follicept - what's this?
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BS to this working. It's snakeoil until it's proven to be better than minoxidil. A guy pandering to a forum of desperate ppl, is likely to be full of crap. Just look at how many views this thread has gotten...based on what? -
Well you ask the same question 3 times what do you want me to do?
How is it speculation? Perhaps you'll go argue that the fact that pseudohermaphrodites or AIS people don't display androgenetic alopecia is speculation or not important? I'ts totally relevant to extrapolate data of such genetic diseases to AGA. In fact we have done this and discoveries are often made through this way.
People with Acrogemaly can display AGA, don't they? Then how can the FOXO1 hypothesis occur? Please explain, I'm interested in what you have to say.
You say that I speculate but don't give argumentation of anything at all. Aside from pointing me on carrier proteins (IGFPB family). Anyone on wikipedia can read about that lol.
You can't predict what effect will IGF-1 have on tissue level based on conditions with high circulating IGF-1. That is a speculation. You just don't know.
I have no idea what FOXO1 hypothesis is. I am not giving argumentation because I am not a molecular biologist and I am not pretending to be one. I'm just pointing to a logical fallacy that you committed.Leave a comment:
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Yeah, what I meant was that it could take a while before this will be sold over-the-counter. But indeed, those samples could reach us earlier.Leave a comment:
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Yes. Exact timeline/production tbd, but in a WORST case, it would be a few weeks from the conclusion of the indiegogo, the duration of which is also tbd. But launching indiegogo means "We are 100% confident this works, and samples will be to you within weeks." Again, proceeds would be used to scale up to full production and launch.Leave a comment:
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Please don't patronize me. I don't need you to simplify anything for me. Circulating IGF-1 is not simply "bound to the blood", there are binding proteins that modulate the biological actions of IGFs in target tissues. You do know what this means right ?
Also, your conclusions based on acromegaly are beyond speculation.
How is it speculation? Perhaps you'll go argue that the fact that pseudohermaphrodites or AIS people don't display androgenetic alopecia is speculation or not important? I'ts totally relevant to extrapolate data of such genetic diseases to AGA. In fact we have done this and discoveries are often made through this way.
People with Acrogemaly can display AGA, don't they? Then how can the FOXO1 hypothesis occur? Please explain, I'm interested in what you have to say.
You say that I speculate but don't give argumentation of anything at all. Aside from pointing me on carrier proteins (IGFPB family).Leave a comment:
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I base that from two things as I said people with these genetic defects. Plus the fact that nothing upstream before Androgens > AR happens. Things which can indirectly alter androgens, for instance circulating IGF-1 or for that fact metabolic syndrome or insulin resistance can be bad yes in speeding up AGA. That's obvious. Loading yourself on a diet full of phyto estrogens like soy can slow your hair loss tremendously too. You'll even feminize.
So indeed circulating IGF-1 levels are not directly important to the pathology of AGA. The paracrine action mediated from within the dermal papilla can be of importance of hair follicle biology itself. You do know what this means right? Cells are little machines they can communicate with each other. So the DP may send out IGF-1 to neighboring cells for instance the keratinocytes. Something that circulating IGF-1 which is expressed in the blood can't achieve. The dermal papilla produce IGF-1 and release that.
I don't see it being important for the pathology of AGA though and definitely don't see it doing much at all in relation to AGA. It might not even be important for the DP itself but only for the keratonicytes. If you don't agree then please state with what not and your argumentation. And if you don't understand, then be more specific and I'll simplify it even more.
Thank youLeave a comment:
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See Keki, this is what I mean. The full clinical trials won't start until June 1 if everything goes right and who knows how long those trials will take. You won't be using follicept for another few months and I think this can easily turn into a half year, if not longer.
But if you really want to wait, your call. Just remember that a lot of people have already told you to start with current treatments, not without reasonLeave a comment:
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I base that from two things as I said people with these genetic defects. Plus the fact that nothing upstream before Androgens > AR happens. Things which can indirectly alter androgens, for instance circulating IGF-1 or for that fact metabolic syndrome or insulin resistance can be bad yes in speeding up AGA. That's obvious. Loading yourself on a diet full of phyto estrogens like soy can slow your hair loss tremendously too. You'll even feminize.
So indeed circulating IGF-1 levels are not directly important to the pathology of AGA. The paracrine action mediated from within the dermal papilla can be of importance of hair follicle biology itself. You do know what this means right? Cells are little machines they can communicate with each other. So the DP may send out IGF-1 to neighboring cells for instance the keratinocytes. Something that circulating IGF-1 which is expressed in the blood can't achieve. The dermal papilla produce IGF-1 and release that.
I don't see it being important for the pathology of AGA though and definitely don't see it doing much at all in relation to AGA. It might not even be important for the DP itself but only for the keratonicytes. If you don't agree then please state with what not and your argumentation. And if you don't understand, then be more specific and I'll simplify it even more.
Also, your conclusions based on acromegaly are beyond speculation.Leave a comment:
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I agree, I think most people will continue to use Fin. I think the place that Folliept is coming from is the fact that they don't know how fin and follicept will interact. (According to what Devon said in a recent post.) Stopping minoxidil in order to get the hair back to the shrunken state makes more sense to me, (and I personally don't see how fin and follicept could interact, if anything there may be an additive or synergestic effect here but of course that is just a guess) but then again, I see where Follicept is coming from. They are going based on proof and hard scientific evidence, and right now their evidence will only be from treatment naive patients.Leave a comment:
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For US and Europe? I can't wait. If it works, trust me, i will take my 5 weeks of hollidays in Florida if we can't have it in Europe.Leave a comment:
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Quite curious indeed. The paper later this week should shed some light on it, but it is definitely a strange requirement. I imagine many people on this forum will probably go forward with fin+Follicept anyway (assuming it works well), perhaps this is just their current protocol given that they want to test the efficacy at baseline first. Unless Follicept has some effect on DHT I don't know why fin should be affected.
Then again I know pretty much nothing about this stuff.Leave a comment:
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See Keki, this is what I mean. The full clinical trials won't start until June 1 if everything goes right and who knows how long those trials will take. You won't be using follicept for another few months and I think this can easily turn into a half year, if not longer.
But if you really want to wait, your call. Just remember that a lot of people have already told you to start with current treatments, not without reasonLeave a comment:
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No no i know you are right, maybe i should start using fina at 0.25 at least, anyway it will be interesting to know exactly why a dht blocker isn't necessary at all according to themLeave a comment:
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But if you really want to wait, your call. Just remember that a lot of people have already told you to start with current treatments, not without reasonLeave a comment:
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