Trichoscopy · Staging · CityLink Mall
Pattern hair loss is not hair falling out faster than it should. It is hair growing back progressively thinner, shorter and paler with every cycle until it no longer reaches the surface — a process called miniaturisation, and one that behaves very differently from shedding.
Every follicle on the scalp runs a repeating cycle: a long growth phase called anagen, a brief transitional phase, and a resting phase that ends in the hair being released. Anagen determines how long a hair grows and therefore how thick and how long it becomes before it is shed. In androgenetic alopecia the anagen phase of susceptible follicles is progressively shortened, cycle after cycle, and the hair produced each time is a little finer and a little shorter than the one before it.
The signal driving that shortening is dihydrotestosterone. Testosterone is converted to DHT by the enzyme 5-alpha-reductase within the dermal papilla at the base of the follicle, and DHT binds androgen receptors there. In a follicle that carries the genetic susceptibility, that binding alters the growth signalling of the papilla. In a follicle that does not, exactly the same hormone concentration produces nothing at all — which is why the condition is patterned rather than uniform, and why men with identical testosterone levels can have entirely different scalps.
The visible consequence is miniaturisation. A terminal hair — thick, pigmented, long — is replaced across several cycles by an intermediate hair, then by a vellus hair, the fine colourless down that covers most of the body. The follicle is still there and still cycling. It is simply producing something that no longer provides coverage. This is why the scalp appears to thin before it appears to bald: the same number of follicles remain, but the total mass of hair each produces has collapsed.
Distribution follows androgen receptor density, not blood supply, hat-wearing or scalp tension. The frontal hairline, temples and vertex carry high receptor density; the occipital and lateral scalp carry very little. That regional difference is the entire basis of hair transplantation — follicles taken from the back of the head retain their resistance to DHT after they are moved, which is why a transplanted hairline persists while the native hair around it continues to recede.
Classification
The most consequential thing a consultation establishes is not how much hair has gone but which disease removed it. Miniaturisation, shedding, autoimmune attack and tension injury present to the same reader as thinner hair and respond to entirely different management. The distinction that matters most is whether the follicle is intact or has been replaced by scar.
Hair loss is a diagnosis before it is a treatment. Four conditions look identical in a mirror and only one of them responds to what most people buy for it.
Timing
Androgenetic alopecia is progressive by definition, and the practical consequence is that every treatment decision is really a decision about how much hair there is left to keep. A miniaturised follicle can be pushed back toward terminal calibre because the machinery is still present. A follicle that has been miniaturised for long enough undergoes perifollicular fibrosis, and at that point the ground is empty — the surface looks the same as it did the year before, but nothing will grow there again.
This is why the first question at consultation is density and calibre rather than symptom duration. Trichoscopy shows hair shaft diameter variability long before a mirror does, and standardised photography establishes the baseline against which anything is later judged. Without that baseline, a year of treatment produces an argument rather than an assessment, because hair changes too slowly for memory to be a reliable instrument.
Management is then built in layers rather than chosen from a menu. Medical therapy addresses the hormonal driver and is what stops the disease progressing; non-pharmacological follicle stimulation and regenerative approaches work on the follicles that remain; surgical redistribution moves DHT-resistant follicles into areas that have already been lost. The sequence matters — transplanting into a scalp whose native hair is still actively miniaturising produces a result that unravels around the graft within a few years.
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