Dihydrotestosterone — DHT — is the central hormonal driver of androgenetic hair loss in both men and women. A complete understanding of what DHT is, how it causes hair loss, and how it can be targeted therapeutically puts patients in a much stronger position to make treatment decisions.
DHT is produced from testosterone through the action of the enzyme 5-alpha reductase. There are two isoforms of this enzyme: type I (found predominantly in skin and liver) and type II (found predominantly in the hair follicle, prostate, and liver). Finasteride inhibits type II 5-alpha reductase; dutasteride inhibits both type I and type II.
DHT binds to androgen receptors in the dermal papilla cells of susceptible hair follicles. This binding triggers a cascade that progressively shortens the anagen phase of each successive hair cycle — producing shorter, finer, less pigmented hairs until the growth cycle becomes too brief to produce visible hair. This is miniaturisation.
The susceptibility of individual follicles to DHT is determined by the density of androgen receptors expressed in those follicles — a genetically determined characteristic. Follicles in the donor zone at the back and sides of the scalp have low androgen receptor expression and are largely DHT-resistant. Follicles in the frontal and crown regions are more likely to express high androgen receptor density in susceptible individuals.
Serum DHT levels do not predict hair loss severity. Two people with identical serum DHT can have completely different hair loss patterns, because follicle sensitivity — not circulating DHT level — is the relevant variable.
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