Prevent Hair loss, don't Regrow?

Article by HairlossTalk.com

Drug treatments: manipulating androgen metabolism to retard male pattern hair loss

The most promising treatments modulate the metabolism of androgens in the scalp. Currently, only one pharmaceutical is available to the physician for the treatment of men with AGA. Finasteride (Propecia) is a potent, specific inhibitor of the type 2 5a-reductase that is responsible for the conversion of testosterone to DHT. Given orally, Finasteride reduces DHT levels systemically and in the target tissues (i.e. scalp). In an animal model of AGA, the stump-tailed macaque, daily oral Finasteride given over a period of 6 months significantly reduced circulating DHT levels and increased scalp hair weight. 8 Finasteride at a dosage of 1 mg/day has recently been approved by the Food and Drug Administration (FDA) for the treatment of male pattern hair loss in men. Its efficacy has been demonstrated in three double-blind, placebo-controlled, randomized studies. Men with AGA, aged between 18 and 41 years, were given either oral Finasteride 1 mg/day or a placebo. Assessed by scalp hair counts, self-assessment by patients using a validated questionnaire, investigator assessment using a standardized seven-point rating scale of hair growth from baseline, and an independent expert review of photographs taken every 6 months, Finasteride treatment was evaluated as resulting in improvement. Finasteride produced a progressive increase in hair counts at 6, 12 and 24 months, while placebo treatment resulted in significant hair loss. By 24 months, 72% of patients on placebo had lost hair compared to baseline, while 83% of patients on Finasteride had experienced no further hair loss. Similarly, at 14 months, the expert panel considered 66% of Finasteride-treated patients greatly, moderately, or slightly improved vs. only 7% of those on placebo. There was little difference in the incidence of side-effects reported by men on Finasteride (4.2%) vs. placebo (2.2%) which resolved after discontinuation and in many of the men who remained on drug treatment.

These results are in line with our current understanding of the effect of DHT on hair physiology. Although, as mentioned previously, the molecular details of the mechanism by which androgens affect hair growth are not known, it is apparent that, in the androgen-sensitive scalp of genetically susceptible individuals, they cause a gradual miniaturization of the follicles and conversion of long, thick pigmented terminal hair to short, fine, unpigmented vellus hair. Prevention of the androgen-mediated miniaturization will inhibit or retard the process leading to hair loss, and in some cases result in new hair growth. Furthermore, there is demonstrable heterogeneity in 5a-reductase activity in scalp hair roots from patients with AGA, which may account for some of the variation in response to Finasteride.

Conclusions

The likelihood is that the modulation of androgen metabolism will prevent further hair loss in the majority of patients, and induce hair growth in a smaller proportion, depending on the extent of their condition and their genetic background. It is vital therefore for the prescribing physician to bear in mind that the patient may suffer anxiety over the possible progression of hair loss in the future, while being able to tolerate his present condition. For many patients, prevention of further hair loss alone will constitute acceptable management. For the physician, the important message is that the best therapeutic prospects lie in drug modalities that utilize our increased understanding of normal and pathologic hair growth. Although topical minoxidil was the first effective drug to benefit some of these patients, targeting of type 2 5a-reductase in the scalp hair follicle using oral Finasteride is now a realistic option for the prevention of further hair loss in the patient with male pattern baldness.

Marcia Ramos-e-Silva, MD, PhD
International Journal of Dermatology

HLT

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