Nutritional Management of Polyendocrine Metabolic Ovarian Syndrome: Current Evidence on Dietary Strategies, Supplementation, and Lifestyle Support.

Polyendocrine metabolic ovarian syndrome (PMOS), formerly known as polycystic ovary syndrome (PCOS), is a heterogeneous endocrine and metabolic disorder associated with reproductive dysfunction, hyperandrogenism, insulin resistance, chronic low-grade inflammation and an increased risk of long-term cardiometabolic disease. Lifestyle intervention remains the cornerstone of management; however, the optimal nutritional strategy continues to be debated. This narrative review summarizes current evidence on nutritional management of PMOS, including dietary approaches, the role of the gut microbiota, dietary supplementation and complementary lifestyle interventions. Current evidence indicates that no single dietary model is universally superior for all women with PMOS. Instead, different dietary approaches may improve selected anthropometric, metabolic, endocrine, and reproductive outcomes, although the consistency of these effects varies across interventions and outcomes. The most consistent benefits are observed for body weight, insulin resistance, glycolipid metabolism and cardiometabolic risk, whereas improvements in reproductive and hyperandrogenic outcomes are generally more variable. Gut microbiota modulation represents a biologically plausible mechanism linking diet with metabolic and reproductive function, although its role as a mediator of dietary effects remains insufficiently established. Adjunctive supplementation, particularly with inositols, vitamin D, omega-3 fatty acids, and selected probiotics or synbiotics, may improve selected metabolic and reproductive outcomes, although the certainty and consistency of these effects vary across supplements. Such approaches should be considered complementary to, rather than a replacement for, lifestyle management. Physical activity, behavioural support, adequate sleep and stress management further contribute to comprehensive care, although evidence is strongest for structured exercise interventions. Lifestyle approaches may also have a role in early risk modification, particularly through the prevention of excess weight gain and promotion of physical activity, although direct evidence for primary prevention of PMOS remains limited. Overall the findings support individualized and sustainable nutritional and lifestyle strategies rather than a universal therapeutic approach. Future research should focus on well-designed long-term randomized trials and the development of personalized approaches that account for clinical and metabolic heterogeneity in PMOS.