When will Aderans release it\'s phase 2 data?

Are the rest of you sitting on pins and needles waiting for Aderans phase 2 results? I am!!!

I want to see what Aderans phase 2 results look like. I think that Aderans phase 2 results are the wild card that could set the tone for the remainder of the battle against baldness. If Aderans phase 2 results are good or even great then that could affect what Aderans competitors do. It could put their competitors on the defensive and then perhaps their competitors would be more agreeable to early release and stuff like that. And if their competitors won’t cooperate then Aderans will get all of our business and Aderans competitors will be kicking themselves in their collective butts for being the big losers in the GREAT CURE-FOR-HAIRLOSS race as Aderans gets all of the glory and all of the profits.

I don’t care which of these companies I give my money to so if Aderans will give me what I want, but Histogen won’t, then I will give my money to Aderans instead. It all gets down to Aderans study results to be released very soon. I am so looking forward to this.

i hope they take their time.

last thing we need is for them to blow 15 years of research in one careless move.

take the time to get it right before diving into phase 3.

» Are the rest of you sitting on pins and needles waiting for Aderans phase 2
» results? I am!!!

So far Aderans has disappointed big time. This process is taking a RIDICULOUS amount of time (over 10 years – far longer than I expected) and now they keep lowering expectations. At first it was supposed to be “designer hair”, now we’re talking about bald spots being improved ever-so-slightly with a few extra hairs around the outer edges. Nothing that clearly takes a balding person and makes him look like he isn’t balding. Which was exactly what they were shouting to high heaven about when they started. So it’s really disappointing.

The one factor which might change this bad news, however is COMPOUNDABIILITY.

The reason for this is the following: Let’s say a “bad” treatment is something that only gives 1/10 of the results you’d like.

Well, even a bad treatment can be repeated 10 times. If results are compoundable, then repeating that bad treatment 10 times might result in a “good treatment” with truly cosmetically useful results.

Remember, Aderans is NOT a drug. It’s something completely different from Propecia or Rogaine. Drugs aren’t really “compoundable” in the same sense. You start using them and either they work or they don’t. If they work, you’ll see a gradual improvement, and then you’ll reach a plateau, where no further improvement is possible.

Of course, you MIGHT be able to improve the results of Propecia dramatically if you, say, took 20 pills a day. But then you’d also die. Or you could improve the results of Rogaine dramatically if you rubbed it into your scalp all day, every day. But again, if you did that, you’d die.

All drugs have a TOXICITY related to dosage. Their efficacy be compoundable in theory, but not in practice, because if you go beyond a certain point in dosing, you get extremely sick, or you die. Sure, you can go into “maintenance” mode and keep using the drug every day for the rest of your life. But that’s not the same as increasing the daily dosage. If you increase the daily dosage beyond a certain point, it may actually be GREAT for your hair, but you will get very sick and you may die.

That’s why nobody takes 20 Propecia tablets a day.

HT is definitely not compoundable except in the most limited sense. The doctors will tell you the more grafts you get, the more coverage you’ll get, but very soon you’ll hit a concrete wall. You run out of donor hair. And all the while they’re doing irreparable damage to your scalp.

Aderans’ treatment different in that there is no perceived toxicity to it, and there’s no brick wall hit from depleting donor hair or savaging the scalp. They’re injecting a culture of your own cells. So it is literally something you could have done safely, an unlimited number of times, depending of course on your funds.

I have my own theories about what contributes to Aderans’ efficacy or lack thereof, in any given situation.

Injecting cells into the scalp is like a crap shoot. Unlike in the embryo where proto-follicles are held together by naturally occurring embryonic chemicals and growth factors (which are very specific to the embryo and fetus and no longer exist in the adult), the cells injected by companies like Aderans and Replicel, once they get into your scalp, are NOT naturally held together in a ball to form a proto-follicle. So as soon as they’re injected, they tend to want to flow apart. Some of them may be absorbed by nearby hair follicles, which incorporate them into their structures and in this way become larger. But I believe this is rare. That’s why I say it’s like a crap shoot. Most of the cells injected float away and are wasted. Maybe 90% of the cells are wasted. They never contribute to any new hair growth at all. Maybe 10% are lucky enough to get incorporated into existing follicles, which might enlarge vellus follicles and in some cases turn them into terminal follicles. That is what probably accounts for the slight “new” hair growth seen in the Aderans patients. The remainder of the injected cells simply drift apart, never to be heard from again. They may be taken up by the bloodstream, eaten by macrophages, or just float away and die.

There is almost no way to address “crap shoot” problem in a single application. Aderans has tried using various tiny matrixes (matrices) or biodegradable scaffolds to hold the injected cells together long enough to form a follicle. I don’t know what the specific results of that idea are, because to my knowledge they haven’t been reported anywhere. The fact that such results haven’t been reported, even just in passing, to me is not promising. Maybe these scaffolds aren’t working nearly as well as they had conceived. This scaffold/matrix idea might be great in theory, but maybe it’s too complicated and fraught with problems to work in practice. That might be why we’re not hearing much about it. Sure there are various patents for it, but has the idea actually panned out?

However, forgetting about the scaffold idea, even a really disappointing treatment in which 10% of the injected cells cause some improvement, and 90% of the injected cells are wasted, should be, by its very nature, compoundable. If 10% of the injected cells are lucky enough to get incorporated into nearby follicles in each injection, causing those follicles to grow and become cosmetically visible, then of course that is a very low yield. But repeating that poor-yield procedure 10 times, would perhaps give you an impressive end result.

Unlike with drugs or HT, where you increase risk the “more” of the procedure you use, with Aderans procedure you do not increase risk on successive treatments. And each time, you have the same odds of growing hair. With the same odds each time and zero increased risk, results should be compoundable.

I’m not sure about this theory… Only time will tell. But that’s what I’m relying on now for Aderans. I think I’m right on this. But if this theory doesn’t pan out, Aderans may become yet another colossal failure.

I think 2012 was a big year for information on the status of MPB research. Unfortunately, the news was almost all bad. I would love to be optimistic, as i was before the start of 2012, but, based on the information that has come out, i don’t see much reason for it.

What we’ve learned is that the cell based approach is probably on it’s last legs. Unless replicel or aderans release some very dramatically improved results, that therapeutic approach is almost certainly dead. So far, three companies have made attempts at it and all of them have failed. Intercytex couldn’t grow new hair, replicel replicated (hey!) their results, and now we’ve seen that Aderans (after 10 grueling years of research)can’t grow hair either. I can’t see companies continuing to throw money down this wishing well. My guess is that the executives at Aderans will review the data from phase II, which is most likely to be unimpressive as we saw from their presentation, and will then pull the plug on the clinical trials. Phase III is by far the most costly expense in the clinical process and companies don’t engage in it unless they have a high level of confidence in their protocol. From the outside what we’ll see are repeated delays in the initiation of phase III, probably some confusing press releases and eventually total silence from them.

Histogen looks ok so far. It’s certainly not going to restore hair to the levels that they initially indicated in their first trial. They’ve back pedaled a lot on expectations for regrowth - and i think that tells us quite a bit about how it’s working. The photos they’ve released have been for women, which is good and all, but, is not quite a NW5 scalp of a bald man. There is probably good reason we haven’t seen results from that level of baldness. I’m guessing at best this will help slow down hairloss and will be good for the next generation of baldies who are yet to start down the tortured path of mpb - those in their teens now.

Follica is dead as a door nail.

Lauster is more than 15-20 years out. He hasn’t even grown a full hair follicle yet. So, it will be years before he can do that. Once that is worked out, he can then begin clinical trials which, as we’ve seen, take 7-10 years on average. This treatment will not be available in time for anyone who is now over 20.

So, as it stands right now, it looks like hair transplants are the only treatment that can provide significant hair. Perhaps Dr Cole with his minimal depth fue will be the next thing. Gho seems to be having some success with hst, so maybe that is a way (a very expensive way) forward? But even with that, surgical wounding limits the density that can be achieved. And in my opinion transplant density, even the very good ones, is not too good looking.

I agree on a lot of that.

But I don’t think Aderans is at so much risk of stopping now. As long as they can make a plausible case to their investors that their posted phase-II results can be achieved for the average patient, then I think they will push forward to market.

Yes I know that’s not guaranteed but hopefully one of their protocols is more consistently successful than others and shows more promise. (And if there is any hope of compounding gains from repeated sessions then I would be pushing forward even if the progress was still very weak.)

People are quick to point out that ARI is struggling to improve on the results of Fin & Minox. But they are not offering the same thing. They are offering something that needs no ongoing daily maintenance and should have no side effect problems. That carries more weight in the mainstream market than it does on here. Guys in the MPB community are desperate for visible cosmetic improvement at all costs. But a lot of the mainstream market is more easily put off by downsides to any treatment. Right now the vast majority of men with MPB have never tried to do anything about it at all.

That’s a pretty fair assessment Mr. Z. I’m not as well versed in the science of hairloss as some of the posters on here, but I totally agree with your assessment.

Replicel hasn’t shown any real evidence that their treatment is actually effective.

The way Histogen presented their photos and results really turned me off. There was a huge difference in lighting/flash in the before and after pictures. The macro photographs they also presented showed either no improvement in hair count or two completely different areas of the scalp!

Aderans is probably the best bet out of all three but even their photos were somewhat underwhelming considering how much time and research has gone into it.

Even if one or more of those options turns out to be an effective treatment, I don’t see any single one ending up as a cure. It might increase your density but it won’t turn a NW7 into a NW1. In this case, you’ll probably still need to supplement the treatment with a hair transplant.

The hair transplant procedures that preserve the donor area seem to be the most promising at this very moment. Even the work of Dr. Lauster or the Tsuji Lab will require surgical implantation at the recipient end. So in all of these treatments the aesthetic results still depend on the artistic skill of your surgeon. In other words, you won’t be able to get back your “true” hair pattern mother nature designed before the onset of MPB.

In terms of the density issues, it will probably be a while until you can get your natural density back but i think technology will improve on the implantation side of things that will allow for higher densities in the future. I don’t think this has been a research priority given how limited the donor supply is with traditional hair transplant procedures. Regardless, I’ve seen some impressive results in terms of density from some docotors, even with a limited donor.

You know, I think that Aderans has made a good case that they can grow hair with their cells utilizing the follicles that already exist on your scalp but they can not produce new follicles. I think that this means that if you have short thinning hairs they can turn them back into thick terminal hairs. The thing is that Aderans might be a good treatment to add if you can find a treatment that will give you some fine short hairs and then use Aderans to turn those fine short hairs into thick terminal hairs. I’m thinking a treatment like PS1 which creates new follicles - get PS1 first and then get the aderans treatment after using PS1.

What do you all think about that idea?

» That’s a pretty fair assessment Mr. Z. I’m not as well versed in the
» science of hairloss as some of the posters on here, but I totally agree
» with your assessment.
»
» Replicel hasn’t shown any real evidence that their treatment is actually
» effective.
»
» The way Histogen presented their photos and results really turned me off.
» There was a huge difference in lighting/flash in the before and after
» pictures. The macro photographs they also presented showed either no
» improvement in hair count or two completely different areas of the scalp!
»
» Aderans is probably the best bet out of all three but even their photos
» were somewhat underwhelming considering how much time and research has gone
» into it.
»
» Even if one or more of those options turns out to be an effective
» treatment, I don’t see any single one ending up as a cure. It might
» increase your density but it won’t turn a NW7 into a NW1. In this case,
» you’ll probably still need to supplement the treatment with a hair
» transplant.
»
» The hair transplant procedures that preserve the donor area seem to be the
» most promising at this very moment. Even the work of Dr. Lauster or the
» Tsuji Lab will require surgical implantation at the recipient end. So in
» all of these treatments the aesthetic results still depend on the artistic
» skill of your surgeon. In other words, you won’t be able to get back your
» “true” hair pattern mother nature designed before the onset of MPB.
»
» In terms of the density issues, it will probably be a while until you can
» get your natural density back but i think technology will improve on the
» implantation side of things that will allow for higher densities in the
» future. I don’t think this has been a research priority given how limited
» the donor supply is with traditional hair transplant procedures.
» Regardless, I’ve seen some impressive results in terms of density from some
» docotors, even with a limited donor.

Roger_that,

I wonder if Aderans is injecting growth factors with the cells or if Aderans is just injecting cells that have been treated with growth factors??? I think this could make a big difference. If they are just injecting cells that have been treated/cured in growth factors then that could be why we aren’t seeing more regrowth. You see, these cells are large…perhaps too large to get inside of the follicles that have shrunk down to peach fuzz size. This is why Aderans should inject growth factors with the cells so the growth factors can enlarge the follicles enough to make it possible for the follicles to allow the cells entry into the follicles. I think that follicles would have to be intermediate size to be big enough for the newly injected cells to find an entry way big enough to get inside the follicles. When these cells are injected into the skin they might be sailing right past all of our peach fuzz follicles simply because those follicles are too small for the cells to find an entry-way into.

Is there a product that can turn a lot of peach fuzz into a lot of intermediate hairs? I wonder if bimatoprost can do that.

» I think 2012 was a big year for information on the status of MPB research.
» Unfortunately, the news was almost all bad. I would love to be optimistic,
» as i was before the start of 2012, but, based on the information that has
» come out, i don’t see much reason for it.
»

I broadly agree with what you say here. We have a ridiculously long way to go, and a lot of science to understand before we can grow hair regularly. To talk of “release date in 2013/14/15” is sheer idiocy.

The cell-culturing method sounded really promising, but it seems that there are many steps that need to be worked out. You’re taking dissociated cells and somehow trying to form a hair follicle out of it. It’s really cutting edge science. It may yet work, but it’s likely a lot more work is needed. It was mistaken to expect Replicel to succeed where ARI, a far better funded and more experienced operation has struggled. In addition to the notion that Replicel’s patent was about a cell that nobody else recognizes as a distinct cell type. I had felt that if anybody would get there first, it would be ARI.

I suspect Follica did grow hair, but it’s unlikely that they grew cosmetically significant results. A smattering of intermediate or vellus hairs won’t do us any good. Like ARI, their overall idea might be very promising, but one failed trial can derail a small startup. It is a shame because this was the most talented team and professionally run operation in a field full of snake oils and shills.

I think it’s a bad idea to put much faith into these little one man operations like Lauster and Gho. When they raise millions in funding and build out a deep scientific team, then we can talk.

Take your fin/dut daily.

» I think it’s a bad idea to put much faith into these little one man
» operations like Lauster and Gho. When they raise millions in funding and
» build out a deep scientific team, then we can talk.

The research facility of the Berlin Charité is not exactly “a one man show”. Many scientific and advancements have been achieved in academic environment.

» Roger_that,
»
» I wonder if Aderans is injecting growth factors with the cells or if
» Aderans is just injecting cells that have been treated with growth
» factors??? I think this could make a big difference. If they are just
» injecting cells that have been treated/cured in growth factors then that
» could be why we aren’t seeing more regrowth. You see, these cells are
» large…perhaps too large to get inside of the follicles that have shrunk
» down to peach fuzz size. This is why Aderans should inject growth factors
» with the cells so the growth factors can enlarge the follicles enough to
» make it possible for the follicles to allow the cells entry into the
» follicles.

No. This theory is wrong for a number of reasons, because the amount the follicles have miniaturized does not cause them to be too small for cells to enter. Even a miniaturized follicle is still on the order of 10-100 thousands of times bigger than individual cells. In any event, it doesn’t matter because the cells aren’t trying to “enter” anything. It’s more like the injected cells get close to the follicle, maybe at the dermal papilla, and “glom onto” the follicle, adhering with it and uniting with it. It’s not a matter of comparative size at all. And even if they had to enter a “door” (i.e., a space) somewhere along the side of the follicle, those spaces wouldn’t be any different in size in a vellus follicle as compared with a terminal one.

I think that follicles would have to be intermediate size to be
» big enough for the newly injected cells to find an entry way big enough to
» get inside the follicles. When these cells are injected into the skin they
» might be sailing right past all of our peach fuzz follicles simply because
» those follicles are too small for the cells to find an entry-way into.

Again, this is not because of size. Even if the follicles were full-sized terminal follicles, it would be a problem because of the scale of the relative DISTANCES within the epidermis/dermis which are much too big to expect that injected cells will always hit a follicle. The spacing between the follicles is just too vast, period – whether the follicles are big or small doesn’t matter. The relative differences in size between terminal and vellus follicles is negligible when you compare it to the “vast” distances between follicles, period. The “vast” distances between the follicles are equally vast in comparison to the size of cells, whether the follicles are terminal or vellus.

To get an idea of the kinds of scales we’re talking about here, and the task at hand, think of this analogy. Picture an Olympic-sized swimming pool, with some kind of buoys, 3-5 feet wide in size, spaced every 15 feet or so apart, all the way up and down the length and breadth of the pool (that’s 50 buoys by my calculation). Then picture someone on a platform hanging from the roof, 75 feet above the pool, throwing handfuls of grapes at the water. They’re trying to aim for the buoys. The position of the platform can be moved anywhere over the pool, but the height can’t. What are the chances that the entire handful of grapes will hit a buoy when thrown from that height? What percentage of the grapes do you think will hit the buoy on each throw?

That is SOMETHING like what I’m talking about here.

I think the idiocy is coming from you. Any person with a 3-digit IQ can see that Histogen is the silver bullet and some of these other things might pan out if we can figure out a way to use them effectively. For example, Aderans clearly turns intermediate hairs into terminal hairs so the problem is how to turn vellus hairs into intermediate hairs and then we’re home free. Bimatorost might do that for all we know. I think that there is more info coming over the next few months that will clear up the picture and I think that the news is going to be all good news. I think I’m right. Let’s wait a few months and see what news comes from Histogen, Allergan (bimatoprost), and Aderans and then let’s see who ends up being the idiot. I’m highly confident that it will be YOU and the people who agree with YOU.

» » I think 2012 was a big year for information on the status of MPB
» research.
» » Unfortunately, the news was almost all bad. I would love to be
» optimistic,
» » as i was before the start of 2012, but, based on the information that
» has
» » come out, i don’t see much reason for it.
» »
»
» I broadly agree with what you say here. We have a ridiculously long way to
» go, and a lot of science to understand before we can grow hair regularly.
» To talk of “release date in 2013/14/15” is sheer idiocy.
»
» The cell-culturing method sounded really promising, but it seems that there
» are many steps that need to be worked out. You’re taking dissociated cells
» and somehow trying to form a hair follicle out of it. It’s really cutting
» edge science. It may yet work, but it’s likely a lot more work is needed.
» It was mistaken to expect Replicel to succeed where ARI, a far better
» funded and more experienced operation has struggled. In addition to the
» notion that Replicel’s patent was about a cell that nobody else recognizes
» as a distinct cell type. I had felt that if anybody would get there first,
» it would be ARI.
»
» I suspect Follica did grow hair, but it’s unlikely that they grew
» cosmetically significant results. A smattering of intermediate or vellus
» hairs won’t do us any good. Like ARI, their overall idea might be very
» promising, but one failed trial can derail a small startup. It is a shame
» because this was the most talented team and professionally run operation in
» a field full of snake oils and shills.
»
» I think it’s a bad idea to put much faith into these little one man
» operations like Lauster and Gho. When they raise millions in funding and
» build out a deep scientific team, then we can talk.
»
» Take your fin/dut daily.

» » Roger_that,
» »
» » I wonder if Aderans is injecting growth factors with the cells or if
» » Aderans is just injecting cells that have been treated with growth
» » factors??? I think this could make a big difference. If they are just
» » injecting cells that have been treated/cured in growth factors then that
» » could be why we aren’t seeing more regrowth. You see, these cells are
» » large…perhaps too large to get inside of the follicles that have
» shrunk
» » down to peach fuzz size. This is why Aderans should inject growth
» factors
» » with the cells so the growth factors can enlarge the follicles enough to
» » make it possible for the follicles to allow the cells entry into the
» » follicles.
»
» No. This theory is wrong for a number of reasons, because the amount the
» follicles have miniaturized does not cause them to be too small for cells
» to enter. Even a miniaturized follicle is still on the order of 10-100
» thousands of times bigger than individual cells. In any event, it doesn’t
» matter because the cells aren’t trying to “enter” anything. It’s more
» like the injected cells get close to the follicle, maybe at the dermal
» papilla, and “glom onto” the follicle, adhering with it and uniting with
» it. It’s not a matter of comparative size at all. And even if they had
» to enter a “door” (i.e., a space) somewhere along the side of the follicle,
» those spaces wouldn’t be any different in size in a vellus follicle as
» compared with a terminal one.
»
» I think that follicles would have to be intermediate size to be
» » big enough for the newly injected cells to find an entry way big enough
» to
» » get inside the follicles. When these cells are injected into the skin
» they
» » might be sailing right past all of our peach fuzz follicles simply
» because
» » those follicles are too small for the cells to find an entry-way into.
»
» Again, this is not because of size. Even if the follicles were full-sized
» terminal follicles, it would be a problem because of the scale of the
» relative DISTANCES within the epidermis/dermis which are much too
» big to expect that injected cells will always hit a follicle. The spacing
» between the follicles is just too vast, period – whether the follicles are
» big or small doesn’t matter. The relative differences in size between
» terminal and vellus follicles is negligible when you compare it to the
» “vast” distances between follicles, period. The “vast” distances between
» the follicles are equally vast in comparison to the size of cells, whether
» the follicles are terminal or vellus.
»
» To get an idea of the kinds of scales we’re talking about here, and the
» task at hand, think of this analogy. Picture an Olympic-sized swimming
» pool, with some kind of buoys, 3-5 feet wide in size, spaced every 15 feet
» or so apart, all the way up and down the length and breadth of the pool
» (that’s 50 buoys by my calculation). Then picture someone on a platform
» hanging from the roof, 75 feet above the pool, throwing handfuls of grapes
» at the water. They’re trying to aim for the buoys. The position of the
» platform can be moved anywhere over the pool, but the height can’t. What
» are the chances that the entire handful of grapes will hit a buoy when
» thrown from that height? What percentage of the grapes do you think will
» hit the buoy on each throw?
»
» That is SOMETHING like what I’m talking about here.

I hope you’re right because if you are then that bodes well for the idea of compoundability.

You see, any fair-minded person can see that there is some regrowth in the before and after pic involving the most talked about test subject. Clearly he has some new terminal hairs at the outer part of the bald spot on his crown and he even has some new terminal looking hairs in the inner center area of the crown. If these were intermediate hairs that Aderans turned into terminal hairs then that means we would have to turn our vellus hairs into intermediate hairs before we can expect more from Aderans but if those are vellus hairs turned into terminal hairs then that means that Aderans can turn vellus hairs into terminal hairs and all we have to do is get follow/up injections and each time we do so we will turn more and more vellus hairs into terminal hairs.

All of that having been said I would like to point out that when researchers do a presentation about male pattern hair loss they always show animated illustrations of follicles miniaturizing due to AGA and it’s pretty clear that AGA follicles do shrink dramatically. Now if you’re right and that shrinkage is not preventing Aderans cells from getting into the follicle then I do think that the treatment is likely compoundable. But if the follicles shrink down small enough that Aderans cells can’t get inside of the follicles then I think that Aderans is not compoundable unless you can first enlarge the follicles to the intermediate size. I hope you’re right because Aderans did get some follicles to go terminal so if you’re right then repeated injections should do the same thing again - get more follicles to go terminal (compoundable).

» All of that having been said I would like to point out that when
» researchers do a presentation about male pattern hair loss they always show
» animated illustrations of follicles miniaturizing due to AGA and it’s
» pretty clear that AGA follicles do shrink dramatically. Now if you’re
» right and that shrinkage is not preventing Aderans cells from getting into
» the follicle then I do think that the treatment is likely compoundable. But
» if the follicles shrink down small enough that Aderans cells can’t get
» inside of the follicles then I think that Aderans is not compoundable
» unless you can first enlarge the follicles to the intermediate size. I
» hope you’re right because Aderans did get some follicles to go terminal so
» if you’re right then repeated injections should do the same thing again -
» get more follicles to go terminal (compoundable).

I still don’t know what you’re talking about. You’re talking as if the cells have to enter some sort of “opening” in the follicle which is big if it’s a terminal follicle and gets smaller if the follicle is miniaturized. This is a huge misunderstanding of the biology here; you’re not even close in your understanding. What you’re saying is completely unscientific. It’s way off the mark!

» It is a shame
» because this was the most talented team and professionally run operation in
» a field full of snake oils and shills.

Other than the fact that Cotsarelis licensed them some of his research, what about them constituted a “talented team and professionally run operation”? So they recruited a bunch of well-credentialed names to appear on their website as part of their “Board of Directors”. What exactly have any of these people done to make Follica a success?

» » if the follicles shrink down small enough that Aderans cells can’t get
» » inside of the follicles
then I think that Aderans is not compoundable
» » unless you can first enlarge the follicles to the intermediate size. I
» » hope you’re right because Aderans did get some follicles to go terminal
» so
» » if you’re right then repeated injections should do the same thing again
» -
» » get more follicles to go terminal (compoundable).
»
» I still don’t know what you’re talking about. You’re talking as if the
» cells have to enter some sort of “opening” in the follicle which is big if
» it’s a terminal follicle and gets smaller if the follicle is miniaturized.
» This is a huge misunderstanding of the biology here; you’re not even
» close in your understanding. What you’re saying is completely
» unscientific. It’s way off the mark!

This is truly hilarious.

» » Roger_that,
» »
» » I wonder if Aderans is injecting growth factors with the cells or if
» » Aderans is just injecting cells that have been treated with growth
» » factors??? I think this could make a big difference. If they are just
» » injecting cells that have been treated/cured in growth factors then that
» » could be why we aren’t seeing more regrowth. You see, these cells are
» » large…perhaps too large to get inside of the follicles that have
» shrunk
» » down to peach fuzz size. This is why Aderans should inject growth
» factors
» » with the cells so the growth factors can enlarge the follicles enough to
» » make it possible for the follicles to allow the cells entry into the
» » follicles.
»
» No. This theory is wrong for a number of reasons, because the amount the
» follicles have miniaturized does not cause them to be too small for cells
» to enter. Even a miniaturized follicle is still on the order of 10-100
» thousands of times bigger than individual cells. In any event, it doesn’t
» matter because the cells aren’t trying to “enter” anything. It’s more
» like the injected cells get close to the follicle, maybe at the dermal
» papilla, and “glom onto” the follicle, adhering with it and uniting with
» it. It’s not a matter of comparative size at all. And even if they had
» to enter a “door” (i.e., a space) somewhere along the side of the follicle,
» those spaces wouldn’t be any different in size in a vellus follicle as
» compared with a terminal one.
»
» I think that follicles would have to be intermediate size to be
» » big enough for the newly injected cells to find an entry way big enough
» to
» » get inside the follicles. When these cells are injected into the skin
» they
» » might be sailing right past all of our peach fuzz follicles simply
» because
» » those follicles are too small for the cells to find an entry-way into.
»
» Again, this is not because of size. Even if the follicles were full-sized
» terminal follicles, it would be a problem because of the scale of the
» relative DISTANCES within the epidermis/dermis which are much too
» big to expect that injected cells will always hit a follicle. The spacing
» between the follicles is just too vast, period – whether the follicles are
» big or small doesn’t matter. The relative differences in size between
» terminal and vellus follicles is negligible when you compare it to the
» “vast” distances between follicles, period. The “vast” distances between
» the follicles are equally vast in comparison to the size of cells, whether
» the follicles are terminal or vellus.
»
» To get an idea of the kinds of scales we’re talking about here, and the
» task at hand, think of this analogy. Picture an Olympic-sized swimming
» pool, with some kind of buoys, 3-5 feet wide in size, spaced every 15 feet
» or so apart, all the way up and down the length and breadth of the pool
» (that’s 50 buoys by my calculation). Then picture someone on a platform
» hanging from the roof, 75 feet above the pool, throwing handfuls of grapes
» at the water. They’re trying to aim for the buoys. The position of the
» platform can be moved anywhere over the pool, but the height can’t. What
» are the chances that the entire handful of grapes will hit a buoy when
» thrown from that height? What percentage of the grapes do you think will
» hit the buoy on each throw?
»
» That is SOMETHING like what I’m talking about here.

BTW when I used the word doorway or entry way in the context of cells getting inside of follicles I was not referring to an actual location where injected cells could enter follicles. I meant that more figuratively than literally. Of course I realize that follicles do not come equipped with doorways/entry-ways for injected cells. What I meant is that these injected cells have to get inside of the follicles in order to affect hair growth and getting injected cells inside of follicles would require some things such the follicles being big enough to accept these cells. So when I used the term doorway or entry way I meant that in a sense that the follicles would have to be able to of the right size to accept and contain these cells, which are larger than the cells already inside of miniaturized cells. I’m sure you realize that I meant that but some readers may not so I wanted to clarify that.

» » All of that having been said I would like to point out that when
» » researchers do a presentation about male pattern hair loss they always
» show
» » animated illustrations of follicles miniaturizing due to AGA and it’s
» » pretty clear that AGA follicles do shrink dramatically. Now if you’re
» » right and that shrinkage is not preventing Aderans cells from getting
» into
» » the follicle then I do think that the treatment is likely compoundable.
» But
» » if the follicles shrink down small enough that Aderans cells can’t get
» » inside of the follicles then I think that Aderans is not compoundable
» » unless you can first enlarge the follicles to the intermediate size. I
» » hope you’re right because Aderans did get some follicles to go terminal
» so
» » if you’re right then repeated injections should do the same thing again
» -
» » get more follicles to go terminal (compoundable).
»
» I still don’t know what you’re talking about. You’re talking as if the
» cells have to enter some sort of “opening” in the follicle which is big if
» it’s a terminal follicle and gets smaller if the follicle is miniaturized.
» This is a huge misunderstanding of the biology here; you’re not even
» close in your understanding. What you’re saying is completely
» unscientific. It’s way off the mark!

I definitely understand that there is not literally a built-in doorway for injected material to get inside of follicles. I don’t mean it literally when I use the terms “opening” or “doorway” or “entry way”. I mean those terms in a virtual sense rather than a literal sense. I mean that the follicles have to have the right characteristics, including size, in order to receive and intake the cells. To give an extreme example, it would obviously be impossible for cells to get inside of follicles if the cells are larger than the follicles and the cells would not have to be larger than follicles in order to make penetration of the cells impossible. When I use terms like “doorway” or “entry-way” or “opening” I’m using those terms as synonyms for the concept of “an opportunity created.” I’m saying that the follicles have to have characteristics (including, but not limited to, size) that create an opportunity for the cells to get inside of the follicles.

» BTW when I used the word doorway or entry way in the context of cells
» getting inside of follicles I was not referring to an actual location where
» injected cells could enter follicles. I meant that more figuratively than
» literally. Of course I realize that follicles do not come equipped with
» doorways/entry-ways for injected cells. What I meant is that these
» injected cells have to get inside of the follicles in order to affect hair
» growth and getting injected cells inside of follicles would require some
» things such the follicles being big enough to accept these cells. So when
» I used the term doorway or entry way I meant that in a sense that the
» follicles would have to be able to of the right size to accept and contain
» these cells, which are larger than the cells already inside of miniaturized
» cells. I’m sure you realize that I meant that but some readers may not so
» I wanted to clarify that.

Where are you getting the idea that there’s a “right size” for the follicles to accept injected cells? I can think of no scientific reason for this.

Also, you wrote: “… the follicles would have to be able to of the right size to accept and contain these cells, which are larger than the cells already inside of miniaturized cells.”

What makes you think the injected cells are larger than the cells already inside the miniaturized follicles??

When a follicle miniaturizes, the SIZE OF THE CELLS DOES NOT CHANGE. The cells stay the same size as they always were, e.g., when the follicle was a big fat terminal follicle.

What changes is the NUMBER of cells. A miniaturized follicle has a lot FEWER cells than a terminal follicle.

The size of the cells DOES NOT CHANGE. A DP cell is a DP cell, and they’re almost exactly the same size. Same for the rest of the different cell types.

» » BTW when I used the word doorway or entry way in the context of cells
» » getting inside of follicles I was not referring to an actual location
» where
» » injected cells could enter follicles. I meant that more figuratively
» than
» » literally. Of course I realize that follicles do not come equipped with
» » doorways/entry-ways for injected cells. What I meant is that these
» » injected cells have to get inside of the follicles in order to affect
» hair
» » growth and getting injected cells inside of follicles would require some
» » things such the follicles being big enough to accept these cells. So
» when
» » I used the term doorway or entry way I meant that in a sense that the
» » follicles would have to be able to of the right size to accept and
» contain
» » these cells, which are larger than the cells already inside of
» miniaturized
» » cells. I’m sure you realize that I meant that but some readers may not
» so
» » I wanted to clarify that.
»
» Where are you getting the idea that there’s a “right size” for the
» follicles to accept injected cells? I can think of no scientific reason
» for this.
»
» Also, you wrote: “… the follicles would have to be able to of the right
» size to accept and contain these cells, which are larger than the cells
» already inside of miniaturized cells.”
»
» What makes you think the injected cells are larger than the cells already
» inside the miniaturized follicles??
»
» When a follicle miniaturizes, the SIZE OF THE CELLS DOES NOT CHANGE.
»
The cells stay the same size as they always were, e.g., when the
» follicle was a big fat terminal follicle.
»
» What changes is the NUMBER of
» cells.
A miniaturized follicle has a lot FEWER
» cells than a terminal follicle.
»
» The size of the cells DOES NOT CHANGE. A DP cell is a DP cell, and
» they’re almost exactly the same size. Same for the rest of the different
» cell types.

I assumed that since in AGA the follicles are getting smaller, then that means that everything inside of the follicles, including the cells, are getting smaller. Are you 100% sure that I’m wrong about this??? I always assumed that the cells inside of follicles shrink in AGA along with the shrinkage of the rest of the follicles. I assumed that, that is why the hair shafts shrink. I assumed that smaller cells produced smaller hairs. Are you 100% sure that I’m wrong???