The association between body composition and arterial stiffness: investigating the influence of inflammatory markers

Body fat distribution may influence arterial stiffness through inflammatory pathways, but evidence from relatively healthy adults and across complementary measures of arterial stiffness remains limited. This study investigated associations between bioelectrical impedance-derived body composition measures and arterial stiffness and assessed whether selected markers of inflammation and endothelial activation explained these associations.

This study utilized cross-sectional baseline data from the MEGA study, involving 219 healthy non-obese (BMI < 30 kg/m²) and obese (BMI ≥ 30 kg/m²) participants with a mean age of 46 ± 12 years. Exposures were visceral fat (L), total body fat (%), fat mass index (kg/m²), and fat-free mass index (kg/m²). Outcomes were carotid-femoral pulse wave velocity (cfPWV, m/s), augmentation index (AIx, %), and central pulse pressure (cPP, mmHg). Tumor necrosis factor-alpha, interleukin-6, and vascular cell adhesion molecule-1 were evaluated as potential intermediate factors. Multivariable linear regression used robust standard errors and false-discovery-rate-adjusted p-values. Mediation analyses examined associations between body composition, arterial stiffness, and inflammatory markers, using 5,000 bootstrap samples.

Visceral fat, total body fat, and fat mass index were positively associated with AIx: The adjusted regression coefficients were β = 0.642 (95% confidence interval, 0.172-1.112; p = 0.032) for visceral fat, β = 0.186 (95% confidence interval, 0.083-0.288; p < 0.001) for total body fat, and β = 0.333 (95% confidence interval, 0.157-0.508; p < 0.001) for fat mass index, respectively. No bioimpedance-derived measure was independently associated with cfPWV or cPP after correction for multiple testing and no indirect associations through inflammatory markers were found.

Higher visceral fat, total body fat, and fat mass index were associated with higher AIx, but the selected inflammatory markers did not explain these cross-sectional associations. Longitudinal studies with broader biomarker panels are needed before causal or clinical conclusions can be drawn.