DHT and Hair Loss: How Dihydrotestosterone Causes AGA
Reviewed by [Reviewer Name, MD] | Last reviewed: August 2026 | Editorial policy
Androgenetic alopecia (AGA) — the most common form of hair loss in men — is driven primarily by dihydrotestosterone (DHT). Understanding this mechanism explains why finasteride works and why blocking DHT is central to evidence-based hair loss treatment.
How DHT Is Made
Testosterone is converted to DHT by the enzyme 5-alpha-reductase (5-AR). Two isoforms exist: Type I (expressed in skin and liver) and Type II (expressed primarily in the prostate and hair follicles of the scalp). DHT binds to androgen receptors with approximately 5× greater affinity than testosterone, making it the dominant androgen at DHT-sensitive tissues.
DHT and Follicle Miniaturization
In genetically predisposed men, scalp hair follicles in androgen-sensitive zones (vertex, frontal hairline) express high levels of androgen receptors. DHT binding triggers a cascade that progressively shortens the anagen (growth) phase, shrinks the follicle dermal papilla, and produces successively finer, shorter, and more lightly pigmented hairs — a process called miniaturization. Left untreated, miniaturization eventually produces vellus hairs so small they are invisible to the naked eye, and the follicle effectively stops producing cosmetically relevant hair.
Why Finasteride Works
Finasteride specifically inhibits Type II 5-alpha-reductase — the isoform responsible for DHT production in scalp follicles. By blocking this enzyme, finasteride reduces scalp and serum DHT by approximately 60–70%, removing the primary driver of follicle miniaturization and allowing partially miniaturized follicles to recover size and resume normal growth cycles.
See: Finasteride mechanism of action | Norwood scale explained | Hair shedding vs. hair loss | Finasteride for AGA