In this cross-sectional study, a nationally representative sample of women in the United States, ≥ 20-years-old, overweight and obese, as indicated by higher VAI scores, was associated with an increased likelihood of SUI after adjusting for demographic and health-related covariates. Additionally, this risk was further increased among participants with eGFR ≥ 60 mL/min/1.73m2.

The association between SUI and obesity has been shown by some studies [14, 15]. Also, the impact of metabolic syndrome and dyslipidemia on urinary incontinence development has been examined [16, 17]. A systematic review by Hunskaar et al. showed that being overweight and obese is a strong risk factor for urinary incontinence [17]. The study suggested that intra-abdominal pressure increases with excess body weight, bladder pressure, and urethral mobility, leading to SUI and also exacerbating detrusor overactivity. Moreover, the prolonged effect on the pelvic musculature, nerve supply, and supporting structures due to chronic strain may cause pelvic floor muscle weakness and negatively impact pelvic organ function.

It has been hypothesized that oxidative stress related to adipose tissue increases the prevalence and severity of urinary incontinence by altering collagen metabolism. Visceral adipose tissue is an endocrine organ. In overweight and obese people, the secretion of inflammatory cytokines and factors, such as tumor necrosis factor-alpha (TNF-a) and interleukin-6 (IL-6), is unbalanced [18]. Leptin activates the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, stimulates the production of reactive oxygen species (such as hydrogen peroxide, H2O2), also increases oxidative stress in obesity [19]. Liu et al. showed that exogenous H2O2 has a bidirectional regulatory effect on collagen metabolism [20]. After incubation with human uterosacral ligament fibroblasts in vitro for 24 h, lower concentrations of H2O2 stimulated the anabolism of collagen type 1 alpha 1 (COL1A1), while higher concentrations of H2O2 promoted catabolism. Notably, with the increase in oxidative stress, the upregulation of transforming growth factor-beta 1 (TGF-b1) and proteolytic enzymes, such as matrix metalloproteinase-2 (MMP-2), promotes collagen catabolism. The results showed that oxidative stress leads to the disorder of collagen metabolism in human pelvic fibroblasts. Therefore, the physiological and biochemical stress of obesity on the neuromuscular system of the pelvic floor might lead to the development of urinary incontinence [21].

BMI is applied to define overweight and obesity in epidemiological studies. However, it is a poor estimate of overall obesity because it cannot distinguish between lean and fat mass and the types of adipose tissue depots, such as visceral and subcutaneous storage [22]. Conversely, several studies have shown that visceral adipose tissue and low lean mass, independent of BMI, are associated with a high risk of SUI [23]. In summary, additional studies are required to understand the biological basis of the obesity paradox [24]. Relying only on BMI to assess the prevalence of obesity could hinder future interventions aimed at the prevention and control of SUI. As an index of adipose tissue dysfunction, VAI has gradually been used as a surrogate marker associated with all metabolic syndrome factors [10]. It indirectly reflects non-classical risk factors, such as altered production of adipocytokines, increased lipolysis, and plasma free fatty acids, which are independent of BMI, WC, TG, and HDL, respectively. On the other hand, obesity leads to insulin resistance, which in turn adversely affects the lipid ratio, resulting in lower HDL cholesterol and higher triglycerides and LDL cholesterol in the blood. These suboptimal cholesterol ratios may lead to the accumulation of atheromatous deposits in the bladder wall, resulting in bladder wall ischemia, urothelial dysfunction, and increased risk of SUI [11]. Therefore, VAI may be a valuable indicator of fat distribution and function. Some recent studies confirmed that VAI is significantly associated with SUI [9, 23]. In the current study, a 44% increase was noted in the incidence of SUI in the highest compared to the lowest VAI group.

Unlike the previous studies, we used a large sample to evaluate the association between VAI and SUI and adjusted for critical variables based on previous studies and expert recommendations. We also performed sensitivity analyses, including different SUI severities as outcome variables. On the other hand, multiple imputations for covariates did not alter the association between SUI and VAI, suggesting that our results are robust and reliable.

Nevertheless, the present study had some limitations. The current data were obtained from a cross-sectional and observational study. Therefore, it was impossible to infer the causal correlation and calculate the incidence of SUI. Since most data were collected in the form of questionnaires, there may be a recall bias. Another limitation was determining the subjects treated with SUI because this information would help determine the limitations of urological treatment. Furthermore, the respondents could not accurately distinguish between UUI and SUI. However, previous studies reported that the accurate answer to the incontinence question was similar to that in the NHANES questionnaire. Due to the limitations of NHANES, we did not conduct a strict severity grading of SUI. The categorization of different SUI in this article is merely part of a sensitivity analysis, thus the conclusions cannot be linked to the severity of SUI. Moreover, this study was only conducted among women, and cannot be extrapolated to the male population. Finally, missing data led to the deviation in our sample; however, only a small subgroup had missing data. Next, we conducted data imputation as a sensitivity analysis to ensure the robustness of the results.