What Actually Causes PCOS? A Mechanistic Reading of Polycystic Ovary Syndrome — The four phenotypes of PCOS and which driver dominates

The Rotterdam criteria recognize four PCOS phenotypes based on combinations of the three diagnostic features. The framework predicts that different phenotypes have different dominant drivers. Phenotype A (hyperandrogenism + oligo-ovulation + polycystic ovaries): The most metabolically severe phenotype. Drivers 1 (gut dysbiosis) and 2 (insulin resistance) are typically dominant. Standard treatment with metformin and combined oral contraceptives produces partial response. Phenotype B (hyperandrogenism + oligo-ovulation, no polycystic ovaries): Similar metabolic profile to Phenotype A but without the classic ovarian morphology. Same dominant drivers. Phenotype C (hyperandrogenism + polycystic ovaries, regular ovulation): Often "lean PCOS." The metabolic profile may be less severe but the gut dysbiosis and chronic inflammation drivers are typically present. Standard treatment is less effective because the conventional weight-loss-centered approach does not address the upstream lesions in patients who are not overweight. Phenotype D (oligo-ovulation + polycystic ovaries, no hyperandrogenism): Often involves prominent ovulatory dysfunction without the hyperandrogenic features. Inflammatory drivers and mitochondrial dysfunction in granulosa cells may be dominant. Standard hyperandrogenism-targeted treatment is less directly applicable. The clinical implication is that phenotype-aware