What Actually Causes PCOS? A Mechanistic Reading of Polycystic Ovary Syndrome — Why the standard PCOS model produces variable results

The dominant clinical model of PCOS identifies insulin resistance as the central driver in most cases, with secondary contributions from hyperandrogenism, inflammation, and adrenal dysfunction. Treatment targets the components that can be pharmacologically addressed. The framework is correct in identifying insulin resistance as central in most cases. It is incomplete in addressing why insulin resistance developed in the first place and why other PCOS phenotypes (lean PCOS, adrenal PCOS, post-pill PCOS, inflammatory PCOS) behave differently. The questions the standard model does not adequately address: what drives the insulin resistance in PCOS patients who are not obese? Why do some PCOS patients have profound metabolic dysfunction while others have mild features? Why does PCOS so frequently co-occur with Hashimoto's thyroiditis (22.8% prevalence per recent Frontiers in Endocrinology data), with endometriosis (15-25% overlap), with autoimmune conditions broadly? Why do lifestyle interventions that target weight loss work well for some patients and produce minimal improvement for others? The research literature has converged on a set of mechanisms that answer these questions. Gut dysbiosis is documented in PCOS patients independent of body weight. Chronic low-grade inflammation precedes the clinical PCOS phenotype in many cases. Mitochondrial dysfunction in granulosa cells affec