Modified allostatic load and stress urinary incontinence in women: Evidence from a hospital-based cohort and NHANES.

ObjectiveStress urinary incontinence (SUI) is common in women and is traditionally attributed to pelvic floor support failure and reproductive factors. However, emerging evidence suggests that systemic metabolic and inflammatory disturbances may also contribute to SUI. Modified allostatic load (MAL) integrates adiposity, blood pressure, glucose-lipid metabolism, and inflammation, but its association with SUI remains unclear. We examined this association in two independent cohorts.MethodsThis cross-sectional study included women from the Third Xiangya Hospital cohort (2017-2025) and the National Health and Nutrition Examination Survey (NHANES, 2005-2020). MAL was constructed from seven indicators: waist-to-height ratio, systolic and diastolic blood pressure, fasting glucose, triglycerides, high-density lipoprotein cholesterol, and white blood cell count. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Dose-response, subgroup, sensitivity, and model-comparison analyses assessed robustness and model discrimination.ResultsThe main analyses included 8,932 women from the Third Xiangya Hospital cohort and 4,964 women from NHANES. Higher MAL was consistently associated with higher odds of SUI. In the fully adjusted model, each 1-point increase in MAL was associated with 15% higher odds of SUI in both cohorts. Compared with Q1, the highest MAL quartile was associated with increased odds of SUI in the Third Xiangya Hospital cohort (OR 1.90, 95% CI 1.66-2.18) and NHANES cohort (OR 1.88, 95% CI 1.48-2.37). The fully adjusted models including MAL showed limited discrimination (AUCs 0.674 and 0.599); adding MAL increased the AUC only slightly (by 0.011 and 0.022). Results were robust in sensitivity analyses, including MAL based on common fixed thresholds.ConclusionsHigher MAL was consistently associated with higher odds of prevalent SUI in two independent female cohorts. These cross-sectional findings support a multisystem physiological dysregulation framework for understanding SUI but do not establish causality or longitudinal predictive utility.