Lakoski et al1 recently reported on data from the Coronary Artery Risk Development in Young Adults (CARDIA) Study regarding the association between C-reactive protein (CRP) concentration and incidence of hypertension. The association reported in crude analysis was no longer significant after adjusting for body mass index (BMI) (calculated as weight in kilograms divided by the square of height in meters). In fact, we believe that it was an expected finding because CRP concentration likely reflects obesity. Recent new insights into the relation between obesity and inflammatory activation show that obese individuals have larger adipocytes and consequently a larger amount of macrophages present.2 Within a representative sample of Portuguese adults, in subjects with a CRP concentration of 1 mg/dL or less and no hypertension at baseline (n = 476) high-sensitivity CRP was associated with increasing BMI, both in men (Spearman correlation, 0.34; P<.001) and women (Spearman correlation, 0.34; P<.001), and the association was even stronger with fat mass (assessed by bioimpedance), particularly among women (Spearman correlation, 0.48 [P = .004] in men and 0.70 [P<.001] in women). In this sample, after a median 4.4 years’ follow-up, the incidence of hypertension was also significantly associated with CRP levels and attenuated and nonsignificant after adjusting for BMI, as in the CARDIA Study (Table 1). When cross-classifying subjects according to CRP concentration and BMI, as shown in Table 2, increasing CRP concentration was still associated with incident hypertension in overweight and obese individuals, but this may result from residual confounding by obesity within each broad class of BMI and CRP categories. It would be most interesting to assess these associations with longitudinal data beginning in childhood, in which case one would be able to appreciate the temporal sequence between obesity, inflammatory activation, and incident hypertension.
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