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Study showing some have more 5-alpha reductase than others

Higher levels of 5a-reductase probably don't contribute very much to balding. The problem in male pattern balding is far more an increased sensitivity to androgens. It may be similar with acne, too, at least in men. There was a study from a few years ago which found that the use of a specific 5a-reductase type 1 inhibitor (the type 1 enzyme is the one that appears in sebaceous glands) had no effect on the course of acne.

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And acne.

So your explanation for the failure in the study I cited above is....?

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The problem in male pattern balding is far more an increased sensitivity to androgens. It may be similar with acne, too, at least in men.

This scares me because my dad is bald, but he never had acne as bad as I did.

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And acne.

So your explanation for the failure in the study I cited above is....?

What study and which specific type 1 inhibitor did that study test? By what methods?

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What study and which specific type 1 inhibitor did that study test? By what methods?

The abstract of the study is below. Note that those are some BIG names in the field of dermatology. The specific type 1 inhibitor they used was MK386, an experimental drug developed by Merck a few years ago.

J Am Acad Dermatol. 2004 Mar;50(3):443-7. "A systemic type I 5 alpha-reductase inhibitor is ineffective in the treatment of acne vulgaris."

Leyden J, Bergfeld W, Drake L, Dunlap F, Goldman MP, Gottlieb AB, Heffernan MP, Hickman JG, Hordinsky M, Jarrett M, Kang S, Lucky A, Peck G, Phillips T, Rapaport M, Roberts J, Savin R, Sawaya ME, Shalita A, Shavin J, Shaw JC, Stein L, Stewart D, Strauss J, Swinehart J, Swinyer L, Thiboutot D, Washenik K, Weinstein G, Whiting D, Pappas F, Sanchez M, Terranella L, Waldstreicher J.

University of Pennsylvania Hospital, 36th and Spruce Streets, Philadelphia, PA 19104, USA.

Excessive sebum production is a central aspect of the pathophysiology of acne vulgaris. Sebaceous gland function is under androgen control and it is hypothesized that dihydrotestosterone is formed by the action of 5 alpha-reductase. Type I is the controlling isoenzyme. This study describes a 3-month, multicenter, randomized, placebo-controlled clinical trial with a potent, selective inhibitor of type I 5 alpha-reductase used alone and in combination with systemic minocycline. Inhibition of type I 5 alpha-reductase was not associated with clinical improvement of acne when used alone and did not enhance the clinical benefit of systemic minocycline. These results indicate the need for further work at the molecular level to better understand the action of androgens on sebaceous gland function.

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So it was a trial of a Merck drug. Topical or oral?

Oral.

Did it inhibit 5-alpha reductase?

Without digging-up that paper again and re-reading it just to be sure, I don't think they did blood tests to determine DHT levels before-and-after, but this drug has been well-researched in the past. It's a proven 5a-reductase type I inhibitor.

Male or female subjects?

Both.

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^ What about reduction in oil? Since that's really all inhibiting DHT would accomplish and wouldn't necessarily reduce acne.

They didn't bother to test for any effect on sebum production, and I consider that to be a serious oversight. I bet now they wish they HAD done that! :)

It's astonishing to me that now we have at least two proven 5a-reductase type I inhibitors: MK386 (the drug used in the aformentioned study), and dutasteride, the dual 5a-reductase inhibitor from Glaxo, and yet STILL there have been no studies having to do with the effect of such drugs on sebum. One would think that dermatologists would be keenly interested in such tests, for obvious reasons.

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