The possible causes of the higher frequency of type 2 diabetes in African-Americans compared with European-Americans has generated much interest. Conventional wisdom might suggest that the disadvantaged socioeconomic position of African-Americans and their increased genetic susceptibility as a group account for the higher incidence of the disease. However, when socioeconomic factors are controlled for the excess, type 2 diabetes risk for African-Americans remains (1). Is this excess risk due solely to a difference in genetic susceptibility? Although genetic susceptibility is likely contributory, risk factors operating perhaps exclusively in the African-American population may also contribute to the unexplained excess of type 2 diabetes in that group.
Bjorntorp (2) hypothesizes that certain individuals who are prone to defeat-oriented responses to environmental stressors may exhibit a dysfunctional response of the hypothalamic-pituitary-adrenal (HPA) axis to stress, resulting in abdominal obesity and metabolic abnormalities including glucose intolerance. This hypothesis has captured our interest regarding its implication for African-Americans. We previously demonstrated in African-Caribbean individuals (3) that internalized racism (4) (i.e., the extent to which blacks agree with racist stereotypes attributed to them) is associated with increased levels of dysphoria and abdominal obesity independent of BMI. To determine whether internalized racism might also be related to glucose intolerance, we conducted a nested case-control study as part of a larger study of diabetes risk factors in the U.S. Virgin Islands (USVI).
Participants were non-Hispanic blacks ≥20 years of age recruited from randomly selected households on the island of St. Croix in the USVI. Fasting blood samples were drawn from all of them. Between November 1999 and February 2000, 27 subjects with newly diagnosed type 2 diabetes (5) and 55 nondiabetic control subjects were recruited. The two groups were frequency matched by age and sex. The distribution of internalized racism scores was divided into high and low levels based on a median split. Each participant signed a consent form approved by the University of Pittsburgh Institutional Review Board.
The study results showed no significant difference between case subjects and control subjects with respect to age (58.7 ± 11.2 vs. 58.1 ± 10.9 years, respectively), sex (51.9 vs. 56.4% female, respectively), or high school completion (44.4 vs. 41.8%, respectively). However, case subjects had a higher level of both internalized racism (63 vs. 40%, odds ratio = 2.5; P = 0.050) and mean hostility score (75.5 vs. 66.3, P = 0.0008) than control subjects. In the entire cohort, internalized racism and hostility score (6) were highly correlated (r = 0.53; P = 0.0001).
The current study suggests that internalized racism is associated with glucose intolerance among African-Americans in the USVI. It might be hypothesized that internalized racism may be a marker of abnormal HPA function and the cascade of metabolic abnormalities reported by Bjorntorp et al. (7). Its relationship to type 2 diabetes may signal the important contribution of a psychosocial stress–mediated pathway in the etiology of type 2 diabetes in African-Americans. Given estimates that 15–50% of African-Americans in the continental U.S. may have high internalized racism (8), additional study in this area is recommended.
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Address correspondence to Dr. Eugene S. Tull, Graduate School of Public Health, 512 Parran Hall, 130 DeSoto St., Pittsburgh, PA 15261. E-mail: [email protected].
