Pattern hair loss
Androgen-driven follicular miniaturization↓
Also searched as Androgen-driven follicular miniaturization.
The word 'loss' misleads. In pattern hair loss the follicle survives; each growth cycle simply starts shorter and thinner than the last, so the change is one of duration rather than of presence. That is why nothing here works quickly — you are lengthening the next cycle, not recovering the last one. Two forces are established. DHT binds the androgen receptor in dermal-papilla cells and drives the miniaturization itself. And prostaglandin D2 is measurably elevated in bald scalp compared with haired scalp on the same head, which made it a signature of the condition rather than a consequence of it. Worth knowing where the evidence stops: the human prostaglandin work is a comparison and an explant study, not a treatment trial — the causal proof is in mice.
In depth
Pattern hair loss. The follicle is not lost — it miniaturizes, producing progressively finer and shorter hairs over successive cycles, until what grows is too fine to cover the scalp. Androgen-driven, and the most common cause of hair loss in both sexes.
What drives it
Blocks the hormone that shrinks follicles increases it.
Testosterone is necessary for the development of male pattern baldness. DHT binds the androgen receptor in dermal-papilla cells and drives the follicle miniaturization that is the central molecular cause of pattern hair loss. This edge names the condition rather than the outcome, so the trials that studied AGA specifically have a node that matches what they measured. Garza 2012, Sci Transl Med 4(126):126ra34. PMID 22440736
Quiets the hair-suppressing prostaglandin increases it.
Prostaglandin D2 synthase (PTGDS) is elevated at mRNA and protein level in bald scalp compared with haired scalp of the same men with AGA, and PGD2 itself is similarly elevated. PGD2 inhibited growth of explanted human hair follicles (P<0.001) and acts through GPR44, not PTGDR. A K14-Ptgs2 transgenic mouse develops alopecia, follicular miniaturization and sebaceous gland hyperplasia — all hallmarks of human AGA. the human limb is a bald-vs-haired comparison plus explant culture, not a treatment trial; the causal demonstration is murine. Garza 2012, Sci Transl Med 4(126):126ra34. PMID 22440736
Prostaglandin F2-alpha reduces it.
The pilot AGA trial is the direct evidence that a PGF2-alpha analog opposes the condition itself rather than only raising a hair count: density and both vellus and terminal hair rose against the placebo minizone on the same head. n=16, described by its own authors as a pilot, and no prostaglandin-pathway drug has ever been approved for scalp hair loss. Blume-Peytavi 2012, J Am Acad Dermatol — randomized double-blind placebo-controlled 24-week trial of topical latanoprost 0.1% in androgenetic alopecia Sources: doi 10.1096/fj.02-0043fje; doi 10.1097/MD.0000000000004297; PMC5265840. doi 10.1096/fj.02-0043fje · PMC5265840
What it drives
It reduces Hair.
The condition suppresses the outcome: AGA is defined by progressive follicle miniaturization and shortening of anagen, so hair growth falls as the condition advances. Drawn so that AGA-specific trial evidence attaches to the condition and its effect on growth is explicit rather than implied. Garza 2012, Sci Transl Med 4(126):126ra34. PMID 22440736
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.