A proposed psychometabolic endotype of polyendocrine metabolic ovarian syndrome: bidirectional interplay between psychological distress, eating dysfunction, sleep disruption, chronic stress, and metabolic deterioration.

Background: Polycystic ovary syndrome was renamed polyendocrine metabolic ovarian syndrome (PMOS) in 2026 to better represent its multisystem biology. Psychological distress, eating dysregulation, sleep disturbance, and metabolic dysfunction frequently coexist, yet clinical care and research commonly treat them as parallel comorbidities. Objective: To define the proposed psychometabolic construct operationally; position it relative to conventional phenotypes and data-driven clusters; and grade evidence for association, temporal prediction, causation, and treatment response across psychological, behavioral, sleep-stress, neuroendocrine, and metabolic pathways. Methods: We conducted a targeted narrative review of PubMed/MEDLINE from inception through 15 September 2026. Seven structured topic blocks returned 1,278 records, 1,009 unique identifiers after PubMed identifier (PMID)-based deduplication, and 1,008 retrievable article records for title/abstract screening. Guidelines, systematic reviews, longitudinal or causal studies, trials, and informative human mechanistic studies were prioritized; general-population and preclinical evidence was used only when its indirectness was explicit. Evidence synthesis: Depression and anxiety, body-image concerns, binge- and bulimia-spectrum symptoms, poor sleep, and obstructive sleep apnea are reported more often in PMOS than in comparison populations, but most estimates are cross-sectional and heterogeneous. One tertiary cohort found that baseline depression and/or anxiety history predicted incident metabolic syndrome over a median seven years (adjusted hazard ratio 1.45, 95% confidence interval 1.02-2.06); this supports prognostic enrichment, not causality. General-population longitudinal and genetic studies support reciprocal depression-metabolic relationships, whereas PMOS-specific causal evidence is inconsistent. Plausible links include insulin-androgen-adipose interactions, neuroactive steroid signaling, ovarian sympathetic input, sleep fragmentation, stress and autonomic regulation, reward-related eating, treatment exposure, stigma, and social context. None validates a discrete endotype. Conclusions: We define a candidate psychometabolic endotype as a cross-cutting, mechanistically coupled pattern that may occur within any conventional PMOS phenotype. Clinical co-occurrence is only an entry profile; endotype status requires replicated longitudinal coupling, incremental prognostic value, interpretable transitions, and preferably treatment-effect heterogeneity. Four overlapping prototypes are working formulations rather than subtypes. A six-step clinical pathway centers shared formulation and nests care-intensity tiers within treatment selection.