[quote]Yes, but my understanding is that it’s exceedingly rare with dermabrasion. It would be more accurate to call it a “rare anomaly” than a reliable phenomenon.
I don’t know if you can turn an anomaly into a viable treatment[/quote]
Maybe the follicle creation is truly a very rare thing or maybe it’s not. It’s certainly not all that rare for wounding to HEAL a follicle back to terminal in some way or another.
How many guys in MPB forums can tell you about needling/scraping the scalp and ending up with one or more odd random terminal hairs sprouting back very thick & strong? That’s pretty common. Its just not something anyone has been able to control & reproduce at will.
Are these healed follicles, or new ones? It seems strange that the process would not produce any gain on thousands of existing half-balded follicles and yet it occasionally heals one back to 100%. Maybe it makes more sense to conclude that the process occasionally produces an all-new follicle, and logically that follicle shows up without any MPB damage. I don’t know what the real story is here, but I have learned to never under-estimate how much basic stuff scientists haven’t bothered to learn about MPB.
Personally I have seen this happen on my head. And I also abraded one side of my hairline a few times a few years ago. I am convinced that side emerged in better shape than the other side. It is still thin, it is still losing, but the rate of loss slowed down noticeably compared to the other side that I left alone. I sometimes wonder about the therapeutic possibilities of simply dermabrading the scalp in balding areas periodically, all drugs aside. You wouldn’t want to be doing it 3-4 times a year but I wonder about once every 12 or 18 months. Its not going to make anyone into Elvis but the MPB community is still grasping at pathetic little pharmaceutical straws for any measurable improvement at all.
My point is that regardless of what is going on with Follica at this stage, their basic premise of using the wounding process to treat MPB makes more sense than anything else ever investigated. Including any kind of cellular manipulation & reinjection.
I would really hate to see Follica go under because they are the only ones in the entire HM game to take a sensible path to finding a treatment. Everyone else seems to start with a treatment idea they like and then trying to make it work on MPB. Follica actually started by looking at what is proven to work against MPB and then trying to understand & use it.
If I thought dermarolling + Minox would produce gains beyond what is dependent on continuing the drug, I would get interested. But I don’t want to mess with Minox just for “offset growth” and take on a permanent daily commitment to the stuff.
I have read many cases with pics of hypertrichosis occuring in wounds.,
Via dermabrasion, bone fractures w/ cast application, henna tatoos, ink tatoos, the list goes on and on. Its not too far fetched to believe that Follica has created new follicles in humans. Type of hair is a different story.
I’m not saying Follica hasn’t created new follicles with this method. I certainly think it’s possible. I just doubt it can create a huge amount of follicles. As jarjarbinx said, it probably works a little, sometimes. I like the word he used – a “herky-jerky” treatment.
If is an immature technology because Follica got ahead of itself. They are trying to base a company on what amounts to half a technology. They have the one half – the wounding part – which probably activates stem cells in the skin to some extent.
But they don’t have the “magic compound” part yet. They don’t have the amazing compound which optimizes skin perturbation to take it from a “sometimes a little hair grows” to a reliable grower of lots of hair.
The problem with this is, how do you continue to finance and run a company when you only have half a technology?
How do even apply for clinical trials when you have one part of the protocol, but the drug part is still unkown?
How long do you wait around for Dr. Cotsarelis to discover that amazing compound in his lab?
If their research staff is really disbanded, and if Garza says anything commercial is “years away” then we might as well declare them dead. Nothing is coming soon and nobody is preparing anything in the medium term.
Follica remains a wild card though, because Cotsarelis might stumble onto the right drug in the future and it might not take long for us to be able to get it onto our heads after that. The FDA would not let it happen for another XXX years but there are plenty of other places on earth that will.
[quote][postedby]Originally Posted by cal[/postedby]
If I thought dermarolling + Minox would produce gains beyond what is dependent on continuing the drug, I would get interested. But I don’t want to mess with Minox just for “offset growth” and take on a permanent daily commitment to the stuff.[/quote]
Not sure if I understood your post, but the study compared DA+minox to just minox and DA did produce gains well beyond minox.
Yeah I get that part. But I see no reason to think the gains are caused by anything other than a heavier dose of Minox to the scalp. Which means that the gains are still going to immediately start falling out as soon as you stop dosing with Minox every 24 hours for the rest of your life. It isn’t restoring any actual MPB damage, it is just giving some extra growth to offset it.
Hello,
do you know here why histogen use Wnta rather than WNT10b wich seems more powerful ? Also why they expect result when DHT and PGD2 seems still there… I mean… dont you think they are just pure bullsht ?
[quote][postedby]Originally Posted by Tom Vercetti[/postedby]
Hello,
do you know here why histogen use Wnta rather than WNT10b wich seems more powerful ? Also why they expect result when DHT and PGD2 seems still there… I mean… dont you think they are just pure bullsht ?[/quote]
Certain “flavors” of Wnt are less likely to cause “tumors”, that’s why.
I know… But it still possible to stimulate wnt10 for exemple. Still the problem of long term effect of these injction (effective or not) and the problem of androgen and pgd2 inthe scalp very high…
[quote][postedby]Originally Posted by Tom Vercetti[/postedby]
Hello,
do you know here why histogen use Wnta rather than WNT10b wich seems more powerful ? Also why they expect result when DHT and PGD2 seems still there… I mean… dont you think they are just pure bullsht ?
[postedby]Originally Posted by goata007[/postedby]
Certain “flavors” of Wnt are less likely to cause “tumors”, that’s why.[/quote]
It is entirely possible that Wnt3a or Wnt7a would work just as well as Wnt10b, all three are canonical Wnts. To be honest there hasn’t been enough research done to say conclusively which Wnts are actually playing a role in hair growth and which ones are not, or which would be better for hair growth. For instance the outer root sheath produces more Wnt3a the closer to the matrix and dermal papilla you get (as defined by George Cotasrelis’s group), which would make you think that it might be fairly important. Similarly it has been shown that Wnt10b is upregulated in the matrix of the hair follicle (can’t remember who showed this off the top of my head). The dermal papilla secretes Wnt5a, which is a noncanonical wnt, typically, which would indicate that non-canonical wnt signaling may actually play a large role in follicle development as well by inhibiting canonical wnt signaling. Then again, if the correct receptors, such as certain frizzled receptors and LRP5/6, then you can get canonical signaling with Wnt5a. So it is very ambiguous at the moment. However, it is certainly true that without nuclear β-catenin then you cannot form a hair follicle and continued growth of the hair follicle is impossible. The accumulation of nuclear β-catenin does not happen without the Wnts or IGF-1/insulin and various other growthfactors so β-catenin signaling is absolutely vital. New follicles will form in wounds of mice that overexpress Wnt7a. Tumors did not develop at the time frames reported with Wnt7a overexpresion. That’s probably our best lead so far. Also, FGF9, but that really just leads to the expression of wnts so it may not be necessary in the long run. Who knows, that’s what makes this kind of research exciting!
Thank you for your answer. What about possible result for histogen according to you ? I mean without anti DHT… or PGD2 bloker… what can be achieve you think ?
I think everyone here would greatly appreciate it if you would live up to your word and provide us with an update on your procedure. It has been months since we saw any pictures. Really this is so disappointing.
Do you still intend on keeping us informed, or have you given up on that?
hairman
[quote][postedby]Originally Posted by Tom Vercetti[/postedby]
Thank you for your answer. What about possible result for histogen according to you ? I mean without anti DHT… or PGD2 bloker… what can be achieve you think ?[/quote]
[quote][postedby]Originally Posted by Tom Vercetti[/postedby]
Thank you for your answer. What about possible result for histogen according to you ? I mean without anti DHT… or PGD2 bloker… what can be achieve you think ?[/quote]
Histogen may be successfull, it’s very difficult to know at the moment. They claim that the fibroblasts produce vegf, which is thought to be a contributing factor with how minoxidil works. So in that case you may see a benefit without 5aR inhibitors. As for prostaglandinD2 blocker I’m not sure there is any evidence that it will help (no NSAID has ever been reported to grow hair and neither did the PGD2 antagonists that went through clinical trials). That said, I don’t know…I would guess that high levels of PDG2 is more of a secondary effect of hair loss rather than a causative agent. Cotsarelis’s paper on the topic wasn’t the most convincing paper I’ve ever read.
IMO the most damning piece of evidence against the idea of PGD2 being a game-changer is the fact that Cots has already gone public with it. He never reveals anything of practical use nor anything indicative of where his current thinking is.
Cal, maybe it’s true that he never reveals anything of practical use, but what do we have to compare this with? Has there been anything he discovered that he didn’t reveal at first, but then later came out and proved to be of practical use?
I don’t think we can say the wounding study qualifies, because hair growth after wounding was already known, plus he didn’t conceal that information at first.
By your logic, we would only know if Cots has discovered something useful if he DOESN’T reveal it. But if he doesn’t reveal it, how would we know the discovery was made?
sorry its not 3 month then… so difficult to say… but… i was in belgium to mwamba clinic few days ago… and we checked the density at the 4 strip donor area, and… density is exact same… Soon we will make a patch test on 10 peoples to test and defiitely know more about this technique… But peoples wil have to make semi permanent very small tatoo in 4 different area at donor.
Who are you referring to when you speak of “we”. You mean Dr. Mwamba will do a patch test on 10 patients? Or are you speaking of Dr Nigam.
[quote][postedby]Originally Posted by Tom Vercetti[/postedby]
hey bro,
sorry its not 3 month then… so difficult to say… but… i was in belgium to mwamba clinic few days ago… and we checked the density at the 4 strip donor area, and… density is exact same… Soon we will make a patch test on 10 peoples to test and defiitely know more about this technique… But peoples wil have to make semi permanent very small tatoo in 4 different area at donor.
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