Overactive bladder (OAB) is a chronic lower urinary tract dysfunction syndrome characterized by symptoms such as urinary urgency, urinary frequency and nocturia, which seriously affects patients’ quality of life and psychological health (1). The global prevalence is about 10%–16%, and the prevalence of OAB is on the rise with the aging of the population (2). According to epidemiologic estimates, more than 460 million adults worldwide are afflicted by OAB, and its direct medical costs and indirect economic burden are increasing each year, with associated health expenditures projected to increase by 42% by 2030 (3). The pathogenesis of OAB is complex and involves a multifactorial interaction of bladder sensory nerve abnormalities, detrusor overactivity, and imbalance of central nervous system regulation (4). In addition to non-modifiable risk factors such as age and gender, lifestyle factors, such as fluid intake patterns and sedentary habits, have been shown to be strongly associated with symptom exacerbation in OAB (5, 6), suggesting that intervening with these modifiable behavioral factors may be an important direction in the management of OAB.

Behavioral therapy is the first-line treatment strategy for OAB, and studies have shown that lifestyle modifications such as bladder training and fluid management are effective in relieving symptoms in 30%–50% of patients (7, 8). In recent years, more and more studies have begun to focus on the potential impact of sleep on bladder function, which is considered to be a central aspect of circadian rhythm regulation and may play an important role in bladder function through the neuro-endocrine-immune axis (9). Clinical observations have found that abnormal sleep duration is closely associated with increased frequency of nocturia and decreased bladder capacity (10, 11), while sleep disorders such as insomnia and sleep apnea, which are linked to sympathetic activation and can also exacerbate headaches and orofacial pain, may further destabilize the urethral muscle (12–14). In addition, there may be a bidirectional relationship between sleep quality and OAB symptoms: increased frequency of nocturia may lead to sleep fragmentation, while sleep deprivation may exacerbate sensory hypersensitivity of the bladder through elevated levels of inflammatory factors (e.g., IL-6, TNF-α) (15).

However, existing studies have mainly focused on a single sleep dimension, with fewer systematic explorations of the combined effects of sleep duration and sleep disorders. Despite the growing interest in the potential value of sleep health in the management of OAB, there is still a lack of cross-sectional evidence based on large sample populations to elucidate the independent and synergistic effects of sleep duration and sleep disorders on OAB. Therefore, using data from a nationally representative health survey, this study is the first to comprehensively assess the association patterns between sleep duration and sleep disorders and the risk of OAB, aiming to provide a new scientific basis for multidimensional behavioral interventions for OAB. We hypothesize that both short and long sleep durations are associated with an increased risk of OAB, and that this effect is modified by the presence of sleep disorders.

This study explored the non-linear association between sleep duration and overactive bladder (OAB) risk using NHANES 2005–2018 data. Restricted cubic spline (RCS) analysis revealed a significant non-linear relationship (P < 0.001), with an inflection point identified at 6 h. Specifically, among individuals with sleep durations of less than 6 h, the risk of OAB decreased as sleep duration increased (OR = 0.94). In contrast, prolonged sleep duration (> 6 h) was progressively associated with higher OAB risk (OR = 1.60, 95% CI: 1.56–1.65, P < 0.001). This U-shaped pattern was further supported by a segmented linear regression model, which confirmed the threshold effect at 6 h.

While Table 3 presents results from categorical logistic regression based on predefined sleep duration groups, the evidence for a non-linear U-shaped association was primarily derived from the RCS and threshold effect models (Figure 2 and Table 4). These methods allowed for a more flexible and detailed characterization of risk across the full spectrum of sleep duration—capturing trends that may not be evident in categorical comparisons alone.

These findings are consistent with previous studies emphasizing the critical role of sleep quality in OAB risk. For example, Lu et al. reported a significantly higher risk of OAB in individuals with poor sleep patterns (OR = 1.38), a finding consistent with our finding of sleep disruption as a risk factor for OAB (20). In addition, Ge et al. (21) associated sleep disruption with more severe OAB symptoms, while Cheng et al. documented a synchronization of increased sleep disorders with increased prevalence of OAB among men in the United States (22, 23). However, unlike these studies, studies focusing on specific populations, such as Guzelsoy et al. and Clerget et al. have focused on hypoxia-driven OAB in patients with obstructive sleep apnea (OSA) (24). In contrast, our population-based study identified sleep disorders as an independent risk factor for OAB, suggesting that there may be broader mechanisms beyond OSA-associated hypoxia, such as circadian rhythm disruption or autonomic dysfunction.

An innovative aspect of this study was the identification of a threshold of 6 hours of sleep duration, a finding that has not been previously reported in epidemiologic studies. Unlike intervention-based studies, such as Mirzayeva et al. who observed linear improvements in the relief of nocturnal urinary frequency with Briverm treatment and Li et al., who included sleep in a composite index of cardiovascular health (LE8), the non-linear association we found emphasizes the dual role of sleep duration in the pathophysiology of OAB that may reflect differences in biological pathways between short and long sleep duration (20, 25). These new insights expand our understanding of sleep-OAB interactions and highlight the need for personalized interventions targeting sleep quantity and quality in reducing the burden of OAB.

The observed non-linear association between sleep duration and OAB risk may be attributed to different physiologic mechanisms operating at different sleep thresholds. Short sleep duration (< 6 h) may cause sympathetic nervous system (SNS) overactivity, which may paradoxically inhibit urethral muscle overactivity in the acute phase through β3-adrenergic receptor-mediated bladder relaxation, as shown by sleep deprivation in animal models (26). However, chronic sleep restriction may disrupt neurotransmitter homeostasis, particularly serotonin and dopamine, which are critical for regulating bladder afferent signaling and central inhibitory pathways (27, 28). Conversely, prolonged sleep may reflect underlying systemic inflammation or circadian rhythm misalignment. Elevated levels of pro-inflammatory cytokines (e.g., IL-6, TNF-α) associated with excessive sleep have been shown to increase bladder permeability and sensitize afferent nerves, which may exacerbate OAB symptoms (29, 30). Further, circadian rhythm misalignment due to irregular sleep-wake patterns may impair hypothalamic regulation of bladder function, including control of urinary aquaporin-2 channels and nocturnal urine production in the supraoptic nucleus (31–33). These bidirectional mechanisms highlight the complexity of the role of sleep duration in the pathophysiology of OAB.

In addition to the findings on the U-shaped relationship between sleep duration and overactive bladder (OAB), it is important to note that sleep hygiene guidelines generally recommend a minimum of 7 h of sleep per night for optimal health. Consistent with current sleep recommendations, this amount of sleep is essential for restorative functions, including physical recovery and cognitive performance, and may play a role in managing OAB symptoms. Sleep durations shorter or longer than this threshold can potentially disrupt physiological processes, contributing to various health issues, including bladder dysfunction.

Furthermore, the subgroup analyzes shown in Figure 3 revealed a complex relationship between sleep duration and OAB risk, which was significantly moderated by age, diabetes status, and drinking habits. Firstly, the moderating effect of age may be closely related to physiological changes during aging. With aging, the body’s metabolic and neuroregulatory capacity gradually declines, especially in the control of urinary tract and the regulation of nocturnal awakenings. The higher risk of OAB in people over 60 years of age may be due to the circadian clock misregulation and nervous system dysfunction caused by aging (34), which makes the effect of sleep on bladder function more significant. The weakening effect of diabetes on the relationship between sleep and OAB may be related to the dysfunction of autonomic nervous system caused by diabetes. Diabetic patients are often accompanied by neuropathy, especially in the sensory and motor nervous systems of the bladder, resulting in reduced sensitivity and functional regulation of the bladder (35), thereby weakening the effect of sleep on the risk of OAB. In addition, metabolic dysregulation in diabetic patients may further affect the physiological mechanisms of nocturnal urine production and excretion (36). In terms of drinking status, the significant association among moderate drinkers may be related to the effect of alcohol on sleep quality. Alcohol can aggravate OAB symptoms by disrupting the structure of sleep, especially during deep sleep and rapid eye movement (REM) sleep stages (37). The diuretic effect of alcohol may also exacerbate frequent urination at night and increase the risk of OAB (38). However, although the association with OAB was stronger between heavy drinkers and never drinkers, the difference in effect size suggests that drinking frequency and the effects of alcohol on the neuroendocrine system have an important modulatory role (39).

The positive association between sleep disorders and OAB risk may involve interrelated pathways in the neuroendocrine and autonomic nervous systems. Sleep disorders such as insomnia or OSA persistently activate the hypothalamic-pituitary-adrenal (HPA) axis, leading to elevated levels of cortisol and catecholamines, which may directly potentiate the excitability of bladder afferent nerves and the contractility of the forced urethra (40). In OSA, intermittent hypoxia-reoxygenation cycles induce oxidative stress and endothelial dysfunction, which may damage bladder neuromuscular junctions and promote overactivity (41). In addition, sleep fragmentation disrupts thalamo-cortical pathways responsible for regulating bladder sensation during non-rapid eye movement sleep, thereby lowering the threshold of awareness of urinary urgency (42). Neuroimaging studies further suggest that chronic sleep disorders alter functional connectivity between the insular cortex, which is associated with visceral perception, and the prefrontal cortex, which is responsible for inhibitory control, potentially amplifying the importance of bladder signaling (43–45).

This study explored the relationship between sleep duration and OAB while controlling for key confounders. However, several limitations must be considered. First, OAB diagnosis was based on symptomatic criteria, not urodynamic validation, which may lead to misclassification of bladder disorders. Second, self-reported sleep duration is prone to measurement errors, with participants often overestimating or underestimating their sleep by 30–60 min. This could lead to non-differential misclassification, especially in individuals with sleep disorders or chronic conditions. If the error is systematic in the OAB group (e.g., individuals with nocturnal urgency reporting shorter sleep), it may introduce bias. Moreover, although we utilized the harmonized SLQ012 variable to maintain consistency in sleep duration measurement across all NHANES cycles, it is important to acknowledge the underlying heterogeneity in the original data collection methods. Earlier cycles (2005–2014) directly asked participants to report their usual sleep duration in whole hours, whereas later cycles (2015–2018) estimated sleep duration based on reported bedtimes and wake-up times. Although SLQ012 standardizes these inputs, variations in data precision and recall bias may introduce subtle misclassification or measurement error. Future studies using objectively measured sleep duration (e.g., actigraphy) are needed to validate these findings. Additionally, due to the cross-sectional design, causality cannot be determined. OAB may cause nocturnal awakenings and shorter sleep, or longer sleep may result from health deterioration associated with OAB. This reverse causality could explain the “short sleep ? lower OAB risk” relationship observed in our study. Future prospective cohort studies with objective sleep measurements (e.g., actigraphy or polysomnography) and standardized urodynamic assessments are needed to clarify the causal relationships between sleep and OAB.

This study reveals a significant U-shaped non-linear relationship between sleep duration and the risk of overactive bladder (OAB). Specifically, individuals with sleep durations of less than 6 h exhibited a reduced risk of OAB, while those with prolonged sleep durations (≥ 9 h) had a significantly higher risk. These findings underscore the importance of managing sleep patterns as part of the clinical approach to OAB.

Given the clinical implications, it is crucial to consider both sleep quality and duration when evaluating and managing OAB in patients. Behavioral interventions, such as sleep hygiene education, could be beneficial. Recommendations may include promoting a consistent sleep schedule, reducing caffeine and alcohol intake in the evening, and creating a comfortable sleep environment. Additionally, interventions like bladder training and fluid management can complement sleep-based treatments, potentially reducing the frequency and severity of OAB symptoms. Implementing these personalized sleep and behavioral interventions could significantly improve patient outcomes and enhance the overall management of OAB.