Associations of estimated glucose disposal rate and overactive bladder and the potential mediating role of systemic inflammation: NHANES 2005–2018

Abstract Background Insulin resistance (IR) is linked to overactive bladder (OAB), with chronic inflammation serving as a common pathophysiological mechanism in both conditions. As a robust marker of IR, estimated glucose disposal rate (eGDR) was selected as the exposure variable to examine its relationship with OAB, with a specific focus on the mediating role of inflammation. Methods We conducted a cross-sectional study using data from the 2005–2018 National Health and Nutrition Examination Survey (NHANES). We utilized weighted logistic regression to assess the association of eGDR with OAB, while restricted cubic splines (RCS) helped characterize potential nonlinear patterns in this relationship. Subgroup analyses and interaction tests were performed to assess heterogeneity in the eGDR-OAB association across different subgroups. Mediation analysis was used to explore whether systemic inflammatory biomarkers statistically explain part of the eGDR-OAB association, while acknowledging that causal inference is limited by the cross-sectional design. Results 31,351 participants were included in this study, of whom 6,356 (20.27%) were diagnosed with OAB. In the fully adjusted Model, each one-unit increment in eGDR was associated with a 11% reduction in OAB risk (OR = 0.89; 95% CI: 0.87–0.91; P < 0.001) and a 48% decreased risk of OAB for the highest eGDR quartile (Q4) compared to the lowest quartile (Q1) (OR = 0.52; 95% CI: 0.42–0.64; P < 0.001). RCS analysis showed a significant nonlinear inverse association between eGDR and OAB, and this association was consistently observed across nearly all subgroups. Mediation analyses revealed that systemic inflammatory biomarkers statistically mediated the relationship between eGDR and OAB, explaining approximately 0.64–3.15% of the total effect, suggesting that inflammation accounts for only a small fraction of the eGDR–OAB association, while other mechanisms (e.g., autonomic dysfunction, microvascular damage, urothelial changes) likely contribute more substantially. Conclusions Our research confirmed the correlation between eGDR, inflammation and OAB. The potential mediating effect of inflammation between eGDR and OAB provides a meaningful direction for future research and targeted interventions.