Androgenetic Alopecia

Androgenetic alopecia (AGA), or pattern baldness, affects up to 70% of men and 40% of women lifetime, driven by genetics and dihydrotestosterone (DHT) shrinking scalp follicles. In men, it forms an "M" receding hairline and crown baldness; women show widening parts with preserved frontal hair. Follicles transition from thick terminal hairs to fine vellus ones, shortening the growth (anagen) phase. Over 380 genetic loci, including androgen and WNT pathways, influence susceptibility.

Causes and Risk Factors

Primary triggers are genetic predisposition and androgens like DHT, produced by 5?-reductase from testosterone, binding follicle receptors in susceptible scalps. Age accelerates onset post-puberty; men peak by 50, women post-menopause. Family history dominates (80% heritability); inflammation, fibrosis, and stress may worsen it. Rare in prepubescents.

Symptoms and Diagnosis

Men notice temple recession and vertex thinning (Norwood scale); women experience Ludwig-pattern diffuse loss. Diagnosis is clinical via pattern recognition, pull tests, or dermoscopy showing miniaturized follicles. Trichoscopy reveals >20% vellus hairs. Biopsy confirms if needed. Impacts quality of life via anxiety.

Treatment Options

FDA-approved: topical minoxidil (2-5%) stimulates growth; finasteride (1mg oral, men) cuts DHT by 60-70%, boosting counts 9-15%. Women use spironolactone or minoxidil. Adjuncts: PRP, low-level laser, transplants from resistant areas. Emerging: peptides, mRNA therapies. Continuous use required; early intervention best.