CGA and polycystic ovary syndrome: Looking forward, two design refinements would strengthen causal interpretation: (i) comparison with metabolically matched non-PCOS controls (matched on BMI, HOMA-IR, and inflammatory profiles) to test whether CgA elevation persists beyond comorbidity, and (ii) integration of unbiased inflammatory/metabolomic panels (guided by Mendelian randomization signals) to localize CgA within specific inflammatory–metabolic pathways (10, 11, 13).