Decoding the gut-adipose-ovary axis in polycystic ovary syndrome: from metabolic dysregulation to oncological risk modulation.

Polycystic ovary syndrome (PCOS) is traditionally managed as a localized reproductive disorder, but emerging evidence redefines it as a systemic metabolic-endocrine continuum with profound long-term health implications. This review comprehensively synthesizes the pathogenic role of the nutrition-mediated "gut-adipose-ovary axis" in bridging PCOS-associated metabolic dysfunction with an elevated risk of gynecological malignancies. Aberrant nutritional intake acts as the primary environmental catalyst, driving gut microbiota dysbiosis and metabolic endotoxemia. These gut-derived signals provoke visceral adipose tissue dysfunction, initiating a self-reinforcing cascade of systemic insulin resistance, hyperandrogenism, and chronic low-grade inflammation. Crucially, the convergence of these systemic insults continuously remodels the localized ovarian microenvironment. By sustaining proliferative signaling, forcing metabolic reprogramming, and fostering immune evasion, these convergent insults may contribute to a permissive pre-neoplastic microenvironment in susceptible patients with PCOS. To dismantle this pathogenic network, we outline a multi-dimensional therapeutic framework that integrates precision nutrition, microbiome modulation, and targeted pharmacological agents. Ultimately, this systems-biology perspective mandates a paradigm shift in clinical practice: moving beyond empirical symptom palliation toward proactive, risk-stratified interventions that interrupt the disease continuum and reduce long-term oncological risk in appropriately stratified women with PCOS.