Cnn - Cotsarelis And Christiano Interview 10/18
- Thread starter Breyfogle
- Start date
Nope. And I think more people need to become uber fans of science instead of placing any faith whatsoever in anonymous people posting juvenile comments.
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Yeah, see, that's just the thing: The people (scientists included) saying this isn't going to work for Androgenetic Alopecia are saying so because the science thus far indicates it won't work.
That dude who had AA was cured but still revealed he had Androgenetic Alopecia, but "oh the topical is going to function sooooo much differently", right? What basis do you have for believing so? Your only defense is "We have to wait and see" based on the false assumption that because something hasn't been tested specifically, we can't make accurate predictions to its efficacy based on what is already known — its mechanism is unrelated to the underlying cause of Androgenetic Alopecia.
This is like someone saying "Don't jump off that cliff; you'll die" and then you being like "Well, you don't know that! You don't know how high it is! Wait until we test it!" and then acting like everyone else has a problem for thinking you're crazy.
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I just have to point out in your quote that an "ELITE HAIR FOLLICLE BIOLOGOY SCIENTIST" gave it a 1/10 chance.... You realize that means that even an "ELITE SCIENTIST", which you praise, can't predict with 100% certainty that a topical formulation will work, right?
Does it look good from photos showing people still have Androgenetic Alopecia pattern after regrowing hair? Well, no obviously not any ignoramous with a bad spray tan could tell you that, but there's still a chance and if people want to be hopeful let them. Take your broscience and ridiculous claims that you know it won't work 100% b/c you did the "research" elsewhere. You're just a meathead that thinks he is a PhD b/c he can say 99.9% of products won't be a cure. Anyone can do that b/c most of these things don't work out. It doesn't make you right about anything.
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No, I know with 100% certainty actually. Science doesn't lie. And lay down the hardcore drugs, they are bad for your mental health.
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I agree with anyone that says this will probably not work. I don't agree with anyone that says it won't work 100% bc thats just ignorance. You haven't seen it tested in a topical formulation with a specific vehicle made for it. Again, does it look good? Not at all, but seriously, stop saying science doesn't lie, because you are literally lying and trying to quote science. You sound like an idiot.
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Yea, it probably won't work. It's not looking good, but people need to stop acting like they know everything and have all the answers. The fact is no one knows for sure, we can make educated guesses, but until it's tried NO ONE knows 100%.
I wouldn't be making any bets on this that's for sure.
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It probably won't work for Androgenetic Alopecia but i am sure Everyone would prefer it actually does work even if it proved them wrong.
The almost evolutionary pessimism of people that suffer hairloss is unerstandable. But saying it will probably won't work without any knowledge is ridiculous.
This company wouldn't try so hard if they had no something successful to rely on. It's alot of money there. Do you really think they would spend SO MUCH money and TIME for this sh*t, while Histogen, Replicel, Tsuji are breathing on their back, if they didn't have something in their hands?
Seriously. If you were the owners of that company, would you keep spending efforts on marketing (yes, that website and smartphone app included), trials, researching in that situation?
This company wouldn't try so hard if they had no something successful to rely on. It's alot of money there. Do you really think they would spend SO MUCH money and TIME for this sh*t, while Histogen, Replicel, Tsuji are breathing on their back, if they didn't have something in their hands?
Seriously. If you were the owners of that company, would you keep spending efforts on marketing (yes, that website and smartphone app included), trials, researching in that situation?
He could be legit. I think he said he graduated with magnus opus lauder distinction from What's the Matter U. or some such.
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I think you have proven yourself enough. You are not only dumb but bat sh*t crazy. A woman had to even call you out for your strange ultra pro feminism behavior. Must be hard being a brittle dumb old guy like you in life lol
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@InBeforeTheCure,
I actually never have asked you about this matter. You are one of the most knowledgeable guys if not the most on this forum so your opinion is welcome.
Tofacitinib IC50 of 1nM towards JAK3 (less selective against JAK1 and JAK2)
Finasteride IC50 of 4.2nM towards 5ar2. (remember that finasteride fully saturates 5ar2 at 1mg orally).
Take that as a rough model.
You obviously understand that since both topical formulations and oral formulations work for AA it must mean that the drugs exert their biological activity sufficiently towards JAK3 somewhere at or around the hair follicle (tofactinib is most selective for JAK3).
This makes per definition the notion of A.M Christiano flat out wrong in this article, since topical formulations are on the market already that do penetrate the skin. In fact there is a pharmacy that has released one that works on people with AA. Not only that Brett King has even made a topical formulation that works.
But let's get on the oral side because that's where I'm at. Remember to keep the pharmacology and pharmacokinetics in mind of Tofacitinib and that it has been tested across of hundreds if not thousands people of Androgenetic Alopecia orally over a long period of time. The dosage that already shows to be effective is twice a day dosage of 5 mg a day for AA. But it has been trialed in people across long periods of time at even higher dosages.
Now this means similarly that the drug exerts it's biological activity and saturates one of the JAK enzymes in close proximity of the bulb when taken orally. If it didn't after all it wouldn't work for AA. But it's most selective for JAK3.
Now the only legit comment I have heard out of the camp of Aclaris is the following from the CEO that isn't flat out laughable;
This is actually the same point I made before the CEO said this which is funny, but I said that it is highly damn unlikely that the drug doesn't exert it's biological activity sufficiently at the bulge but only does on the bulb when taken orally. Why? Well observations support this again since oral JAK inhibitors work for many other ailments like psoriasis, vitiligo, keratosis etc. These ailments for instance vitiligo and psoriasis take place in the epidermis, which as you know is actually the outermost layer of the skin and pretty much non-vascularized. So these observations support that these drugs exert their biological activity in the whole skin, including the outermost layers. Not only at the height of the bulb.
Now ok these are observations which are pretty important. They make his reasoning already very weak. But what really checkmates Aclaris is that even a study has shown that tofacitinib rapidly exerts it's biological activity in the epidermis after a single (!!!!) dosage (not even repeated dosing...)
The study confirms the observations with data and came out recently from a phase 2 trial
http://www.sciencedirect.com/science/article/pii/S0091674916001263
The picture says all, tofacitinib has a rapid effect on keratinocytes;
The picture speaks for itself top right corner keratinocytes which are located in the epidermis. The epidermis is highly non-vascularized as you know.
"The epidermis has no blood supply and is nourished almost exclusively by diffused oxygen from the surrounding air.[6] It is 95% keratinocytes"
Rapid inhibition of JAK/STAT signalling even towards JAK1 where tofactinib has less potency too lol....
So not only observations but data from a clinical trial totally contradicts the statement of the CEO of Aclaris.
Now do you agree with me that this is quite a hopeless endeavor?
The worst thing about this is the whole context. A.M Christiano literally looks at a mice model and draws a (weird) conclusion while totally neglecting observations and data in actual HUMANS.
Besides after all the mice that got the drug orally grew hair anyway, it just wasn't as quick and robust. But they did grew hair. A more logical conclusion for instance would be that a topical distributes itself quicker to the target location than when taken systemically.
Anyway can you understand why I find this the worst endeavor in many years for hair loss? In fact I find it beyond hopeless. I have never seen such a bad display of science throughout the years.
I actually never have asked you about this matter. You are one of the most knowledgeable guys if not the most on this forum so your opinion is welcome.
Tofacitinib IC50 of 1nM towards JAK3 (less selective against JAK1 and JAK2)
Finasteride IC50 of 4.2nM towards 5ar2. (remember that finasteride fully saturates 5ar2 at 1mg orally).
Take that as a rough model.
You obviously understand that since both topical formulations and oral formulations work for AA it must mean that the drugs exert their biological activity sufficiently towards JAK3 somewhere at or around the hair follicle (tofactinib is most selective for JAK3).
This makes per definition the notion of A.M Christiano flat out wrong in this article, since topical formulations are on the market already that do penetrate the skin. In fact there is a pharmacy that has released one that works on people with AA. Not only that Brett King has even made a topical formulation that works.
But let's get on the oral side because that's where I'm at. Remember to keep the pharmacology and pharmacokinetics in mind of Tofacitinib and that it has been tested across of hundreds if not thousands people of Androgenetic Alopecia orally over a long period of time. The dosage that already shows to be effective is twice a day dosage of 5 mg a day for AA. But it has been trialed in people across long periods of time at even higher dosages.
Now this means similarly that the drug exerts it's biological activity and saturates one of the JAK enzymes in close proximity of the bulb when taken orally. If it didn't after all it wouldn't work for AA. But it's most selective for JAK3.
Now the only legit comment I have heard out of the camp of Aclaris is the following from the CEO that isn't flat out laughable;
This is actually the same point I made before the CEO said this which is funny, but I said that it is highly damn unlikely that the drug doesn't exert it's biological activity sufficiently at the bulge but only does on the bulb when taken orally. Why? Well observations support this again since oral JAK inhibitors work for many other ailments like psoriasis, vitiligo, keratosis etc. These ailments for instance vitiligo and psoriasis take place in the epidermis, which as you know is actually the outermost layer of the skin and pretty much non-vascularized. So these observations support that these drugs exert their biological activity in the whole skin, including the outermost layers. Not only at the height of the bulb.
Now ok these are observations which are pretty important. They make his reasoning already very weak. But what really checkmates Aclaris is that even a study has shown that tofacitinib rapidly exerts it's biological activity in the epidermis after a single (!!!!) dosage (not even repeated dosing...)
The study confirms the observations with data and came out recently from a phase 2 trial
http://www.sciencedirect.com/science/article/pii/S0091674916001263
The picture says all, tofacitinib has a rapid effect on keratinocytes;
The picture speaks for itself top right corner keratinocytes which are located in the epidermis. The epidermis is highly non-vascularized as you know.
"The epidermis has no blood supply and is nourished almost exclusively by diffused oxygen from the surrounding air.[6] It is 95% keratinocytes"
Rapid inhibition of JAK/STAT signalling even towards JAK1 where tofactinib has less potency too lol....
So not only observations but data from a clinical trial totally contradicts the statement of the CEO of Aclaris.
Now do you agree with me that this is quite a hopeless endeavor?
The worst thing about this is the whole context. A.M Christiano literally looks at a mice model and draws a (weird) conclusion while totally neglecting observations and data in actual HUMANS.
Besides after all the mice that got the drug orally grew hair anyway, it just wasn't as quick and robust. But they did grew hair. A more logical conclusion for instance would be that a topical distributes itself quicker to the target location than when taken systemically.
Anyway can you understand why I find this the worst endeavor in many years for hair loss? In fact I find it beyond hopeless. I have never seen such a bad display of science throughout the years.
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KO1
Established Member
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Says who?
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- 1,004
VERY INTERESTING
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- 1,004
I, and I suposse that others people, Know that alopecia areata can be solved withouth any treatment, only passing the time.
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Hi hairblues,
You must know that it is essential do not to wash the hair or hair products two or three days before the interview in order to observe better scalp and hair conditions.
Sorry for the off-topic
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Yes, THIS is a great difference between AA y Nadrogenetic Alopecia. AA is reversible but common hair loss don´t.