In this ARIC analysis, blacks had about two to three times higher incidence rates of ischemic stroke compared to whites in each obesity quintile. However, obesity, regardless of the measure, was a risk factor for ischemic stroke, without statistical evidence for differences by race or sex.
For whites, ARIC findings were consistent with most previous studies. Prior studies in blacks have shown less association of obesity with stroke, except for the Northern Manhattan Stroke Study which found that obesity defined as a high sex-specific WHR was significantly positively associated with ischemic stroke incidence.13
The Black Pooling Project, a meta-analysis of cohort studies using individual data, did not find association between BMI and stroke mortality in blacks (incidence not examined).24
The unadjusted prevalence of obesity defined by sex-specific WHR did not differ among black ischemic stroke cases and controls in the South London Stroke Register Study25
though the controls were seven years younger than the cases, and included more women (64% versus 52%). Finally, the lowest BMI quartile was associated with a surprisingly higher non-hemorrhagic stroke incidence in the NHANES Epidemiologic Follow-up Study (NHEFS).11
One of the reasons for the discrepancy between ARIC and NHEFS, a cohort study like ours, may be differences in the average degree of obesity. The median BMI values of black women (29.8 kg/m2
) and men (27.1 kg/m2
) at baseline (1987-89) in ARIC were 2.5 kg/m2
greater than those at baseline (1971-75) in NHEFS (27.4 kg/m2
in women and 24.5 kg/m2
in men). The rightward shift of the BMI distribution in blacks over the decades, which was greater than in whites (0.2 and 1.3 kg/m2
increase in white women and men, respectively) may account for significant positive association between BMI and ischemic stroke incidence in ARIC blacks. Further, NHEFS included only 955 blacks compared to 3,694 in the present study, which made our analysis more powerful. In addition, about half of NHEFS participants were aged 65 to 74 at baseline in contrast to ours that included only 45 to 64 years old at baseline. The older age distribution, with possible impact of weight loss in the elderly, might have distorted BMI-stroke association in NHEFS.26
Based on the fact that we consistently found positive associations between obesity measures and ischemic stroke incidence in blacks in the present study, we believe that obesity, however it is measured, significantly increases ischemic stroke risk in blacks as well as in whites. From a public health point of view, the estimated PAF values suggested that 18-20% of ischemic stroke occurrence may be accounted for by BMI >=28.1kg/m2
, waist circumference >=100 cm, or WHR >=0.95. We are aware of debates on PAF calculation methods.23, 27, 28
In the present study we defined the obese group as top 40% of each obesity-measure and calculated the PAF using a multivariate (Model I) adjusted HR23
. Since disease risk in relation to obesity measure is expected to be continuous, misclassification due to the selection of a certain cutoff points is likely to underestimate PAF.29
Although there might be possible inaccuracies related to the method employed to calculate PAF, we considered such errors would not be critical.
In all race-sex groups, significant positive associations of obesity measures with ischemic stroke incidence were largely explained by mediators related to obesity. In fact, either blood pressure or diabetes mellitus alone in Model II could have eliminated significant associations between obesity measure quintiles and ischemic stroke incidence. Yet, obesity did not fully account for the higher blood pressure and stroke risk of blacks compared to whites. For example, the mean systolic blood pressure in the lowest quintile of BMI in blacks was comparable to the systolic blood pressure in the highest quintile in whites (125.2 versus 126.3 mmHg).
Hypertension did not modify the associations of obesity measures with ischemic stroke incidence. In other words, in subjects both with or without hypertension, there were significant positive associations between obesity measures and ischemic stroke incidence. These associations were, however, significantly attenuated with additional adjustment for systolic blood pressure. Given the strong association between obesity and hypertension and other risk factors including diabetes mellitus, obesity would be an important target for the prevention of ischemic stroke.
Strengths of the present study included the prospective design; large sample size and number of ischemic strokes which allowed race-sex specific analyses; the long duration of follow-up, systematic surveillance and confirmation of outcome events; the detailed assessment of potential confounding and mediating variables; and the standardized recording of multiple obesity measures. As a limitation, although our goal was a careful description of ischemic stroke incidence using anthropometric measurements relevant in the field of public health, formal comparison among these measures for the prediction of ischemic stroke should be considered. Second, most of the blacks were from one field center and the whites from three other centers, limiting the generalizability of our findings to other cultural or socio-economic contexts.
In conclusion, the degree of obesity defined either by BMI, waist circumference or WHR was a significant risk factor for ischemic stroke incidence regardless of sex or race. Prevention and control of obesity has a potential to reduce the incidence of ischemic stroke.