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  1. #21
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    hi, I'm writing from Turkey we have a hair forum and we also think that the autoimmune system has a hit on mpb but our search is just starting and it seems like you guys are way ahead of us.We also watch this topic and will try to do our best to help starting with IL-6 which as far as I concern is playing a role in inflammation and can be inhibited with estrogen I don't know if it can be done with something else like I said we recently started searching the ai system experimenting with indomethadin which seems to cause an initial shed and then almost halt the loss-well, according to other guys on American forums- we and also I started using indo it's not even a week anyway what I'm trying to say is this thing what you guys are doing here is important and I think just like others mentioned we're close to something so let's keep pushing.

  2. #22
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    Quote Originally Posted by hellouser View Post
    Proof that follicles never die, they just shrink. Also further proof that anti-inflammatory drugs work. BIG clue here.

    I wonder if anyone has ever tried benoxaprofen as a topical solution.

    This is incredibly interesting and promising. I think that after a very long time follicles do die, but this offers some hope that even after quite a few years we can still revive them. i wonder if christiano and the other guys know about this. It seems like they should be able to narrow down what this drug does and create a better and more side effect free drug for MPB. People should definitely email them this article. Also I'm really curious for one of the crazies on here to try using a topical version of Christianos AA cure. I don't think it's out of the question for us to get a really good treatment out of nowhere, i just hope it doesn't have sides if it does come, but thats probably too much to ask.

  3. #23
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    Quote Originally Posted by cichlidfort View Post
    Based off the picture above, it seems the hair follicles don't die with cases such as AA. But what about hair follicles that were affect by AGA? Is it possible those hair follicles die?
    No, follicles in AGA are not dead. Dr. Cotsarelis confirmed this in this year's World Hair Congress in South Korea. They're miniaturized, but not dead or gone.

  4. #24
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    Quote Originally Posted by sdsurfin View Post
    This is incredibly interesting and promising. I think that after a very long time follicles do die, but this offers some hope that even after quite a few years we can still revive them. i wonder if christiano and the other guys know about this. It seems like they should be able to narrow down what this drug does and create a better and more side effect free drug for MPB. People should definitely email them this article. Also I'm really curious for one of the crazies on here to try using a topical version of Christianos AA cure. I don't think it's out of the question for us to get a really good treatment out of nowhere, i just hope it doesn't have sides if it does come, but thats probably too much to ask.
    Kyle Rhodes (the AA patient) didn't get sides from Xeljanz. A topical application is less likely to give them.

  5. #25
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    AGA really is a matter of ROS/oxidative stress guys. The idea behind it is simply beautiful simple. Simply said due to stress caused by the androgen receptor/androgens the body shuts proliferation of the cells down and puts them in a quiescent state. Meaning instead of a beautiful terminal hair follicle we are left with a shitty tiny miniaturized non pigmented hair follicle.




    These are important molecular mechanisms of the hair follicle guys. They are of utmost importance. Most of the wnt, fgf, hedhegog, prostaglandin family, etc... Lay downstream of these incredibly important regulators. Red being anti-apoptotic and black being pro-apoptotic. They are master regulators of the hair cycle, and they are completely whack out of line in our scalp leading to these shitty tiny hairs.

    Interestingly I was just reading a article about stem cells not even related to hairloss but stumbled upon some interesting stuff;

    Some types of injury or irritation can activate regenerative processes. A dermatology journal described the case of an old man who had been bald for many years who fell head-first into his fireplace. As his burned scalp healed, new hair grew. In the U.S., experimenters (Ito, et al., 2007) have found that injuring the skin of mice stimulates the formation of stem cells that are able to become hair follicle cells, supporting the regeneration of cells that had been absent. A brief exposure to estrogen, and other stress related signals (nitric oxide, endorphin, prostaglandins) can initiate stem cell proliferation.


    Obviously the grandpa was lucky. But yet again it proves that reverting is possible. So who is going to lit up his barbeque .

    Take a 5ar2 inhibitor or a anti-androgen and what do you see? In most cases you hold your hair and you get some of your hair back right? You even shed (!) seeing thicker hair and some new hair coming back. Especially if you see some new hair coming back consider yourself lucky cause your cells still had the capability to regenerate themself with the help of fin/dut/ru whatever. At the time of adding in these treatments you maintain normal status of the apoptotic molecules leading to a normal hair cycle again. If you are to late however and extensive DNA damage is done simply said the molecular mechanisms creates a "lockdown" on the hair cycle. Here are some studies about it;

    http://www.ncbi.nlm.nih.gov/pubmed/18702626
    http://www.plosone.org/article/info%...l.pone.0079434
    http://www.ncbi.nlm.nih.gov/pubmed/17989730
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929555/

    Now minoxidil works differently, we like to call it a "growth agent". It does not prevent damage but rather stimulates growth. If you will go on a anti-androgen or 5ar2 inhibitor you may notice less body hair or less beard hair. Minoxidil works everywhere and stimulates hair everywhere right? Why is that? It literally changes these apoptopic molecules. As A.M Christiano (1) points out in her journal minoxidil opens adenosine sensitive potassium channels (stimulate ATP) in the dermal papilla and increases BCL-2/BAX ratio. Meaning that by adding minoxidil you literally force hair follicles to enter a different cell cyle. If you stop you revert to the state when you started minoxidil and often you will have a massive shed 2-3 months later because the balance of the apoptopic molecules is back as it was. Look at how BCL-2/bax is incorporated also in the picture here above and a other study pointed out that minoxidil also had influence on P53 (antagonizing it)



    As you see here minoxidil coupled with ATRA significantly also has a effect on P53. These molecules are master regulators guys. I'm pretty sure most of the other studies about it improving FGF2, VEGF, and b-catenin in the dermal papilla is simply because all these pathways lay downstream of these powerfull regulators as P53 as I have pointed out. They literally decide if the hair goes in catagen, telogen, anagen etc..

    But really if these cells have DNA damage as said even finasteride, or minoxidil won't help you. Look at the burned guy here above. Obviously the wound caused probably apoptosis or some sort of perhaps (specific) injury to the cells. Leading to repairing of these cells and getting them pre-mpb normal state. As said the grandpa is just lucky because perhaps the injury was even in specific cell lines who the heck knows, but hey he got his hair back in the temple area being a grandpa.

    This chlorine dioxide, I was fascinated that it supposedly does something. Because it is a strong oxidating agent and the general idea seems to say that AGA is caused by ROS/oxidative stress. Do you get the picture now though? Albeit probably not specific and it not being the cure it probably damages the cells (creating apoptosis) wherein some of the hair comes back because the body literally replaces the cells with healthy pre-mpb ones. After all it is a extremely regenerative organ but instead of preventing damage using finasteride or stimulating the cells using minoxidil I think indeed this is important as pointed out;

    There is increased DNA damage that would be beyond the capacity of cells to repair in advanced cases. An alternative pathway would take place in order to eliminate the damaged cells through apoptosis.
    Jup, I agree these cells need to go back to original state and specific injury or damage may break the chain leading to healthy pre-mpb cells. It is possible guys, the man here above is living proof period.

    Anyways I hope A.M Christiano picks up AGA, because as hellouser pointed out really ironically the quality of hair researchers is generally not very high researching AGA. You can easily see that by the lack (!!!!) of questions asked at the hair congress when presentations are done, it's ridiculous. It's like they don't want to learn from each others work.

    There are also some pretty interesting small molecules in pre-clinical trials at the moment which alter specific pathways high upstream of AGA, for instance on these apoptopic pathways. Secretly I hope one of them might cause hair growth as a side effect who knows?!

    (1.) Regenerative medicine and hair loss: how hair follicle culture has advanced our understanding of treatment options for androgenetic alopecia - Claire A Higgins & Angela M Christiano

    https://www.dropbox.com/s/gb62waj5a0...pecia.pdf?dl=0

  6. #26
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    all this information needs to be sent to the researchers. chances are they haven't ever seen it. the stuff about the guy regrowing hair after being burned is fascinating, and if they can tie together similarities between that process and the way that that one drug regrew hair, there might be an answer hidden. This is also very relevant to cotsarellis' wound healing experiments. Something about the way the burning changed the skin, or possibly whatever was applied to the skin after this guy burned it was responsible for growing hair. i wonder if they know what was put on the old guy to help him heal. its also possible that he was taking another medication orally, and after his skin got burned, it initiated new hair growth. this makes me think that follica's research really does have promise- maybe a topical version of those JAK inhibitors would regrow hair in a wound. i think if these forums are useful for anything, its pulling up random information from the past and sending it to current researchers. whoever reads this should forward all that stuff to cots and christiano and everyone. if they get emails from enough people they are bound to check it out.

  7. #27
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    Quote Originally Posted by sdsurfin View Post
    all this information needs to be sent to the researchers. chances are they haven't ever seen it. the stuff about the guy regrowing hair after being burned is fascinating, and if they can tie together similarities between that process and the way that that one drug regrew hair, there might be an answer hidden. This is also very relevant to cotsarellis' wound healing experiments. Something about the way the burning changed the skin, or possibly whatever was applied to the skin after this guy burned it was responsible for growing hair. i wonder if they know what was put on the old guy to help him heal. its also possible that he was taking another medication orally, and after his skin got burned, it initiated new hair growth. this makes me think that follica's research really does have promise- maybe a topical version of those JAK inhibitors would regrow hair in a wound. i think if these forums are useful for anything, its pulling up random information from the past and sending it to current researchers. whoever reads this should forward all that stuff to cots and christiano and everyone. if they get emails from enough people they are bound to check it out.
    I agree. The case is fascinating and I would love to have more information on the grandpa.

    What is interesting too, AA and AGA definitely have pathways in common no doubt, but AGA is on a different level and not immune response driven. But for instance a important regulator which is dis balanced between both AA and AGA is caspase.

    http://www.ncbi.nlm.nih.gov/pubmed/22404322 Caspase-1 level is higher in the scalp in androgenetic alopecia.
    http://www.ncbi.nlm.nih.gov/pubmed/11399535 Androgen responsive genes as they affect hair growth.

    Caspases have much to do with inflammation but are powerful too as they can innate apoptosis; http://www.cell.com/abstract/S0092-8674(04)00490-8

    Downstream they have effect on the IL family which are pro inflammatory cytokines and present and are extremely important in AA, but are also upregulated in AGA.

    The ruxolitinib guy cured his AA. Well ruxolitinib is a JAK antagonist , but JAK pathways are connected to caspase again. There are more articles on this too , but here is one; http://www.nature.com/jid/journal/v1...d2013110a.html

    In both AA and AGA these powerful modulating molecules get unbalanced causing for complete absence of hair follicles or in our case miniaturized hair follicles. AA seems way easier to get full (or partial) reversal. We have seen that with anti-inflammatory compounds like strong corticosteroids and immuno suppresive drugs like ciclosporin this can be done.

    I agree though for instance with wounding and specific factors, perhaps hair can be regrown. I think that even causing manual apoptosis in specific cell lines will cause new cells pre-mpb and I think that is what has happened with the guy here above but that is just a guess.

    Nonetheless, exciting drugs are possibly coming through which modulate these crucial cell cycle molecular mechanism most are still pre-clinical ; http://www.nature.com/cdd/journal/v1...4401556t1.html

    But as you see they are doing testing with even p53 modulating compounds, bcl-2 modulating compounds. Most likely scenario short term is that a drug will cause hair regrowth as a side effect. Let's hope so.

  8. #28
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    Hi
    I dont know if this helps the research at all, but oh well... Just wanted to tell that my derm is going to prescribe arthitis drug for me in couple months. So i get chance to test how those drugs affect my MPB. Im also going to be on fin while on it, or if i can get dutas, then that.

    What arthisis drug? idk yet. Will see in couple months.
    List of some arthisis drug avaible in my country: leflunomide, Methotrexate(this is what they usually prescribe for psoriasis), Chloroquine, Etanercept, Adalimumab, Infliximab AND RUXOLITINIB!(i doubt she gives me that but i can try to convince her )

    I think i get to choose/wish for some drug, so if u have any suggestions what should i try... im going to have a thread and have pics in it about my progress

    I also have access to depression drugs, but idk if theres anything to try out for MPB?

  9. #29
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    Quote Originally Posted by hairbackpls View Post
    Hi
    I dont know if this helps the research at all, but oh well... Just wanted to tell that my derm is going to prescribe arthitis drug for me in couple months. So i get chance to test how those drugs affect my MPB. Im also going to be on fin while on it, or if i can get dutas, then that.

    What arthisis drug? idk yet. Will see in couple months.
    List of some arthisis drug avaible in my country: leflunomide, Methotrexate(this is what they usually prescribe for psoriasis), Chloroquine, Etanercept, Adalimumab, Infliximab AND RUXOLITINIB!(i doubt she gives me that but i can try to convince her )

    I think i get to choose/wish for some drug, so if u have any suggestions what should i try... im going to have a thread and have pics in it about my progress

    I also have access to depression drugs, but idk if theres anything to try out for MPB?
    Ask for Tofacitinib. Ruxolitinib inhibits JAK 1 and 2 while Tofacitinib inhibits JAK 1, 2 and 3. AFAIK, Tofacitinib is also supposed to upregulate CD200 cells, which is what men with AGA are lacking in the follicle. If you can do that while being on Fin/Minox it may give you some results. HOWEVER, keep in mind that CD34+ progenitor cells are ALSO missing, perhaps promoting that could give you full regrowth? Try all sorts of things along with deep dermarolling.

    Also, ruxolitinib costs $9,000/month while Tofacitinib is about $2,400/month.

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