PCOS hair loss in London: the endocrine story, and the treatments that actually work

PCOS hair loss is one of the most under-treated conditions in London women's health. Patients often circulate for years — GP to gynaecologist to trichologist to salon — before anyone connects the parting widening on the crown with the ovarian ultrasound in their notes from age 22.

This guide is written jointly with a consultant endocrinologist colleague. It's the treatment map we would draw together for a London patient in her twenties, thirties or forties who has PCOS and is losing hair — and what to do at each step.

The mechanism, in one paragraph

Polycystic ovary syndrome produces excess ovarian and adrenal androgens (testosterone, DHEAS). In the scalp, androgen-sensitive follicles on the top and crown convert testosterone to dihydrotestosterone (DHT) via 5-alpha reductase. DHT progressively miniaturises those follicles — shorter anagen phase, thinner shaft, eventually vellus-only. The pattern is Ludwig I–III central thinning, sometimes with frontal accentuation.

PCOS hair loss is androgenetic alopecia driven by an endocrine cause. Everything we do treats both ends — dampen the androgen signal, and stimulate the follicle to reverse miniaturisation.

The London workup: bloods and imaging

A proper PCOS hair workup is a single 45-minute visit and one blood draw, ideally in the early follicular phase (day 2–5 of the cycle if regular) — otherwise any day, with interpretation adjusted.

• Total testosterone, SHBG (calculate free androgen index) — elevated in PCOS.
• DHEAS — screens adrenal androgen contribution.
• LH, FSH — LH:FSH ratio often >2 in PCOS.
• Prolactin — rules out prolactinoma as differential.
• 17-hydroxyprogesterone — screens non-classical CAH, which mimics PCOS.
• TSH, free T4 — thyroid disease coexists and confounds.
• HbA1c, fasting insulin — insulin resistance is core PCOS.
• Ferritin, vitamin D, B12 — coexisting deficiencies aggravate hair loss.
• Pelvic ultrasound — polycystic ovarian morphology (12+ follicles per ovary or >10 ml volume).
• Trichoscopy of scalp — confirms miniaturisation and rules out coexisting scarring alopecia.

The evidence-based treatment stack

The core stack is anti-androgen + follicle stimulator + hormonal regulation, in that order of impact:

• Spironolactone 100–200 mg daily orally: the most useful single agent. Blocks androgen receptor and mildly inhibits testosterone synthesis. Off-label but well-supported. Slow onset — 6+ months for hair effect. Monitor potassium and blood pressure.
• Topical minoxidil 5% foam once daily, or 2% solution twice daily: extends anagen and increases shaft diameter. Foundational.
• Low-dose oral minoxidil 1.25–2.5 mg daily: increasingly the London first-line where topical is impractical. Cardiovascular screen first. Off-label.
• Combined oral contraceptive (COC) containing drospirenone (Yasmin) or cyproterone (Dianette): if pregnancy not planned, useful adjunct — regulates cycles, dampens ovarian androgens.
• Metformin: primarily for insulin resistance and metabolic health; modest indirect hair benefit through improved ovulation and reduced androgens.
• Finasteride 2.5–5 mg or dutasteride 0.5 mg orally: second-line in women. Effective. Pregnancy strictly avoided — reliable contraception mandatory.
• Cosmetic and adjunctive: PRP or low-level laser as accelerators, not stand-alone. Scalp micropigmentation for visible parting if density falls behind desire.

Lifestyle: what actually moves the needle

Weight loss of 5–10% of body weight, where BMI is elevated, meaningfully lowers androgen levels and improves ovulation. This is not vanity advice — it is disease-modifying.

Insulin resistance responds to low-glycaemic diets, resistance training and adequate sleep. Anything that reduces circulating insulin reduces ovarian androgen production. Coffee is fine. Alcohol above modest amounts worsens insulin sensitivity.

Inositol (myo-inositol 2g twice daily with D-chiro-inositol 50 mg) has reasonable evidence in PCOS for menstrual regularity and modest androgen reduction. Cheap, safe, worth adding.

Timeline and expectations

Shedding usually settles by 3 months on spironolactone + minoxidil. Visible short regrowth appears at 6 months. Peak density restoration is 12–18 months. Treatment is long-term — pattern loss returns if medication is stopped.

For patients planning pregnancy: stop finasteride, dutasteride and spironolactone well in advance; minoxidil is generally advised against during pregnancy/lactation. Discuss with your endocrinologist. Expect some hair loss during pregnancy hormonal windows.