What Is Polycystic Ovary Syndrome: Hormones, Symptoms, and Management

This article is for informational purposes only. Consult a qualified healthcare professional for medical advice, diagnosis, or treatment.

What Is Polycystic Ovary Syndrome?

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder affecting women of reproductive age, estimated to affect 5–13% of women globally — approximately 116 million women worldwide according to the World Health Organization. Despite its name, the syndrome does not require the presence of cysts on the ovaries; rather, it is defined by a constellation of hormonal abnormalities and clinical features. PCOS is a leading cause of female infertility and is associated with significant long-term metabolic risks, including type 2 diabetes, cardiovascular disease, endometrial cancer, and mood disorders. The condition is heterogeneous — no two patients present identically — making diagnosis and management individualized.

Diagnostic Criteria: The Rotterdam Criteria

The most widely accepted diagnostic framework is the 2003 Rotterdam Criteria, which requires at least 2 of the following 3 features (after excluding other causes):

Other conditions must be excluded before diagnosing PCOS: congenital adrenal hyperplasia (21-hydroxylase deficiency), Cushing's syndrome, thyroid dysfunction, hyperprolactinemia, and androgen-secreting tumors.

Underlying Pathophysiology

PCOS involves three interrelated hormonal disruptions:

Gonadotropin Dysregulation

The hypothalamic-pituitary axis releases gonadotropin-releasing hormone (GnRH) in pulses; in PCOS, GnRH pulse frequency increases, which preferentially stimulates pituitary secretion of luteinizing hormone (LH) over follicle-stimulating hormone (FSH). The resulting elevated LH:FSH ratio stimulates ovarian theca cells to overproduce androgens (primarily testosterone and androstenedione) while insufficient FSH prevents follicular maturation, leading to multiple small antral follicles that arrest development — the polycystic appearance on ultrasound — and chronic anovulation.

Hyperandrogenism

Excess androgens drive the most visible symptoms: hirsutism (affecting 70% of women with PCOS), acne, and androgenic alopecia (thinning of scalp hair in a male pattern). Androgens also contribute to anovulation by suppressing the aromatase enzyme in granulosa cells and promoting follicular atresia (cell death), further disrupting follicle selection and ovulation.

Insulin Resistance and Hyperinsulinemia

Approximately 65–70% of women with PCOS have insulin resistance, often independent of body weight. Hyperinsulinemia amplifies ovarian androgen production (insulin directly stimulates theca cell androgen synthesis), suppresses sex hormone-binding globulin (SHBG) production in the liver (increasing free androgen levels), and drives the metabolic features of the syndrome. The exact molecular defect causing insulin resistance in PCOS — which differs from the insulin resistance of type 2 diabetes in some post-receptor signaling characteristics — remains an active research area.

Clinical Features and Associated Conditions

Diagnosis and Workup

Initial evaluation includes:

• Menstrual history and symptoms: Detailed characterization of cycle irregularity, skin and hair changes
• Blood tests: Total and free testosterone, DHEAS, LH, FSH, AMH (anti-Müllerian hormone — characteristically elevated in PCOS), SHBG, thyroid function, prolactin, fasting glucose, and insulin; HbA1c if metabolic risk factors present
• Pelvic ultrasound: Transvaginal ultrasound (preferred) assesses follicle count and ovarian volume; transabdominal if transvaginal not acceptable

AMH levels correlate strongly with antral follicle count and are elevated 2–3 times higher in women with PCOS versus controls, making AMH a useful diagnostic biomarker even in women on hormonal contraceptives (which suppress LH, FSH, and androgen levels).

Management Strategies

Lifestyle Modification

For overweight or obese women with PCOS, weight loss of 5–10% body weight can restore menstrual regularity, reduce androgens, improve insulin sensitivity, and restore ovulation in up to 55% of cases. Even without weight loss, regular aerobic and resistance exercise improves insulin sensitivity and androgen levels. Dietary approaches reducing glycemic load are particularly beneficial.

Pharmacological Treatment

• Combined oral contraceptive pill (OCP): First-line for menstrual regulation and hyperandrogenism. Estrogen increases SHBG (binding testosterone), while progestin suppresses LH and thus androgen production. Progestin component selection matters — anti-androgenic progestins (e.g., drospirenone, cyproterone acetate) are preferred.
• Metformin: Improves insulin sensitivity, restores menstrual cycles in approximately 50% of women, reduces androgen levels. NICE guidelines recommend metformin for PCOS with metabolic features even without diabetes.
• Letrozole (aromatase inhibitor): Current first-line ovulation induction agent for PCOS-related infertility, with higher live birth rates than clomifene citrate in the LETTRE trial (2014). Blocks peripheral estrogen synthesis, allowing FSH to rise and stimulate follicular development.
• Spironolactone: Androgen receptor blocker used for hirsutism and acne when OCPs are inadequate or contraindicated.
• Inositol (myo- and D-chiro-inositol): Dietary supplement with emerging evidence for improving insulin signaling in PCOS; not yet a standard-of-care recommendation but increasingly used.

Long-term management requires regular screening for metabolic and cardiovascular risk factors. Women with PCOS who are not trying to conceive should be offered progestogen-induced withdrawal bleeds at minimum every 3–4 months to prevent endometrial hyperplasia from unopposed estrogen exposure.