Conroy SM, et al. – This study is performed to better comprehend the pathogenesis of inflammatory–related diseases after menopause, researchers study the adiposity–independent relationship between endogenous sex hormones and C–reactive protein (CRP), a biomarker of inflammation. Prospective and systems epidemiological studies are needed to comprehend whether or not the cross–sectional associations they observed, independent of adiposity, between CRP–SHBG, CRP–total testosterone, and CRP–free estradiol, are causal.

Methods

• For this study, they conducted a secondary, cross–sectional analysis.
• In this study, they examine the baseline data from the Alberta Physical Activity and Breast Cancer Prevention Trial (2003–2007).
• Total 319 healthy, postmenopausal women not utilizing hormone therapy were enrolled in this study.
• Multivariable linear regression models associated serum CRP levels to estrogens, androgens, and sex hormone–binding globulin (SHBG), all on the natural logarithmic scale.
• Models were adjusted for age, lipids, medication, and former menopausal hormone therapy use, and also for adiposity (body mass index [BMI], per cent body fat [via whole–body dual x–ray absorptiometry], or intra–abdominal fat area [via computed tomography]).

Results

• Without adiposity adjustment, estrone, total estradiol, and free estradiol were significantly positively connected with CRP, whereas SHBG was significantly inversely connected with CRP.
• Of all adiposity measures, adjustment for BMI caused the greatest attenuation of CRP–estrogen associations; only free estradiol (β = 0.24, 95% confidence interval [CI] 0.06, 0.43) and SHBG (β = –0.37, 95% CI –0.60, –0.13) associations remained significant.
• Inverse associations between CRP–total testosterone became stronger with BMI adjustment (β = –0.20, 95% CI –0.40, –0.01).
• Differential relationship across categories of BMI, former hormone therapy utilization, and years since menopause were suggestive, but not statistically important (Pheterogeneity > 0.05).