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Male androgenetic alopecia is a common condition, which eventually affects at least half the world's adult male population. It is an inherited condition, which is thought to be dominantly inherited, with variable penetrance [1-4]. The gene or genes have not yet been identified. Its presumed androgen dependance is based on the observation that it is prevented by early castration but can develop if the castrate is treated with androgen replacement [5]. Furthermore, males who lack the enzyme type 2 5alpha-reductase do not produce much dihydrotestosterone (DHT) and do not become bald [6, 7]. The characteristic balding of the crown, as hair loss diseases pattern baldness evidenced by bitemporal recession of hair and vertex baldness, is diagnostic of male pattern alopecia [8]. The underlying change responsible for the balding process is a progressive miniaturization of terminal hairs on the crown [9-11]. Although the traditional view of miniaturization has been that of a gradual, step wise progression, there is mounting evidence that the process can occur, or be reversed, abruptly [12], perhaps in one hair growth cycle. The first drug approved for the treatment of male pattern alopecia, over a decade ago, by the US Food and Drug Administration was topical minoxidil [13]. Its mechanism of action is stop hair loss with propecia pattern baldness still unclear, but it has no apparent effect on androgen metabolism. Although minoxidil has a definite effect in initiating and prolonging the anagen phase of the hair growth cycle, its visible effects on hair growth are often not striking. In general, it is better at preserving than restoring hair. In more recent years finasteride, a potent inhibitor of type 2 5alpha-reductase, was developed. It directly affects androgen metabolism by reducing the amount of DHT converted from testosterone. Finasteride was designed to resemble the structure of testosterone, so as to block the production of DHT and mimic the biochemical profile of type androgenetic alopecia pattern baldness 2
