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.
You should cause you don't even know what you're arguing
But as Inb4TheCure, easily the forum's most knowledgeable member posted, studies have shot this bullshit down for decades.
You should cause you don't even know what you're arguing
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.
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.
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.
How do you explain that balding matches the expected tension distribution of the galea?
How do you explain that Botox therapy to the scalp can increase hair growth significantly?
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.
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.
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?
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),
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.
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.
@InBeforeTheCure what does our future hold? With all your knowledge what do you foresee being the answer for most people?
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.
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.
Not after at least 15 years in humans
Lord Tsuji is our best hope.
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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.
What do you think of Replicel/Shiseido, O wise one?
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.