Whatever Happened To All The Replicel/shiseido Hype?

Trichosan

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And, he actually needs to remove hair to establish an esthetic hairline. That condition must be less than .1% of the human population. :eek:
 

That Guy

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That's not exactly what I did and not exactly what I've said.

First of all, DHT is absolutely important as an inflammatory mediator of hair loss. That is why blocking DHT stops hair loss. And there is absolutely such a thing as "DHT resistant" hair. The question is how permanent that DHT resistance can be expected to be in the context of this model. We will return to this point in a bit.

I believe Tsuji is absolutely unlikely to develop a commercially available method for mass hair cloning in the next 18 months. I think they have overpromised. I do not know what if anything they will offer in 18 months.

I have said it would be incredibly helpful if he can do this because it creates unlimited donor supply.

However I am honestly not sure (and I don't think anyone could be in the context of this new research) about how permanently androgen-resistant and galea-resistant the hairs would be.

If the transplanted hairs re-fuse to the galea and with time this increases androgen sensitivity gene expression, as it does for native balding scalp follicles over time, then these hairs could start a new "balding countdown clock" upon transplantation.

If on the other hand, the surgical process of transplantation keeps the hairs mechanically unloaded from the galea and/or the epigenetic switches that were thrown by having those hairs develop in the occiput are resistant to being "re-switched" by the move the galea, then the hairs will be pretty permanent.

I dont think anyone could know for certain, as this is a relatively new concept. With further research in the next 5-10 years that question should be answered.

If I had to speculate based on all the information reviewed and posted in this thread, I would guess that like anything else this may be individualized. In some men the transplanted hairs may be more sensitive to the new galeal stress than others. So some men can probably get away with doing nothing. While others may get thinning and deterioration of their transplants in another 10-20 years of they don't combine the procedure with an anti-androgen.

The articles I linked commented that in those researcher's opinions we need large long term 10-20 year studies of human hair transplants in men who have taken anti-androgens and those who have not before we can know for sure. I would tend to agree.

The world isn't rock 'em sock 'em robots or a UFC ring. This isn't a competition about who knows more or who is "calling bullshit" on who. It's meant to be an open discussion to share and learn so we can all advance our knowledge and hopefully the entire science of hair loss in the process.

I absolutely hope Tsuji is successful in his endeavors and he's done fantastic work in my opinion already so far.

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Mykonas

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That Guy

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You should cause you don't even know what you're arguing

You stated that follicles aren't DHT resistant at the back of the head, that the skin is and that's why transplants work.

Except for the unfortunate problem that as Inb4 linked to, this has been investigated, the matter is resolved, and your statement is incorrect. There is nothing to argue.

Since when knowledge means being right ? If that was the case we won't even be here on a hairloss forum cause such thing won't exist.

Uh, no. That's not how any of this stuff ever works.

Just because the condition is not presently "cured" by any technology presently on the market, does not mean we do not have any cold, hard facts about the condition.
 

InBeforeTheCure

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I know you don't personally believe in this explanation for hair loss. However, I don't think anything you've said refutes the principle of the galea being the underlying cause of hair loss or the recent studies that have been published to support this explanation.

Not "personal belief", but a conclusion based on mountains of evidence, and a finding that all real researchers in hair follicle biology also accept (as far as I know).

Nordstom's findings were reflected upon here, in the study where they analyzed expected galeal stress patterns and found them to match the Norwood hair loss pattern exactly:

The involvement of mechanical stress in Androgenetic Alopecia implies that hair follicles do not have genetically preprogramed androgen sensitivity. It is imperative at this point to mention the ingenious experiment by Nordstrom, who transplanted hair follicles from both balding and occipital scalp to the forearm. The result was the loss of hair from the balding scalp whereas the occipital hair continued growing.[32] This study is considered a proof of genetic follicle preprograming, but according to the approach of the present paper, it would be necessary to know the strain supported by the forearm skin and to realize that the hair follicles close to receding hairline have already started a countdown toward the miniaturization, but not the occipital follicles. In hair transplantation, the grafted follicles start a new "balding clock," but hair growth would be guaranteed for many years even without preventive pharmacotherapy.​

And one of the experiments I already posted debunks this - the one where they transplanted occipital hair to frontal scalp in stump-tailed macaques and they survived for eight years, twice as long as the macaques had even been alive up to that point, and like 100 times longer than native frontal hair takes to start miniaturizing in response to androgens at puberty.

How do you explain that balding matches the expected tension distribution of the galea?

Does it? It looks to me like it only matches some patterns, but not others. Let's see the same analysis done on men with different balding patterns. Also, let's see the same analysis done on balding non-human primates like macaques, uakaris, chimpanzees, bonobos, and orangutans to rule out coincidence.

How do you explain that Botox therapy to the scalp can increase hair growth significantly?

Imagine the Botox study was done before any of these hair transplant studies. You could then hypothesize: "Well, maybe tension explains the pattern of hair loss." And then you could do the transplantation studies and you would find this hypothesis to be wrong. As for the mechanism, I don't know because it hasn't been investigated (and I sort of agree with the things d3nt3dsh0v3l said here, but ultimately it's irrelevant because the conclusions you try to pull from it are already known to be false.

Here is the conventional explanation for the effectiveness of Botox for hair growth, which also recognizes tension as a primary mediator of androgenic hair loss:

The proposed mechanism for hair growth in androgenic alopecia after botulinum toxin A treatment is that paralysis of the scalp muscles enhances blood flow to the scalp by reducing the tension on the scalp skin. Because the conversion to dihydrotestosterone (DHT) is enhanced in a low-oxygen environment, oxygenated blood reduces this conversion and increases conversion to estradiol. This might be the same mechanism by which minoxidil affects androgenic alopecia. The 18% increase in hair count is similar to that achieved with finasteride. How injecting BTX A into scalp muscles could be protected as intellectual property is difficult to see.

https://www.jwatch.org/jd201111100000001/2011/11/10/growing-hair-with-botox

This explanation as a whole suggests that the galea likely causes epigenetic changes to the hair follicles, by inducing specific genes to upregulate (androgen production and androgen sensitivity) in response to tension during development and lifespan.

Now you're contradicting yourself. I thought you said that once miniaturization started, due to a positive feedback loop, miniaturization would continue even after transplantation to a different site??? That's how you explained away the Nordstrom study. But according to what you're now saying, Botox has the same effect as anti-androgens (i.e. stops and partially reverses hair loss). In other words, maintaining this tension is critical for continuing hair loss just as androgens are, and we should expect that once (like androgens) we remove this tension, hair loss should stop. And according to you, regional muscle tension on the galea is where this tension comes from. But AGAIN, the Nordstrom study contradicts this contradictory claim of yours, and I already posted yet another experiment that shows this is wrong: The experiment where they transplanted frontal hair to occipital scalp in ovariectomized macaques before giving them testosterone.

Transplantation is a difficult thing to speculate on in the context of this model, because we don't know how long it would take to reverse the positive genetic switches that the occipital scalp turns on and replace them with the negative switches the galea would turn on.

Not after at least 15 years in humans, and not after at least 8 years in macaques. None of these studies has ever found evidence for what you're claiming.

We also don't know how much of the mechanical stress from the galea will transmit to transplanted hair compared to native hair over time to change these switches.

Dermis associated with native hair in balding prone scalp is considered to be "fused" to the galea. What about dermis associated with transplanted hair? Transplantation is an artificial surgical process. Would the same "fusion" occur to equally transmit mechanical stress?

Now AGAIN you're ignoring the frontal-to-occipital transplant study done in ovariectomized macaques. I posted those studies for a reason, FFS.

If transplanted hair truly does survive very well (decades) even in young balding men in the absence of anti-androgens like finasteride (and I am highly skeptical this is the case as I have seen disastrous examples of guys who have had transplants and not taken their meds after),

Any links to studies comparing transplant survival rates in men who take finasteride vs. those who don't?

it would suggest primarily that either the epigenetics induced by developing in the occipital scalp are resistant to change or that the mechanical process of transplantation keeps the transplanted hair "unloaded" from the galea.

And AGAIN (how many times do I have to say this), you're ignoring the frontal-to-occipital transplant study done in ovariectomized macaques. This nullifies all this muscletensionpatternexplainshairloss conjecture. Why do you keep ignoring this?

So I don't think anything you're saying undermines the basic principle of this model. This model still best explains the distribution of hair loss that is seen with male pattern baldness. It just suggests we don't really know how transplanted hair reacts to relocation in the context of this model.

Only in Fantasyland is a failed hypothesis the "best explanation" for anything. Meanwhile, the exact same principles that guide biological pattern formation in most other contexts, and which ARE consistent with REALITY - nah, that's not the best explanation.
 

IdealForehead

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Not "personal belief", but a conclusion based on mountains of evidence, and a finding that all real researchers in hair follicle biology also accept (as far as I know).

And one of the experiments I already posted debunks this - the one where they transplanted occipital hair to frontal scalp in stump-tailed macaques and they survived for eight years, twice as long as the macaques had even been alive up to that point, and like 100 times longer than native frontal hair takes to start miniaturizing in response to androgens at puberty.

I think those studies are actually really important to reflect on so thanks for posting them. They would suggest in the context of this model that either one of two things has occurred: (1) the transplanted hair by virtue of the surgical transplantation process is not subjected to the same mechanical stresses from the galea as native hair in this area, ie. it is surgically "unloaded", and/or (2) there are epigenetic switches mediating androgen sensitivity set during development based on which area of the scalp the hairs develop in (ie. the tension region of the scalp) that cannot be easily changed thereafter.

Nordstrom's findings as well as the testosterone therapy in macaques could be best explained by #2. And that explanation can be applied without refuting mechanical tension as the underlying epigenetic and inflammatory cause of hair loss.

Does it? It looks to me like it only matches some patterns, but not others. Let's see the same analysis done on men with different balding patterns. Also, let's see the same analysis done on balding non-human primates like macaques, uakaris, chimpanzees, bonobos, and orangutans to rule out coincidence.

You'll probably have to wait decades for those studies to be done unless you propose to download ANSYS yourself and start building models of primate heads. But I expect that modeling will be done in time. This initial modeling study is only 2.5 years old, and there is no money to be made in this.

We know that currently the predicted tension pattern of the human scalp matches the Norwood pattern exactly. We also know mechanical stress can induce androgen sensitivity. That is hard to ignore as "coincidence".

You haven't offered any explanation for how Botox works for hair loss or why the scalp tension pattern matches the Norwood pattern. Nor have you offered any explanation for research showing that there known chemical signalling chains whereby androgen sensitivity is mediated by mechanical stress.

Not after at least 15 years in humans

From what I can see, Orentreich 1970 is the only "study" you have provided on human hair transplant survival rates and it's just the anecdotal experience/opinion of one transplant surgeon. Are you aware of any longitudinal quantitative studies that assess this? Ditto with the survival of transplants in men who take finasteride vs those who do not?

As far as I know no one has done a quantitative long term human transplant study.
 
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IdealForehead

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View attachment 84354

Alright. I'm done wasting time to repeat evidence, only for you to selectively ignore it in your replies. Sayonara.

But I acknowledged your evidence. You suggested Nordstrom's study, the fact that occipital and frontal scalp hairs can be swapped while retaining their source characteristics, and macaque longitudinal studies as evidence that scalp tension cannot be responsible for hair loss.

I suggested that in fact, all of these findings can be folded into the galeal tension theory if galeal tension sets the epigenetics that dictate areas of high tension and androgen sensitivity from an early developmental stage. ie. The hairs are epigenetically different, but set into these differences in the Norwood pattern by galeal tension.

Why could this not be the case?

Furthermore, I think it is very careless to try to dismiss:

- Findings that the scalp tension pattern mirrors the Norwood pattern exactly.
- Findings that cellular mechanical stress proteins can induce upregulation of androgen sensitivity genes.
- Findings that Botox to relieve mechanical stress can alleviate hair loss equally well after 1 year as finasteride.

All of these strongly suggest mechanical stress is an important part of setting the stage for how baldness occurs and mediating the chemical cascade that enacts it. I do not claim to have all the answers (no one yet does). But I don't believe these are "coincidences", and I think any comprehensive theory of hair loss must address what they together suggest.
 
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Trichosan

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QUOTE="InBeforeTheCure, post: 1646760, member: 109694"]Lord Tsuji is our best hope.[/QUOTE]

Praise unto him! (Otherwise I don't have a Chinaman's chance in Hell of getting hair in my lifetime).

I know we have to consider all possibilities now, but the real cure will come and it will be via genetics. In fact, when that does happen, it will overlap with genetic selection before conception. There will be those with altered characteristics created after birth existing with those whose genetic, close to perfection, patterns were created before birth. Given human nature, it would create a brave new world of discrimination. 100 years? Perhaps, 300?
 

Iah11

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But I acknowledged your evidence. You suggested Nordstrom's study, the fact that occipital and frontal scalp hairs can be swapped while retaining their source characteristics, and macaque longitudinal studies as evidence that scalp tension cannot be responsible for hair loss.

I suggested that in fact, all of these findings can be folded into the galeal tension theory if galeal tension sets the epigenetics that dictate areas of high tension and androgen sensitivity from an early developmental stage. ie. The hairs are epigenetically different, but set into these differences in the Norwood pattern by galeal tension.

Why could this not be the case?

Furthermore, I think it is very careless to try to dismiss:

- Findings that the scalp tension pattern mirrors the Norwood pattern exactly.
- Findings that cellular mechanical stress proteins can induce upregulation of androgen sensitivity genes.
- Findings that Botox to relieve mechanical stress can alleviate hair loss equally well after 1 year as finasteride.

All of these strongly suggest mechanical stress is an important part of setting the stage for how baldness occurs and mediating the chemical cascade that enacts it. I do not claim to have all the answers (no one yet does). But I don't believe these are "coincidences", and I think any comprehensive theory of hair loss must address what they together suggest.

You keep saying that it matches the balding pattern exactly and thats wrong though. The first place I, and many many others, lose hair was not on the top of my scalp but on the lateral sides in the temporal region. This is not in the region of the galea.
 

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What do you think of Replicel/Shiseido, O wise one?

bump. I think it will maintain existing hair and is great for those of us that have most of their hair still but will not do much if you are already in advanced stages of balding. Would be interested in what INB4 thinks.
 

IdealForehead

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You keep saying that it matches the balding pattern exactly and thats wrong though. The first place I, and many many others, lose hair was not on the top of my scalp but on the lateral sides in the temporal region. This is not in the region of the galea.

According to this diagram we can have a temporal fascia in the area of the temporal points which would work the same. Also note that at the back of the scalp there is yet another fascia connecting the occipitalis to the skull where some people get retrograde thinning.

Probably there are natural variations in the anatomy and highest tension points accordingly.

galeatomie_haaruitval.png
 
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