What Actually Causes PCOS? A Mechanistic Reading of Polycystic Ovary Syndrome — The PCOS-Hashimoto's-endometriosis cluster

PCOS frequently co-occurs with other women's-health conditions in patterns that the standard model does not fully explain. Hashimoto's thyroiditis has a 22.8% prevalence in PCOS patients compared to 5.7% in the general population. Endometriosis has 15-25% prevalence in PCOS patients. The overlap with hEDS-POTS-MCAS triad conditions is also elevated. The framework explains these co-occurrences as expressions of shared upstream lesions. The gut dysbiosis and barrier failure that drives PCOS also drives the molecular mimicry that produces Hashimoto's (described in the Hashimoto's article) and contributes to the inflammatory milieu that supports endometriosis (described in the endometriosis article). The CD38-NAD+-SIRT3 cascade operates across all three conditions. The mast cell mechanisms described in the MCAS article contribute to multiple of these conditions simultaneously. Treatment that addresses the shared upstream lesions benefits all of the co-occurring conditions. This is one of the strongest arguments for the framework's clinical value. A patient with PCOS, Hashimoto's, and endometriosis treated through the standard medical approach receives three separate specialist treatment cascades that do not communicate with each other. A patient with the same constellation treated through the Host Capacity Model framework receives an integrated approach that addresses the shared le