It doesn’t say how or what protocol they are going to use. Is this a trial or this is the real deal that is being marketed now?
Would you pay up to $10,000 plus airfare for this if it was a trial?
You have to read into what Dr. P.Kemp said. They are testing perhaps on a few selected a few protocols. It’s not happening yet.
It is happening only in the sense that Hair Clone is ready to freeze and store your hair cells, but I don’t think they have an effective protocol yet. Read the long Q&A thread for Hair Clone, it sounds like Dr. Kemp 's intention is to use the money generated by the storage service to fund future hair multiplication protocols.
The more I think about it, the more I think the model of injecting cells into the skin to rejuvenate miniaturized follicles has some very serious limitations that may be impossible to totally overcome. I think the true solution will be cell based, but it’ll be about growing de novo follicles.
Didn’t Jahoda prove that injecting cells should work when he injected cellular material into his wife’s arm and it grew hair? And I think he also did the same thing with his own arm a few years later. Plus, Intercytex, Aderans, and now Replicel have all gotten small regrowth with their cellular injection therapies. I even saw limited regrowth on some of Dr. Nigam’s cell therapy patients. I also have numerous theoretical/hypothetical reasons for why cell injections might not work, but I think the body of hard evidence (Jahoda success plus small success by Aderans, Intercytex, Replicel and even Dr. Nigam) indicates that it could work if the inductivity problem is solved.
It’s not that it can’t work, it’s that it just doesn’t work very well. What I’m saying is that for every injection, perhaps 99% or more of the cells are wasted and never hit their targets.
Dr Jahoda’s experiment was a bit different than just injecting cultured DP cells. He took “fresh” (0th passage) DP cells and implanted them into his wife’s forearm. Apparently it was some kind of surgical implantation with an incision (I think James Bond has explained the details here before). That’s not the same thing as creating a mass culture of cells and injecting them.
I reached my (tentative) conclusion through deductive reasoning. Why has progress in all projects involving injecting dissociated DP cells been so slow? Why have 2 well-funded companies failed? Why has every other effort flopped? And why do researchers nonetheless still continue with this idea?
My reluctant conclusion is that it works “a little bit”, just enough to keep researchers pursuing it. But it possibly doesn’t work well enough to turn into a large-scale commercial solution.
What possible things would cause this lack of progress? To me, it would have to be some kind of serious limitation inherent in the method.
To me, there are 2 possibilities:
(1) Cultured cells lose some inductivity with each passage, until they have little or no trichogenicity; or
(2) Some kind of inherent flaw exists in the method itself.
Knowing something about how cells behave in the body, I think (2) is at least as likely as (1). Yet, only (1) has received the attention of researchers like Drs Jahoda, Christiano, Washenik, etc.
Since alternative (1) has received a lot of attention over the years, and we still seem to be at the same place (little or no progress made), then I think it behooves researchers to start considering alternative (2) a bit.
By the way, there is a good way of testing to rule in or rule out alternative (2), which James Bond hinted at earlier on the forum.
Perhaps the reason they continue to only achieve limited regrowth is because they still haven’t solved that same old inductivity problem. Yes you’re right that this problem has received a lot of attention but just because they’ve put a lot of time into that problem doesn’t change the fact that they still haven’t solved it. And they know with certainty that they haven’t solved that problem because they have tools and methods for testing the amount of inductivity is inside the cells. They can (and do) experiment with different structures and mediums for culturing the cells and they test for the amount of inductivity in the cells during and after culture. They’re making significant progress but they still can’t preserve enough inductivity to know one way or another whether or not solving the inductivity problem alone will make cell injections alone cure hair loss. It’s too early to make that judgment.
That having been said, I’ve kind of had this same issue (that you’re raising) on the back of my mind for quite some time. I worry that perhaps these cells have to land in a very specific target area after being injected and they all can’t land within that area, which I will call the “therapeutic area”. That area is only so big and once it fills up with newly injected cells there’s no more room for injected cells to land there so any other cells that would have landed there go elsewhere, where they serve no useful purpose.
This is why I’m a little excited that Shiseido is doing repeat injections instead of just one treatment date. I’m about 90% sure there won’t be any additional benefit from the repeat treatments but I also think that if only a limited number of the injected cells are able to land on the therapeutic area where they can do some good then additional treatments should result in better hair growth. So I do think that there’s a real chance that Shiseido’s repeat treatments could possibly produce a breakthrough. And if they do then that will mean that both Intercytex and Aderans make a mistake when they discontinued their clinical trials. They would have been better served to add repeat injections.
A couple of things –
- When you say “they test for the amount of inductivity in the cells during and after culture”, I think that’s not exactly what they’re testing for during culture. Actually, they’re testing for the presence of activated genes which are ASSOCIATED with inductivity. This is correlation by association, but it is not a direct test of inductivity.
So what they’re doing is, they look at what genes are activated, and what genes are inactivated, in fully inductive cells. Then they look at what genes are activated and inactivated in cells cultured in different ways. The more concordance they see (matches in genes being active or inactive), the more they will ascribe inductivity to the cultured cells. The goal is go keep refining culturing techniques until the gene profile (active vs. inactive genes) of the cultured cells is as close to, or identical with, the gene profile of the fully-inductive (non-cultured) cells.
This is a good method, but has the potential for error, because one can’t assume that EVERYTHING in the genetic profile of the fully inductive cells is a contributor to their inductivity. Also, there’s potential for other problems. For instance, what if doing one thing to the culture improves the concordance of one gene, but eliminates the concordance of another gene? So, the process is almost like flying blind. It’s a good process when you don’t know that much about what each gene actually does, but there are a lot of variables and unpredictable things that can happen.
- The issue of the “therapeutic area” you discussed – I agree with your description of that, but the problem may even be deeper than that. In order for the injections to work well, a few things have to happen: (A) lots of the cells, per injection, have to land at the therapeutic area; (B) they have to actually stay there; © they have to PENETRATE the epithelium around the follicle, which is almost like a capsule. They have to make their way past several layers or stacks of cells; and (D) they have to be integrated into the tissue of the dermal papilla.
Even if you can get a lot of cells to land at the therapeutic area (A), what guarantee is there they will stay there? What’s holding them there? I would argue not much. THEN, they have to penetrate obstacles – the outer epithelium of the follicle (B). How do they do this? Does the follicle suck the cells inside? I doubt it. There is no magical force pulling the injected cells into the dermal papilla. And if they do get past all this, how are they integrated into the dermal papilla?
The last step might be the easiest, but in order for the last step to occur, steps A, B and C have to work just right.
What percentage of the injected cells do you think are fortunate enough to make it past all that? I would guess it’s quite a low percentage.
This explanation might also answer the question of why injecting cells seems to work “just a bit” – enough to keep researchers interested – but never good enough to say, “OK, success! Now we can turn this into a commercial therapy.”
Maybe what we are seeing is just the “tip fo the iceberg” – the 1% or fewer cells that manage to integrate into follicles. This would explain the technique working just a little bit – having a very low (but, as Dr. Kemp said, “importantly not zero”) success rate.
A technique where only a very small percentage of cells succeed in inducing regrowth, and that works irregularly, and with a low success rate, but still works enough to keep researchers interested, would demonstrate exactly this kind of experimental profile, I think.
If the injected cells have to go through all of these steps then I think that zero would reach the sweet spot. But it would appear that some do reach the sweet spot because all of the efforts (Intercytex, Aderans, and Replicel) have all grown a little bit of hair. And there’s also the issue that the Jahoda & Christiano hanging drop experiment grew some hair, although many hairs were not cosmetically viable. Check out this article below.
Also, regarding the reliability of inductivity analysis, it’s my understanding that in the above linked (Jahoda & Christiano) experiment the scientists did inductivity analysis. It’s also my understanding that the analysis showed improved inductivity with their 3-d hanging drop method versus 2-d culture methods. And it’s my understanding that the improvement in inductivity was significant but nowhere near fully induced cells. And they got some new hairs, although many were not cosmetically viable. Still this (Jahoda & Christiano) experiment seems to show that improving culture methods improves inductivity, which in turn improves the final hair growth results. Doesn’t this mean that the scientific method for analyzing inductivity is working since the analysis showed improvements to inductivity corresponded to improvements in real hair growth results? The changes seen in real hair growth results are what one would anticipate if the scientific analysis of inductivity was working, at least generally. After all, they achieved better induction and they got better hair growth results. Moreover, the inductivity analysis showed that the 3-d hanging drop method only PARTIALLY improved induction and that corresponded to only a PARTIAL improvement in real hair growth results. The inductivity analysis appears to correspond well to the actual hair growth results.
New methods for preserving inductivity during culture have been developed since the Jahoda & Christiano experiment took place. A few studies show dramatic improvements in inductivity preservation, although these studies have been done by academia unrelated to the research groups who have cell-based hair treatments in clinical trials. I don’t know if any of the teams with cell-based hair treatments in clinical trials have incorporated any of these newer techniques.
This discussion about whether iductivity creates new follicles/hairs and whether or not injected cells reach the therapeutic area makes me wonder more and more whether or not inductivity is even necessary for making existing miniaturized follicles enlarge and produce long thick hairs again. Perhaps the only reason injected cells don’t cause more miniaturized follicles to enlarge and produce bigger hairs is because only so many of them land on the therapeutic areas of follicles when the cells are injected. If this is the case, then Shiseido’s plan to do repeat injections of Replice’s technology could result in a breakthrough?
That’s exactly it… if it’s true that few of the injected cells ever make their way into the follicles, then what we’ve seen in trials and experiments thus far – sporadic, unpredictable and poor yields – is exactly how it would show up clinically.
If a cell would really have to go through each step you indicated I really don’t think even one cell would get to where it needs to get to.
No, some would. We’re talking about injections with millions of cells. This is exactly the kind of behavior large populations of cells exhibit – a statistical bell curve. We’re talking about so many cells that there are literally thousands of possible outcomes for each injection.
OK. But it does appear that regrowth happens with a degree of regularity since all 3 research groups (Aderans, Intercytex, and Replicel) reported similar hair growth. All 3 got somewhere between 5% - 10% regrowth. So is “sporadic” really a fair word to use to describe the growth. It looks to me like the growth is kind of consistent. And while Nigam didn’t do proper clinical trials by any stretch of the imagination, I did see limited regrowth with his cell injections as well.
OK so the cells go through a step-process similar to what you’ve described or close to it. And only some of those cells end up where we want them to go. Once that limited number of cells arrive where we want them to go how does the follicle “use” them to produce hairs. Does the follicle consume those cells like food or what?
The injected cells that actually hit that “therapeutic spot” hopefully will get integrated into the Dermal Papilla, which is a structure on the bottom of the follicle which generates more cells, some of which become the hair shaft. (The hair shaft is actually composed of non-living, keratinized cells that were filled up with the protein called keratin, as well as pigment.)
Picture a bowl of peas. The peas are the dermal papilla cells native to the follicle, in the place called Dermal Papilla close to the very bottom of the follicle. In a follicle miniaturized from MPB, there will be fewer and fewer peas in that bowl. Their numbers will keep diminishing because of genetics. The injections are supposed to replenish the bowl with more peas. It’s like dropping a bunch of fresh peas into the bowl, so it’s as full as it was before the MPB process began. The new peas mingle with the old peas and form a much bigger pile of peas. That’s an incredible oversimplification but it’s like a visual picture of what happens.