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  1. #51
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    Quote Originally Posted by HairBane View Post
    The only guy supposedly trialing it that I know of is 'vraf'. He posted on 8th December 2013: The current tests has nothing to do with marketing. The product will be out in a year. Maximum.

    So, at the latest it should be released December of this year.

    I hope it works, but one moment it seems quite legitimate (ie. associated with reputable tech institute, apparently good results pictures on private forums), then the next day it looks like a scammy laser helmet that at most will do barely anything (russian snake-oil site, the whole idea of using some kind of electrolysis to pass zinc ions into the scalp and disrupt Androgen receptors without using anti-androgens or doing any wounding, the convenient 'book of pictures' a random lurker found in a salon in Israel). I want to see some solid evidence or maintenance results at minimum from a few trusted forum members before I'll believe it.
    That's a good summary. There really is a dichotomy in the evidence for pilox, so I definitely want to see as much new information as possible.

  2. #52
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    Quote Originally Posted by walrus View Post
    False. A causal relationship was found, not a mere correlation like you suggest.
    That's not entirely true, they showed that bald areas had higher levels of PGD2 and that PGD2 caused miniaturization. But that doesn't establish causality.

    Consider this:
    1) Dead humans put out lots of methane.
    2) If we "drown" humans in methane then they die.
    3) Therefore, remove all methane from the environment and humans will never die.

    See, doesn't quite work does it?

    (Though perhaps someone who is more of a biologist than I am can correct me if I misread any of the work).

  3. #53
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    Quote Originally Posted by baldymcgee View Post
    That's not entirely true, they showed that bald areas had higher levels of PGD2 and that PGD2 caused miniaturization. But that doesn't establish causality.

    Consider this:
    1) Dead humans put out lots of methane.
    2) If we "drown" humans in methane then they die.
    3) Therefore, remove all methane from the environment and humans will never die.

    See, doesn't quite work does it?

    (Though perhaps someone who is more of a biologist than I am can correct me if I misread any of the work).
    Your hypothetical theory would not stand up to experimentation, like the demonstrated effects of PGD2 of human hair growth did.

    "The product of PTGDS enzyme activity, prostaglandin D2 (PGD2), is similarly elevated in bald scalp. During normal follicle cycling in mice, Ptgds and PGD2 levels increase immediately preceding the regression phase, suggesting an inhibitory effect on hair growth. We show that PGD2 inhibits hair growth in explanted human hair follicles and when applied topically to mice. Hair growth inhibition requires the PGD2 receptor G protein (heterotrimeric guanine nucleotide)–coupled receptor 44 (GPR44), but not the PGD2 receptor 1 (PTGDR)."


    This section in particular:

    "To test the effect of PGD 2 on human hair growth, we used explanted human hair follicles maintained in culture for 7 days. We added increasing amounts (from 0 to 10 mM) of PGD 2 , 15-dPGJ 2 , or vehicle to the culture medium and measured hair length (Fig. 6D). Starting at 5 mM, PGD2 and 15-dPGJ significantly inhibited hair growth. At 10 mM, PGD 2 -treated hair was 62 ± 5% shorter than vehicle, whereas 10 mM 15-dPGJ 2 completely inhibited all hair growth. We tested a variety of other PGD 2 analogs and found them to be capable of inhibiting hair lengthening. Agonism for GPR44 correlated with the ability to inhibit hair lengthening (fig. S3). For example, the weak agonist 11-deoxy-11-methylene PGD 2 (28) had the lowest activity (hair growth inhibition) of the compounds tested. Note that GPR44 has nanomolar affinities for ligands, but as is typical for this type of experiment, higher concentrations were required to overcome tissue penetration and compound lysis. Thus, in both mouse and human, PGD 2 and 15-dPGJ 2 inhibit hair growth, likely through the GPR44 receptor.

    So again, your methane analogy does not stand, since evidence for causation has been provided experimentally.

  4. #54
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    Quote Originally Posted by walrus View Post
    Your hypothetical theory would not stand up to experimentation, like the demonstrated effects of PGD2 of human hair growth did.

    "The product of PTGDS enzyme activity, prostaglandin D2 (PGD2), is similarly elevated in bald scalp. During normal follicle cycling in mice, Ptgds and PGD2 levels increase immediately preceding the regression phase, suggesting an inhibitory effect on hair growth. We show that PGD2 inhibits hair growth in explanted human hair follicles and when applied topically to mice. Hair growth inhibition requires the PGD2 receptor G protein (heterotrimeric guanine nucleotide)–coupled receptor 44 (GPR44), but not the PGD2 receptor 1 (PTGDR)."


    This section in particular:

    "To test the effect of PGD 2 on human hair growth, we used explanted human hair follicles maintained in culture for 7 days. We added increasing amounts (from 0 to 10 mM) of PGD 2 , 15-dPGJ 2 , or vehicle to the culture medium and measured hair length (Fig. 6D). Starting at 5 mM, PGD2 and 15-dPGJ significantly inhibited hair growth. At 10 mM, PGD 2 -treated hair was 62 ± 5% shorter than vehicle, whereas 10 mM 15-dPGJ 2 completely inhibited all hair growth. We tested a variety of other PGD 2 analogs and found them to be capable of inhibiting hair lengthening. Agonism for GPR44 correlated with the ability to inhibit hair lengthening (fig. S3). For example, the weak agonist 11-deoxy-11-methylene PGD 2 (28) had the lowest activity (hair growth inhibition) of the compounds tested. Note that GPR44 has nanomolar affinities for ligands, but as is typical for this type of experiment, higher concentrations were required to overcome tissue penetration and compound lysis. Thus, in both mouse and human, PGD 2 and 15-dPGJ 2 inhibit hair growth, likely through the GPR44 receptor.

    So again, your methane analogy does not stand, since evidence for causation has been provided experimentally.
    I'm not a biologist, so I'm happy to be proven wrong

    This seems like it should be relatively easy to test, especially given that there are known compounds to block the receptor.

    Can someone familiar with the testing processes comment? This should be easy to confirm/falsify.

  5. #55
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    Quote Originally Posted by baldymcgee View Post
    This seems like it should be relatively easy to test, especially given that there are known compounds to block the receptor.

    Can someone familiar with the testing processes comment? This should be easy to confirm/falsify.
    The theory was already tested (see above) on cultured human hair follicles.

    The next step would be a full human trial.

    The real question is can we use this knowledge to regrow lost hair, or 'only' maintain.

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