DHT and Hair Loss: The Full Mechanism Most Explanations Skip
DHT gets blamed for hair loss constantly, but most explanations stop at "it shrinks follicles." The actual biology is more interesting and helps explain why some treatments work better than others — and why the medications that target DHT do so much more effectively than anything that tries to work around it.
01What DHT is
Dihydrotestosterone is formed when testosterone is converted by the enzyme 5-alpha-reductase — primarily Type II in scalp tissue. DHT is more potent than testosterone: it binds to androgen receptors with 5x higher affinity and dissociates more slowly. In most body tissues this potency is appropriate. In scalp follicles with genetic sensitivity, it's destructive.
02The miniaturization cascade
When DHT binds to the androgen receptor in a sensitive follicle, it triggers a cascade that progressively shortens the anagen (growth) phase with each successive hair cycle. The shaft produced each cycle is slightly finer and shorter. Over multiple cycles (each lasting 2–7 years), the follicle produces only miniaturized vellus hair — peach fuzz — before eventually becoming dormant. This is not sudden; it's measured in years and cycles.
Follicles in the back and sides of the scalp express androgen receptors differently — they're not sensitive to DHT-driven miniaturization. This is why they persist in advanced AGA, and why transplanted hair from these zones retains its resistance permanently after being moved to the balding area.
03Why finasteride works — and has limits
Finasteride blocks 5-alpha-reductase Type II, reducing scalp DHT by ~70%. This doesn't stop the miniaturization process; it dramatically slows it by reducing the primary trigger. Follicles that are already significantly miniaturized may not recover even with full DHT suppression — which is why treatment outcome is better the earlier it starts.
Block the trigger at its source