This study analyzed NHANES data to clarify the significant association between total FMI and regional FMIs (trunk FMI, arm FMI, and leg FMI) with OAB. We found that increases in total FMI and regional FMIs significantly increased the risk of OAB. This finding indicates that not only overall obesity but also the distribution of fat in different body regions significantly affects the risk of OAB. Even after adjusting for multiple confounding factors, these results remained statistically significant, indicating the robust independence of the relationship between regional body fat and OAB.

Adipose tissue functions not just as an energy storage unit but also as an active endocrine organ, releasing diverse metabolically active substances like leptin, adiponectin, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) [19, 20]. These substances regulate systemic metabolic processes and may affect bladder function through various pathways. Obese individuals have elevated leptin levels and decreased adiponectin levels in their blood [21,22,23]. Leptin and adiponectin not only affect energy balance and insulin sensitivity but may also influence bladder function directly by acting on bladder smooth muscle cells or indirectly through the central nervous system [24,25,26]. Increased leptin levels may lead to abnormal contraction of the detrusor muscle, causing OAB symptoms [27]. Chronic low-grade inflammation linked to obesity might also contribute significantly to the pathophysiology of OAB. Inflammatory factors such as TNF-α and IL-6 can activate various inflammatory signaling pathways, potentially leading to abnormal bladder smooth muscle and nerve function, resulting in symptoms such as urgency and frequency [28, 29].

Trunk fat accumulation (especially abdominal fat) is associated with metabolic syndrome and may mechanically increase intra-abdominal pressure, affecting bladder storage function [30]. Increased intra-abdominal pressure may reduce bladder capacity and promote abnormal detrusor activity, thereby increasing the risk of OAB. Additionally, abdominal fat accumulation may increase intra-abdominal inflammation levels, further affecting bladder function [31]. While arm and leg fat accumulation may have a smaller direct impact on intra-abdominal pressure, their metabolic and endocrine functions are equally important [32]. Limb fat accumulation may affect the overall metabolic state by secreting various metabolically active substances, indirectly influencing bladder function [33]. Moreover, limb fat accumulation may reflect overall obesity, which is also associated with the risk of OAB.

The distribution of adipose tissue may affect bladder activity by influencing the autonomic nervous system function. Studies have shown that obesity is associated with an imbalance between the sympathetic and parasympathetic nervous systems, both of which play vital roles in regulating bladder function [34, 35]. Specifically, abdominal fat accumulation may stimulate the sympathetic nervous system, leading to hyperactivity of the detrusor muscle and causing OAB symptoms [36]. Additionally, obesity may affect the pelvic nervous system, altering bladder sensory and motor functions [37, 38].

Our study found that female participants were more likely to develop OAB, which may be related to gender differences. Women are generally more likely than men to accumulate fat in the abdomen and lower limbs, which may lead to a higher susceptibility to the effects of regional body fat, increasing the risk of OAB [39, 40]. Moreover, hormonal fluctuations in women, particularly the decline in estrogen levels after menopause, may also affect fat distribution and bladder function, increasing the incidence of OAB [41, 42].

In our study, while most subgroups did not show significant differences in the incidence of OAB, individual subgroup analyses revealed notable exceptions, particularly among females and those categorized as ‘other races’, along with individuals with a higher BMI. These specific findings underline the importance of targeted clinical strategies to address these disparities. Personalized treatment approaches that consider these subgroup-specific susceptibilities could potentially enhance the management of OAB. For instance, interventions tailored to address the unique physiological and hormonal characteristics of women, culturally adapted strategies for diverse racial groups, and weight management programs aimed at reducing body fat in obese patients may significantly improve therapeutic outcomes.

The findings of this study carry significant clinical implications. First, measuring body fat distribution can be part of OAB risk assessment, providing a basis for early intervention in high-risk populations. For individuals with high regional body fat distribution, lifestyle interventions, nutritional adjustments, and appropriate physical activity can reduce the risk of OAB. Second, targeted reduction of trunk and limb fat accumulation may become a new strategy for preventing and treating OAB. Finally, understanding the relationship between regional body fat and OAB can help clinicians consider individual body fat distribution characteristics when treating OAB, allowing for more personalized treatment plans. For example, patients with high abdominal fat may need more aggressive lifestyle interventions and medication to reduce the occurrence and severity of OAB symptoms.

Although this study has several strengths, such as using a large sample size of NHANES data and accurate body fat measurements from DXA, there are still some limitations. Firstly, the cross-sectional nature of the study design precludes us from establishing causal relationships. While we have identified significant associations, the cross-sectional data only reflect a single moment in time, making it challenging to ascertain whether increased body fat precedes OAB or results from lifestyle changes following OAB diagnosis. This limitation is critical in interpreting our findings as indicative of potential links rather than direct causative pathways. Secondly, our use of DXA for measuring body fat does not allow us to distinguish between subcutaneous and visceral fat. This is a significant limitation given that these fat types are metabolically distinct and may differentially impact health. Visceral fat is often more closely linked with metabolic and inflammatory disturbances that could influence OAB, whereas subcutaneous fat might have less of a direct impact on the condition. The inability to differentiate between these fat depots limits our understanding of the specific pathways through which body fat may influence OAB and restricts the generalizability of our findings to broader implications about body fat distribution. Third, while our study employed rigorous statistical controls to adjust for a comprehensive range of confounding factors, the potential for residual confounding remains a concern. This may stem from unmeasured or imprecisely measured variables that could influence the observed relationships between regional body fat and overactive bladder symptoms. Additionally, the use of NHANES data, while providing a robust sample size and diverse demographic representation within the United States, does pose limitations in terms of global applicability. The findings derived from this dataset predominantly reflect the health dynamics of the U.S. population and may not be directly generalizable to other countries with different cultural, dietary, and healthcare landscapes. Lastly, our analysis, which reveals associations between regional and total body fat indices and the presence of OAB symptoms, must be interpreted with caution. It is essential to understand that these associations do not establish causality due to the intricate and multifaceted nature of OAB. The condition comprises various subtypes, each potentially driven by unique mechanisms influenced by body fat distribution. For example, increased abdominal fat may heighten intra-abdominal pressure, exacerbating symptoms such as urgency and frequency. This mechanical effect could influence bladder outlet obstruction differently compared to how metabolic factors associated with obesity might affect detrusor overactivity or bladder hypersensitivity.

To deepen our understanding of how regional body fat contributes to OAB, it is imperative that future studies delve into the molecular and physiological pathways potentially mediating this relationship. Investigating the roles of adipokines such as leptin and adiponectin, which are significantly modulated by body fat distribution, could provide critical insights. Leptin, often elevated in individuals with higher amounts of visceral fat, has been implicated in promoting inflammation and may influence bladder signaling pathways, potentially exacerbating OAB symptoms. Conversely, adiponectin, typically lower in individuals with obesity, could play a protective role that might be compromised in the presence of OAB. Additionally, accurate differentiation between subcutaneous and visceral fat is essential for clarifying their respective impacts on OAB. Advanced imaging techniques such as MRI or CT scans should be employed to precisely correlate specific fat depots with OAB prevalence and severity, thereby providing a clearer picture of the causal relationships. Integrating these findings with longitudinal studies that track changes in body fat and OAB symptoms over time is crucial. Such studies would not only validate the associations found in cross-sectional studies like ours but also help establish a temporal sequence of events. This approach will clarify whether changes in body fat distribution precede the development of OAB or occur as a consequence of the condition. Moreover, expanding this research to include non-U.S. populations is vital. It will enhance the external validity of our results and provide insights into the global applicability of our findings, ensuring that our research contributions are relevant and beneficial for diverse demographic settings. By aligning these approaches, future research can effectively address the gaps identified in our study, offering a comprehensive understanding of the complex interactions between body fat distribution and OAB. We believe this integrated approach will substantially contribute to the field, guiding targeted interventions and informing clinical management strategies for OAB influenced by body fat.

In summary, this study uncovered a noteworthy link between regional body fat and OAB risk through the analysis of extensive epidemiological data. These findings not only enrich our understanding of the etiology of OAB but also provide new ideas for clinical prevention and treatment. Future research should continue to explore the mechanisms of regional body fat and verify these results in different populations to further advance the prevention and treatment of OAB.