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Starting in the second half of the twentieth century, the prevalence of non-insulin-dependent (type 2) diabetes increased substantially in many populations and ethnic groups, including African Americans, Native Americans, Mexicans Americans, and Pacific Islanders. Diabetes is a metabolic disorder characterized by an inability to regulate blood sugar. The increase in this disease is clearly related to shifts in diet and lifestyle. While some researchers have proposed that it is related to genetic factors, other researchers point to stressful and challenging life conditions resulting from poverty and social inequality.


More than 90 percent of all diabetics have type 2 diabetes. Unlike the more rare form of the disease, type 1 diabetes, people with type 2 diabetes produce insulin and therefore seldom need therapeutic insulin at the initial onset of the disease. Type 2 diabetes is considered a late-onset chronic disease and is associated with risk factors such as increased obesity, dietary fat intake, smoking, and low physical activity. Racism, stress, and socioeconomic status have also been implicated in the development of diabetes. Diabetes is diagnosed by measuring the percentage of red blood cells that are bound with glucose. There is no cure for diabetes, but the traditional treatment includes alterations in diet, exercise, and drug therapies to control glucose metabolism.

Prevalence rates follow a strikingly similar pattern in varied populations. For First Nations Canadian men and women, age-adjusted prevalence rates are 3.6 and 5.5 times higher, respectively, than among the general Canadian population. Among Indigenous Australians, the prevalence rates are almost four times higher than the rate for the non-Indigenous population. Researchers comparing age-adjusted prevalence rates for Nigerians and people of African origin living elsewhere found diabetes rates were

2.5 to 5 times higher for those living in the Caribbean and United Kingdom. In the United States, the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) estimates that at least 8 to 10 percent of all Latinos, African Americans, and Native Americans aged twenty years or older have diabetes. The comparable prevalence rates for non-Hispanic whites is 4.8 percent.

According to the U.S. Centers for Disease Control and Prevention (CDC), diabetes is the seventh leading cause of death in the United States. The World Health Organization (WHO) has called diabetes an emerging epidemic, with more than 16 million people affected in the United States and millions more in the rapidly urbanizing Southern Hemisphere and China. According to the WHO, approximately 366 million people worldwide will have diabetes by 2025. The very similar epidemiological patterns that exist for U.S. minorities, First Nations Canadians, Indigenous Australians, peoples of the African diaspora, and peoples of the Pacific Islands strongly indicate that diabetes disproportionately affects subordinated groups around the world.


As a racializing practice, gene-based approaches to diabetes advance the myth that biology can explain social phenomena. In fact, considerable evidence suggests that biology and social phenomena are co-produced, that biological and social phenomena develop in mutually interdependent ways. In its most crude form, this is evident when genetic researchers use social labels to describe human groups, which renders their findings both biological and social in origin. Similarly, researchers using evolutionary models for complex diseases require genetic samples of the populations most impacted by diabetes. They are thus investigating the physiological impact of social stratification and the radical lifestyle transformation required of advanced capitalism.

Viewing complex disease through a genetic lens is a long-established sociocultural phenomenon, one that has been applied to diseases such as sickle-cell anemia, hypertension, and diabetes. For diabetes, the alleged metabolic adaptation within the thrifty genotype hypothesis presumes that hunter-gatherers experienced severe episodes of feast and famine. Selective evolutionary pressures would therefore favor those whose metabolism would best convert glucose to fat for use during periods of food scarcity. Contemporary human groups impacted by diabetes are viewed as genetically predis-posed to the disease by virtue of their current similarity to the lifeways of earlier humans. However, both the extent of the feast-and-famine cycles of hunter-gatherers and the association of contemporary human groups with early human life-ways are unsubstantiated premises, relying on presumed rather than empirically supported benefits of modernity. The widespread adherence to the evolutionary hypothesis of diabetes (and the considerable resources directed toward such studies) is another iteration of a race theory that advances the cultural notion that diabetes affects human groups differently because of innate genetic differences.

Examining diabetes as an evolutionary trait denies the impact of the social dislocation, dispossession, colonization, slavery, racism, and other sociohistorical impact on those groups affected by diabetes. For example, the groups most disproportionately impacted by diabetes, Native Americans, experienced extreme deprivations during the violent dispossession of their lands and subsequent attempts by white settlers to eradicate them. It is the children and grandchildren of those born during this period who now suffer disproportionately from diabetes. These conditions support the fetal origins hypotheses and do not require the logical leap that such recent experiences could have evolutionary significance, and thus result in genotypic human variation. Thus, the widespread adherence to the genetic predisposition thesis for diabetes reflects a dominant cultural way of making sense of relations between groups impacted by the disease.

In order to understand the causes of diabetes, its evolutionary hypothesis must be seen as fitting not the natural history of the disease, but rather the ideological premise of a subordinating majority whose scientists refuse to seriously account for the social history of those peoples most impacted by the disease. Researchers seriously interested in preventing diabetes would greatly benefit by approaching the disease in ethnoracial groups as a biocultural phenomenon. To avoid merely reproducing another unprovable evolutionary genetic predisposition claim, researchers must carefully investigate diabetes as the biological impact of economic and sociocultural changes for human life. This requires uncommon multi-disciplinary methods spanning the biological and social sciences and humanities. More importantly, researchers must actively counter the racialized hypothesis of genetic predisposition, especially in research into health inequalities among minority and emerging majority groups in parts of the world with high levels of ethnoracial stratification and an unequal distribution of resources. In short, researchers must recognize the link between diabetes and institutional racism.


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