). Entire categories of persons were invented by governmental fiat, eg, Hispanic circa 1970. Finally, Asian, European, Mexican, Pima, white and black are continents, nations and colors respectively – not biological categories.
Yet these categories are what geneticists must use to select, talk about, label and conduct research into diabetes among ethnic minority peoples: The NIH and journal policies require it, our disciplinary divides reinforce it. However, when we carefully examine the selection of a group to study, the labeling of that group, the representation of that group in scientific papers, we see a science of population labeling based squarely on sociocultural factors particular to each group, each region and each historical period.
Hence, Haitians or Nigerians stand in for all African Americans, and Mexicans in one community stand in for Hispanic/Latino/Mexicano people everywhere.
Most importantly, it is the historical and sociocultural life conditions of these groups (eg, poverty, geographic isolation, lack of access to health care) that brought them to the attention of researchers in the first place. Thus, ethnic and racially labeled groups in genetics, as elsewhere, are in fact social groups through and through.
Therefore, genetic discoveries for diabetes among ethnic minority people that are based upon DNA labeled with sociocultural terms reference the sociocultural conditions, historical and contemporary, of those groups.
Historically, migration, enslavement, forced relocation, disruption of lifeways and dispossession, as well as contemporary access to health care, affordable housing, experiences of discrimination, and educational attainment are nonrandom sociocultural conditions that directly bear upon a person’s well being.
On matters of human physiology and disease, science and medicine have predominantly adhered to the mind-body dualism set forth by Descartes in the 17th century. Pathology is measured in terms of deviation from norms of physiological functioning, which in turn are measured by increasingly refined biological units.
Sugar in the urine, HbA1c, or recently, genetic markers are used as indicators of pathology or pathological potential. The body is set apart from the social world in which it exists. Even if we know better, our sciences do not seriously conceptualize the mind and the body as part of one in the same system. Social context is a black box.
The endocrinological system is different, however. Evolved over millennia to biologically mediate our external world, the system’s complex ever-adaptive regulation of hormones in response to threats, foods, pleasures and developmental changes holds more secrets than can ever be discerned through the characterizations of proteins up- or down-regulated by genomic codes.
For diabetes in minority groups is nothing if not the manifest result of differential threats, foods, pleasures and responses to developmental changes over generations. Differences, it might behoove us to note, are not genetic any more than language, religion or property, which are all inherited in nonrandom ways.
That ethnic and racial labels used in genetic research are themselves sociocultural phenomenon should give pause to those who first think of type 2 diabetes among minority groups as at base genetic. Further, recognition of the profoundly disparate life conditions of ethnic minority groups should open the way for further explorations into the connections between the mind-body.
That is, we all embody, within and through our endocrine system, among other ways, the sociocultural worlds we inhabit. Genes may shed light on basic mechanisms of human biology but do little to explain the physiological impact of differential life conditions that are responsible for disparities in health.
For more information:
- Michael J. Montoya, PhD, is an Assistant Professor in the Departments of Chicano/Latino Studies and Anthropology in the School of Social Sciences, and is a core faculty for the Program in Medical Education for the Latino Community (PRIME-LC) in the School of Medicine at the University of California, Irvine.
- Paradies YC, Montoya MJ, Fullerton SM. Racialized genetics and the study of complex diseases: The thrifty genotype revisited. Perspectives in Biology and Medicine. 2007;50.
- Steinthorsdottir V, et al. A variant in CDKAL1 influences insulin response and risk of type 2 diabetes. Nature Genetics. Published online: April 26, 2007.
- Frayling TM, et al. A common variant in the FTO Gene is Associated with Body Mass Index and Predisposes to Childhood and Adult Obesity. Science. 2007;316:889-894.
- Risch N, et al. Categorization of humans in biomedical research: Genes, race and disease. Genome Biology. 2002; 3:1-12.
- Hahn RA, et al., The recording of demographic information on death certificates: a national survey of funeral directors. Public Health Report. 2002;117:37-43.
- Montoya, MJ. Bioethnic Conscription: Genes, Race and Mexicana/o Ethnicity in Diabetes Research. Cultural Anthropology. 2007;22.