Abstract 3905: Genetic and Environmental Influences on Inflammatory Markers: A Study of Middle-Aged Male Twins
Introduction: Little is known about the relative influence of genetic and environmental contributions on inflammatory biomarkers, and to what extent correlations among these markers are due to genetic or environmental factors.
Methods: We performed univariate and multivariate genetic analyses of four inflammation markers, interleukin-6 (IL 6), soluble IL-6 receptor (sIL-6R), C-reactive protein (CRP), and fibrinogen, in 154 (82 monozygotic and 72 dizygotic) middle-aged male twin pairs free of symptomatic CHD. Inflammatory markers were measured in plasma. Traditional CVD risk factors such as smoking, hypertension, and lipids were also obtained.
Results: The mean age of the twins was 54 years (age range: 47–57 years). Heritability was substantial for CRP (0.61, 95% CI: 0.46 – 0.72) and moderate to fair for IL-6 (0.29, 95% CI: 0.09 – 0.46), sIL-6R (0.55, 95% CI: 0.32–0.91) and fibrinogen (0.52, 95% CI: 0.31–0.67). Significant correlations were found between IL-6, CRP and fibrinogen, but not for sIL-6R. Multivariate genetic analysis found that these correlations could be best explained by a common pathway model, where the common additive genetic factor could explain, respectively, 10%, 29% and 9% of the variance for each marker (Table⇓). Genetic contributions explained 39% (95% CI: 6%–64%) of the correlation between IL 6 and CRP, and 44% (95% CI: 11%–67%) of the correlation between CRP and fibrinogen. After adjusting for covariates known to influence inflammation levels, including age, BMI, physical activity, smoking status, history of CHD, hypertension, and diabetes, heritability estimates were slightly decreased but the overall results remained similar.
Conclusion: Inflammatory markers are highly heritable and their covariation is due, in part, to common genes.