OBJECTIVES: We explored whether ethnic differences in type 2 diabetes (T2D) explain ethnic disparities in cognitive impairment. DESIGN: Longitudinal study. SETTING: A cohort study of multiethnic community-dwelling elderly persons in Northern Manhattan, New York. PARTICIPANTS: 941 participants aged > or =65 years without prevalent cognitive impairment or dementia (CID) were followed for a median of 7.1 years. MAIN OUTCOMES MEASURES: CID was defined by a clinical dementia rating > or = .5. CID risk attributable to T2D was estimated for each ethnic group using the hazard ratio (HR) relating T2D and CID and the ethnic prevalence of T2D. RESULTS: 448 participants developed CID; 69 (31.4%) non-Hispanic whites (whites); 152 (48.6%) non-Hispanic-blacks (blacks); 227 (55.6%) Hispanics, P < .001. T2D prevalence was 8.2% in Whites, 20.1% in blacks, and 19.6% in Hispanics, P < .001. Controlling for age, sex, education, and APOE E4, the HR relating T2D and CID was 1.63 (95% CI 1.26, 2.09). CID attributable to T2D was higher in blacks and Hispanics compared to Whites (11.4% vs. 4.9%; P = .06). We estimated that reducing the ethnic disparities in diabetes prevalence could reduce the CID ethnic disparities by 17%. CONCLUSIONS: Reducing ethnic differences in T2D prevalence could partially reduce ethnic differences in incident CID.
OBJECTIVES: We explored whether ethnic differences in type 2 diabetes (T2D) explain ethnic disparities in cognitive impairment. DESIGN: Longitudinal study. SETTING: A cohort study of multiethnic community-dwelling elderly persons in Northern Manhattan, New York. PARTICIPANTS: 941 participants aged > or =65 years without prevalent cognitive impairment or dementia (CID) were followed for a median of 7.1 years. MAIN OUTCOMES MEASURES: CID was defined by a clinical dementia rating > or = .5. CID risk attributable to T2D was estimated for each ethnic group using the hazard ratio (HR) relating T2D and CID and the ethnic prevalence of T2D. RESULTS: 448 participants developed CID; 69 (31.4%) non-Hispanic whites (whites); 152 (48.6%) non-Hispanic-blacks (blacks); 227 (55.6%) Hispanics, P < .001. T2D prevalence was 8.2% in Whites, 20.1% in blacks, and 19.6% in Hispanics, P < .001. Controlling for age, sex, education, and APOE E4, the HR relating T2D and CID was 1.63 (95% CI 1.26, 2.09). CID attributable to T2D was higher in blacks and Hispanics compared to Whites (11.4% vs. 4.9%; P = .06). We estimated that reducing the ethnic disparities in diabetes prevalence could reduce the CID ethnic disparities by 17%. CONCLUSIONS: Reducing ethnic differences in T2D prevalence could partially reduce ethnic differences in incident CID.
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