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  1. #1
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    Default If setipiprant worked...

    ...would we still need to use finasteride to try to block DHT? If setipip blocks PGD2, then would there still be a need to block DHT with fin, or is PGD2 the key? I'm a little confused

  2. #2
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    Quote Originally Posted by woodnor View Post
    ...would we still need to use finasteride to try to block DHT? If setipip blocks PGD2, then would there still be a need to block DHT with fin, or is PGD2 the key? I'm a little confused
    Nobody, including Cotsarelis, knows the answer to this question unfortunately.

  3. #3
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    Quote Originally Posted by KO1 View Post
    Nobody, including Cotsarelis, knows the answer to this question unfortunately.
    I see, I figured that was gonna be the answer, thanks for replying

  4. #4
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    Quote Originally Posted by woodnor View Post
    I see, I figured that was gonna be the answer, thanks for replying
    http://files.shareholder.com/downloa...0Deck%209FEB15

    Check out page 8...What it seems to be is that with increased testosterone there is increased DHT, which target follicles that have androgen receptors, upping pgd2 synthase activity, which ups pgd2 production. PGD2 is involved in hair cycling and signaling causing catagen and telogen phases. Because of the consistently heightened level of PGD2 in the scalp, it signals to the follicles to keep going into catagen and telogen, shortening anagen (growth phase), making them smaller and smaller over time until they are so small you can't see them.

    A DHT inhibitor helps block the cascade of these events, but because it doesn't act locally, or that it doesn't directly block what is implicated in hair loss, it most likely won't be as effective as a pgd2 blocker.

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