PCOS Core

Polycystic ovary syndrome is a lifelong metabolic, reproductive, endocrine, and psychological condition. It is not simply a fertility problem and not a disorder defined by ovarian cysts. Excess ovarian androgen production, insulin resistance, compensatory hyperinsulinaemia, and altered gonadotrophin secretion interact. Insulin resistance occurs across BMI categories. Higher insulin levels stimulate ovarian theca cells to produce more androgens and reduce hepatic production of sex hormone-binding globulin, increasing the free androgen fraction. Relatively increased luteinizing hormone secretion can further support androgen production. Follicles then remain arrested at the small antral stage instead of progressing to ovulation. The clinical result is a variable combination of hirsutism, acne, androgenic alopecia, irregular or absent ovulation, and polycystic ovarian morphology. A patient may have a higher body weight, a lower body weight, or no obvious metabolic symptoms and still have PCOS. Weight alone neither establishes nor excludes the diagnosis. An experienced clinician notices the menstrual pattern first because it reveals the reproductive consequence of anovulation. Eight months without a period is not merely an inconvenience: progesterone has not been providing regular opposition to endometrial oestrogen exposure,...