Overactive Bladder as a Bioenergetic Disorder: A Sex‐Convergent Mitochondrial–Oxidative Framework

ABSTRACT Aims Overactive bladder (OAB) is an urgency‐based symptom syndrome that increases with aging in both sexes, but its explanations remain fragmented around benign prostatic hyperplasia/bladder outlet obstruction in men, menopause/estrogen loss in women, and metabolic, sleep‐related, or neurogenic mechanisms. We examine whether these diverse associations can be organized within a sex‐convergent mitochondrial–oxidative framework while distinguishing OAB from urodynamic detrusor overactivity (DO) and broader lower urinary tract dysfunction (LUTD). Methods This hypothesis‐generating Debate article was informed by a targeted narrative search of PubMed/MEDLINE and citation chaining through August 2026. We prioritized direct human lower urinary tract studies, validated symptom or urodynamic phenotypes, causal animal models, and bladder intervention studies; evidence extrapolated from non‐bladder tissues was treated as indirect. Results Evidence supports mitochondrial–oxidative injury in selected bladder ischemia, obstruction, diabetes, aging, and sex‐hormone‐deprivation models, with limited human associations. Diverse upstream exposures may converge on candidate detrusor–urothelial dysfunction, but direct comparative male–female evidence is lacking. Sleep–circadian/endocrine disruption is the most speculative arm; autonomic dysregulation is considered a parallel, potentially interacting route rather than a consequence of mitochondrial dysfunction. Existing OAB treatments may also alter afferent, smooth‐muscle, or neural signaling. The framework therefore generates testable predictions rather than asserting a universal lesion. Conclusions Age‐related OAB may be usefully examined through a bioenergetic framework that integrates detrusor, urothelial, vascular, metabolic, hormonal, and neural influences. Mitochondrial–oxidative dysfunction should currently be regarded as a candidate contributor rather than a universal final pathway, requiring direct bladder‐level and sex‐comparative validation.