Shift work and hormonal-circadian disruption raise urinary incontinence: a narrative review.

Background and Objective: Pelvic floor dysfunction (PFD) is a multifactorial condition that affects a large proportion of women, compromising urogenital support and producing symptoms such as urinary incontinence (UI). The structural and functional integrity of the pelvic floor depends on coordinated interactions among muscular, hormonal, and neuroendocrine systems. Evidence indicates that circadian misalignment, particularly in women exposed to night-shift work, sleep deprivation, and endocrine disruption, can influence pelvic floor physiology through melatonin suppression, cortisol dysregulation, and inflammatory activation. This review intends to synthesize current evidence on the links between circadian rhythm disruption, hormonal imbalance, and PFD, with specific emphasis on occupational shift work as a model of chronic chronobiological stress, highlighting their integrated pathophysiological mechanisms and preventive approaches. Methods: We conducted a narrative literature review using PubMed, Scopus, and Web of Science covering the period from January 2020 to October 2025. Studies investigating the relationship between circadian regulation, hormonal modulation, and pelvic floor function were included. Particular attention was given to research addressing melatonin and cortisol pathways, estrogen modulation, and occupational factors such as night-shift work, sleep deprivation, and physical overload. Eligible study designs included randomized controlled trials, observational studies (cross-sectional and cohort studies), translational and experimental research, and high-quality mechanistic reviews, defined by methodological rigor, comprehensive literature synthesis, and critical appraisal of evidence. Key Content and Findings: Circadian rhythm disruption-characterized by decreased melatonin secretion, altered cortisol levels, and increased oxidative stress-has been associated with inflammation, impaired muscle contractility, and delayed pelvic floor tissue repair. Beyond anatomical alterations, UI is increasingly recognized as a neuroimmunoendocrine disorder in which hormonal dysregulation contributes to tissue instability and loss of urethral support. Women exposed to night-shift work, sleep deprivation, or occupational overload show higher rates of involuntary urine loss, partly mediated by endocrine desynchronization and maladaptive voiding behaviors during chronically misaligned biological rhythms. Preventive measures include supervised pelvic floor physiotherapy, optimization of sleep hygiene, correction of work schedules, and local estrogen therapy when indicated. Chronobiological and immunomodulatory interventions have recently emerged as promising adjunctive strategies. Conclusions: Management of UI should move beyond a purely mechanical perspective toward an integrated model encompassing hormonal, metabolic, and behavioral modulation. Understanding the interactions among circadian rhythms, endocrine control, and pelvic tissue physiology may open innovative avenues for prevention and treatment, promoting precision-based, holistic care in women's health.