Polycystic ovary syndrome (PCOS)
PCOS is usually metabolically driven, so establishing whether yours is insulin-resistant, lean, post-pill or inflammatory decides whether treatment works.
PCOS is a syndrome with distinct presentations. The insulin-resistant phenotype accounts for the majority and responds to metabolic intervention. Lean PCOS, post-oral-contraceptive PCOS and inflammation-driven PCOS behave differently and respond to different things. Treating them all identically is why so many women conclude that nothing works.
Hyperinsulinemia, which drives ovarian androgen production directly, in the majority of cases. Elevated LH relative to FSH. Chronic inflammation. Adrenal androgen excess in a subset. Post-pill hypothalamic recovery. And genetic loading. Insulin resistance is present in a large share of lean patients too, which is why body size does not determine the workup.
Insulin sensitivity as the primary lever: resistance training, protein-forward nutrition, carbohydrate timing. Inositol, which has good evidence for ovulatory function. Metformin or GLP-1 therapy where clinically indicated. Anti-androgen and cycle support where appropriate. Inflammatory load and sleep. Where fertility is the goal, reproductive endocrinology is the right referral and it is made early.
Total and free testosterone, DHEA-S, LH and FSH, SHBG and AMH. Fasting insulin, HOMA-IR and a two-hour glucose tolerance test where indicated. Complete thyroid function and prolactin, since both mimic PCOS. hs-CRP. Vitamin D. Pelvic ultrasound where the diagnosis is not established. And 17-hydroxyprogesterone, to exclude congenital adrenal hyperplasia.
Ready to start with a clear clinical picture?
Start with the fifteen-minute consultation. No cost, and a straight answer on whether this model fits your case.