Serum @entity2690 , @entity28 , and the incidence of @entity164 2 XXXX in black and white adults: the @entity731 risk in communities study: 1987-1998.

@entity1 @entity6 @entity28 @entity2690 @entity4053 @entity164 @entity731 @entity413
OBJECTIVE: In this study, we tested the hypothesis that @entity4053 serum @entity2690 is higher in nonobese black adults than in white adults and that high @entity4053 @entity2690 predicts @entity164 2 @entity6 equally well in both groups. RESEARCH DESIGN AND METHODS: At the baseline examination (1987-1989) of the @entity731 Risk in Communities Study, @entity4053 @entity2690 and BMI were measured in 13,416 black and white @entity1 and @entity1 without @entity6 . @entity1 were examined at years 3, 6, and 9 for incident @entity6 based on @entity4053 @entity413 and American @entity6 Association criteria. RESULTS: Fasting @entity2690 was 19.7 pmol/l higher among nonobese (BMI <30 kg/m(2)) black @entity1 compared with white @entity1 (race and @entity28 interaction term, P < 0.01). There were no differences among @entity1 . Among nonobese @entity1 , the relative risk for developing @entity6 was similar between racial groups: 1.4 (95% CI 1.2-1.5) and 1.3 (1.2-1.4) per 60 pmol/l increase in @entity2690 (P < 0.01) for black and white @entity1 , respectively (interaction term, P = 0.6). Findings were similar among @entity1 . Adjusting for established risk factors did not attenuate this association. CONCLUSIONS: Nonobese black @entity1 have higher @entity4053 @entity2690 levels than nonobese white @entity1 , and @entity4053 @entity2690 is an equally strong predictor of @entity6 in both groups. These results suggest one mechanism to explain the excess incidence of @entity6 @entity1 but do not explain the excess among black @entity1 . Future research should evaluate additional factors: genetic, environmental, or the combination of both, which might explain higher @entity4053 @entity2690 among black @entity1 when compared with white @entity1 .
