Scientists and hair biologists today are of the opinion that the loss of scalp hair in genetically susceptible individuals is mediated by androgens. Aristotle first noted that ‘maleness’ and sexual maturity were required for balding. Later in 1942, Hamilton’s observations on men deprived of testicular androgens by castration ascertained that androgens, in the form of testosterone or its metabolites, were preconditions for the progression of common baldness. Hamilton observed that men who were castrated before puberty did not develop androgenetic alopecia, and that androgenetic alopecia could be triggered in castrated men by injecting testosterone.
This was followed by research and studies in efforts to establish the relation between androgens and androgenetic alopecia. It has been documented that without androgens or their activity, scalp hair grows constitutively while body hair growth is inhibited; and with androgen activity, genetically predisposed persons develop a definite pattern of scalp alopecia manifested as miniaturization of scalp hair follicles. Miniaturization of hair can be described as the transformation of large terminal hairs (thick pigmented hairs) into fine vellus (tiny colorless) hairs.
There is no satisfactory explanation for the contradictory influence of androgens on hair at different body sites. Pre-pubertal pubic, axillary, beard, and chest Vellus hair follicles respond to androgens by growing into terminal hairs, whereas the same androgens transform by miniaturization the pigmented terminal hairs on the scalp into non-pigmented wispy hairs. However, androgen effects on hair growth at particular body areas are believed to be partially attributed to factors such as increased number of androgen receptors, increased local production of high-potency androgens, and/or reduced degradation of androgens.
Effects of androgens in androgenetic alopecia
Loss of scalp hair in androgenetic alopecia occurs gradually over many years in an orderly pattern and depends on factors within each follicle. Studies using both plucked hairs and scalp biopsies have demonstrated an increased DHT production in balding as against non-balding scalps. Thus, it appears that in balding men DHT binds to androgen receptors in susceptible hair follicles and, by an unknown mechanism, activates genes responsible for follicular miniaturization. The prominent role of 5 alpha – reductase in these studies suggests that inhibitors of this enzyme may provide new therapeutic opportunities for patients with androgenetic alopecia. It has also been found that the amount of dihydrotestosterone produced by men in the scalp is small compared with that produced in the prostate.
It is clear that simply blocking androgens does not result in the conversion of miniaturized follicles to terminal ones in advanced androgenetic alopecia. Studies that illustrate the molecular mechanisms by which androgens regulate hair growth would provide greater understanding of this form of hair loss.