Whatever Happened To All The Replicel/shiseido Hype?

Mykonas

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Tsuji is not going to be your savior here's why :

There is a stupid misleading information circulating in every hairloss forum that is the follicles are either "dht resistant" or they're not. Well let me tell you that's not the case. Hair follicles are the same all over your head, however the androgen receptors that are located in the skin that surrounds you hair follicle are different some are resistent to dht some are not. Calcification and fibrosis that comes with male pattern baldness comes in the scalp region, same region where those androgens receptors are affected by dht.
When you transplant your hair from the back of your head it survives not because it's dht resistant but because they also transplant the skin that surrounds the hair follicle and also the dht resistant androgen receptors attached to it.

This what follica are trying to achieve by neogenisis. Rejuvinating all the skin on the top of your scalp so your receptors are refreshed to their initial state. Now tsuji is trying to multiply the donor area which means generating hair follicles with no androgen receptors as it's present in the skin. Once the're transplanted on your scalp they'll be relying on dht non-resistant receptors. In other words loosing your hair all over again.

I'd still take this if it's available one day though
 

d3nt3dsh0v3l

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Tsuji is not going to be your savior here's why :

There is a stupid misleading information circulating in every hairloss forum that is the follicles are either "dht resistant" or they're not. Well let me tell you that's not the case. Hair follicles are the same all over your head, however the androgen receptors that are located in the skin that surrounds you hair follicle are different some are resistent to dht some are not. Calcification and fibrosis that comes with male pattern baldness comes in the scalp region, same region where those androgens receptors are affected by dht.
When you transplant your hair from the back of your head it survives not because it's dht resistant but because they also transplant the skin that surrounds the hair follicle and also the dht resistant androgen receptors attached to it.

This what follica are trying to achieve by neogenisis. Rejuvinating all the skin on the top of your scalp so your receptors are refreshed to their initial state. Now tsuji is trying to multiply the donor area which means generating hair follicles with no androgen receptors as it's present in the skin. Once the're transplanted on your scalp they'll be relying on dht non-resistant receptors. In other words loosing your hair all over again.

I'd still take this if it's available one day though

Oh look, another new user who wants to show up to preach gospel and dispel the work, conjectures, and conclusions of leading researchers in the field, and not provide any peer-reviewed scientific literature on the matter.

Why, let me just go ahead and expunge any information I have learned from renowned experts and instead hit the subscribe button on your channel. Thank you for emancipating me from the clutches of backward thinking perpetuated by the medical community. If your rhetoric doesn't inspire me to turn over a new leaf, your uniquely stylistic deviations from traditional english spelling may just entice me!
 
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Mykonas

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Oh look, another new user who wants to show up to preach gospel and dispel the work, conjectures, and conclusions of leading researchers in the field, and not provide any peer-reviewed scientific literature on the matter.

Why, let me just go ahead and expunge any information I have learned from renowned experts and instead hit the subscribe button on your channel. Thank you for emancipating me from the clutches of backward thinking perpetuated by the medical community. If your rhetoric doesn't inspire me to turn over a new leaf, your uniquely stylistic deviations from traditional english grammar may just entice me!

I would love for you to provide us with some of those renowened experts work you learned from where it's explicitly explained that androgen receptors are not interfering with dht and hence affecting the follicles. While you're at it you can maybe find us some research that denies fibrosis and calcification are only observed within the scalp area where hairloss is predominantly observed.

English is not even my 3rd language, while you were embelishing your texts with unnecessary synonyms, you forgot that the corps is what matters. being a new user doesn't affect in any way my judgement capacity what i've said is true that's the whole concept of neogenisis, i've been an observer for a long time and i've seen so much false interpretation. But hey if you want to stay in your 2020 fullheadz bubble it's your choice buddy but you're just waisting your time and energy.
 

BootyWarrior

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Tsuji is not going to be your savior here's why :

There is a stupid misleading information circulating in every hairloss forum that is the follicles are either "dht resistant" or they're not. Well let me tell you that's not the case. Hair follicles are the same all over your head, however the androgen receptors that are located in the skin that surrounds you hair follicle are different some are resistent to dht some are not. Calcification and fibrosis that comes with male pattern baldness comes in the scalp region, same region where those androgens receptors are affected by dht.
When you transplant your hair from the back of your head it survives not because it's dht resistant but because they also transplant the skin that surrounds the hair follicle and also the dht resistant androgen receptors attached to it.

This what follica are trying to achieve by neogenisis. Rejuvinating all the skin on the top of your scalp so your receptors are refreshed to their initial state. Now tsuji is trying to multiply the donor area which means generating hair follicles with no androgen receptors as it's present in the skin. Once the're transplanted on your scalp they'll be relying on dht non-resistant receptors. In other words loosing your hair all over again.

I'd still take this if it's available one day though

It's such a shame you are not leading any science team. RIKEN should fire Dr. Tsuji and hire you. Looks like you pretty much busted Tsuji there.
 

Mykonas

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It's such a shame you are not leading any science team. RIKEN should fire Dr. Tsuji and hire you. Looks like you pretty much busted Tsuji there.
Are you dense or what ? what is it with people on forums and false interpretation ??

i haven't questionned tsuji's method or procedure. he's promising to deliver follicle multiplication that's it. whether the multiplied hairs are there to stay or not depends on androgen receptors that are present on the skin not on hair follicles.
 

Feelsbadman.jpg

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Tsuji is not going to be your savior here's why :

There is a stupid misleading information circulating in every hairloss forum that is the follicles are either "dht resistant" or they're not. Well let me tell you that's not the case. Hair follicles are the same all over your head, however the androgen receptors that are located in the skin that surrounds you hair follicle are different some are resistent to dht some are not. Calcification and fibrosis that comes with male pattern baldness comes in the scalp region, same region where those androgens receptors are affected by dht.
When you transplant your hair from the back of your head it survives not because it's dht resistant but because they also transplant the skin that surrounds the hair follicle and also the dht resistant androgen receptors attached to it.

This what follica are trying to achieve by neogenisis. Rejuvinating all the skin on the top of your scalp so your receptors are refreshed to their initial state. Now tsuji is trying to multiply the donor area which means generating hair follicles with no androgen receptors as it's present in the skin. Once the're transplanted on your scalp they'll be relying on dht non-resistant receptors. In other words loosing your hair all over again.

I'd still take this if it's available one day though

Utter nonsense. Hair follicles are DHT resistant to varying degrees. The hair on the back and side have the highest resistance but even these are not immune (If people lived long enough, this hair would eventually bald too). Androgen receptors are absolutely located inside the hair follicles. So is 5 alpha reductase type 2. This is why finasteride works, it inhibits the DHT that is produced locally inside the follicle which is the DHT that is responsible primarily for balding, not serum. Type 1 DHT is in the skin and inhibiting it has shown to be ineffective for male pattern baldness (research Mk-386, a selective type 1 5AR inhibitor).

Also, there have been IN VITRO (this means removed from the body) studies where hair follicles are exposed to androgens and they atrophy. Calcification and fibrosis are definitely active in male pattern baldness but they are downstream events. If you are able to confer the protective effects of the DHT resistant Dermal Sheath Cup cells from the back of the head to the rest of the scalp, then Calcification and fibrosis, which can be described as genetic responses to DHT stimulation in the hair follicles to an extent, will largely not occur. Now, damage that has already been done will probably not reverse much.
 

InBeforeTheCure

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dunning_kruger.png


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Source: Choudhry et al.

facepalm.png
 

IdealForehead

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Tsuji is not going to be your savior here's why :

There is a stupid misleading information circulating in every hairloss forum that is the follicles are either "dht resistant" or they're not. Well let me tell you that's not the case. Hair follicles are the same all over your head, however the androgen receptors that are located in the skin that surrounds you hair follicle are different some are resistent to dht some are not. Calcification and fibrosis that comes with male pattern baldness comes in the scalp region, same region where those androgens receptors are affected by dht.
When you transplant your hair from the back of your head it survives not because it's dht resistant but because they also transplant the skin that surrounds the hair follicle and also the dht resistant androgen receptors attached to it.

This what follica are trying to achieve by neogenisis. Rejuvinating all the skin on the top of your scalp so your receptors are refreshed to their initial state. Now tsuji is trying to multiply the donor area which means generating hair follicles with no androgen receptors as it's present in the skin. Once the're transplanted on your scalp they'll be relying on dht non-resistant receptors. In other words loosing your hair all over again.

I'd still take this if it's available one day though

f*****g nailed it!

The same principle is described in detail here:

https://www.sciencedirect.com/science/article/pii/S0306987717310411

Only they don't subscribe to your belief that it is androgen receptors in the skin that make the difference between hair on top and hair in the back. They suggest that whether or not the skin and hair sits over the the galea or not is the fundamental difference.

They discuss how hair transplants are successful only because they take healthy skin with them, and because they haven't been exposed to decades of inflammation already, so might take decades to "fail" even if they inevitably will.

Which is in all honesty the only thing that we've seen that can explain the difference between scalp on top and scalp in the back and geographic pattern of hair loss we see in men:

image001.jpg


For whatever reason, hair/skin that sits over the galea is more susceptible to androgenic inflammation and damage over time. There are a lot of theories one could come up for why this is the case. eg. Some people say it is a scalp tension and blood flow issue.

But I agree with you 100% that the hair itself is not different depending on scalp location. And I think you are also right that Tsuji is therefore pursuing a flawed approach.

I was just looking for any evidence that occipital hair is INTRINSICALLY more "DHT resistant" than hair on top of the head (and not just more resistant due to environmental factors), as transplant surgeons claim, and found nothing. But I did find this post from 2014 that summarized the reality as I now understand it:

There are many new studies that say it has everything to do with the galea, and more importantly, blood flow to the scalp.

We know this to be the case because if you inject botox into a bald person's scalp, they grow hair:

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

The only reason this would work is if baldness had something to do with the scalp muscles, which in turn reduces blood flow when tensed. This simple fact is the nail in the coffin for the idea that some hairs are DHT resistant, and other hairs are not DHT resistant.

If you take two hairs, one on the galea, and one not on the galea, they will contain the same genetic code. The only way they would express different traits, are if there was an environmental component that changed. This environmental component is DHT, which is excessive in the galea when it becomes tight or blood flow gets restricted.

DHT causes the skull to expand, which further exacerbates this problem in a circular fasion.

As for why hair transplants work, the simple truth of the matter is that it is not true that hair restoration is permanent. People who have hair restoration usually continue to take DHT inhibitors like finasteride and vasodiolators like minoxidil even after their hair restoration. If they didn't, we would likely see the miniaturization process in these follicles over time as well.

There have been no studies of hair restoration and users not continuing propecia/minoxidil that I can find. This makes the claim that hair restoration is permanent very fragile in my opinion, and after seeing the 75% effectiveness of botox injections in male pattern baldness, it literally destroys the claim that some hairs are DHT resistant and others are not. Rather, it has to do with the amount of DHT in a region, which has been found to be higher in the scalp for balding men due to an 18% difference in the O2 saturation of their scalps.

DHT/free T ratios sway towards DHT in lower oxygen environments.

I wrote more here: http://www.hairlosstalk.com/interac...rs-Old-was-in-denial-shaved-my-head-yesterday

If you have any comments/questions I would love to hear them.

Anti-androgens work because they block the inflammation cascade that occurs from the galea's negative effects. But the galea is almost certainly the underlying cause.
 

IdealForehead

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The most recent evidence (2015) for the galea theory of hair loss is summarized here (GA = galea):

One study found that mechanical tension from the GA matches the pattern and progression of Androgenetic Alopecia, with peak tension points corresponding to the first places of hair loss. Androgenetic Alopecia-prone hair follicles reside within the dermis and subcutaneous fat layers of the scalp, and these layers are fused with the GA as a singular unit. As such, tension from the GA carries into these fused tissues, and thereby Androgenetic Alopecia-prone hair follicles. The investigators concluded that TGF-β1 expression may result from the tension-mediated induction of the AR coactivator Hic-5/ARA55, and that a “stretch-induced and androgen-mediated mechanotransduction in DP cells could be the primary mechanism in Androgenetic Alopecia pathogenesis” [57].

https://www.sciencedirect.com/science/article/pii/S0306987717310411#b0285
 

hanginginthewire

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Balding is a situation that has no bottom. Just gets worse and worse. It sounds like a horrifying science fiction novel. Satan must exist because only he could devise something so diabolical and evil.

Wondering how retrograde and DUPA factors in though...
 

sunchyme1

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Balding is a situation that has no bottom. Just gets worse and worse. It sounds like a horrifying science fiction novel. Satan must exist because only he could devise something so diabolical and evil.

Wondering how retrograde and DUPA factors in though...

lol sh*t never ends man

just gets deeper and deeper

we need to start a gofundme for ideal to crack this sh*t. it could take a while. and the man needs to be paid

f*** the conferences
 

IdealForehead

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Balding is a situation that has no bottom. Just gets worse and worse. It sounds like a horrifying science fiction novel. Satan must exist because only he could devise something so diabolical and evil.

Wondering how retrograde and DUPA factors in though...

Well in fairness, it's not all bad.

What it suggests is that we can attack hair loss in multiple ways that are essentially accomplishing the same thing.
  • Botox works (partly) but reducing the scalp tension.
  • Anti-androgens work by reducing androgen levels or androgenic effect triggered by the galea.
  • Anti-histamines work by broadly blocking inflammation that contribute to the "itch" of male pattern baldness.
  • Wounding and growth stimulates work by stimulating stem cells to make new hairs to replace dead ones.
  • Stem cell therapies might be useful also for generating new hairs where old ones have died.
But what this also suggests is there is no singular "cure" for hair loss and that is why none has materialized. The only way to "cure" male pattern baldness would be to replace the galea with muscle so that the hair over top can move more naturally/freely and escape the mechanical stresses that trigger its degradation. That's impossible of course. So we must be pragmatic and attack the problem from the angles we can (as listed above).

Retrograde and DUPA are pretty rare. I could only speculate on their differences. Probably if you did a scalp MRI in retrograde you might see some unusual features to the shape of their occipital muscles or galea, but I don't know for sure. I presume in DUPA, the way the hair attaches to the dermis and underlying connective tissue is more "rigid" all over the scalp just like it is for normal men over the galea, so all the hair on the head is afflicted.
 

hanginginthewire

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Well in fairness, it's not all bad.

What it suggests is that we can attack hair loss in multiple ways that are essentially accomplishing the same thing.
  • Botox works (partly) but reducing the scalp tension.
  • Anti-androgens work by reducing androgen levels or androgenic effect triggered by the galea.
  • Anti-histamines work by broadly blocking inflammation that contribute to the "itch" of male pattern baldness.
  • Wounding and growth stimulates work by stimulating stem cells to make new hairs to replace dead ones.
  • Stem cell therapies might be useful also for generating new hairs where old ones have died.
But what this also suggests is there is no singular "cure" for hair loss and that is why none has materialized. The only way to "cure" male pattern baldness would be to replace the galea with muscle so that the hair over top can move more naturally/freely and escape the mechanical stresses that trigger its degradation. That's impossible of course. So we must be pragmatic and attack the problem from the angles we can (as listed above).

Retrograde and DUPA are pretty rare. I could only speculate on their differences. Probably if you did a scalp MRI in retrograde you might see some unusual features to the shape of their occipital muscles or galea, but I don't know for sure. I presume in DUPA, the way the hair attaches to the dermis and underlying connective tissue is more "rigid" all over the scalp just like it is for normal men over the galea, so all the hair on the head is afflicted.

Are you sure retrograde is rare? I have it (well for sure at the nape, perhaps nape thinning does not equal retrograde?). One sees lots of men with a neckline that has creeped way up and virtually thinned completely out.

It’s nice that we have all these angles to attack from but I admit I long for a proper cure. Androgenetic alopecia resembles a monster from a horror movie. You shoot it, set it on fire, drown it, dismember it, and the f****r keeps attacking you. It’s no wonder that so many of us feel like pattern baldness reflects on us as people at some intrinsic, deep level. It is encoded in not only our DNA, but seemingly our very souls.
 

sunchyme1

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Well in fairness, it's not all bad.

What it suggests is that we can attack hair loss in multiple ways that are essentially accomplishing the same thing.
  • Botox works (partly) but reducing the scalp tension.
  • Anti-androgens work by reducing androgen levels or androgenic effect triggered by the galea.
  • Anti-histamines work by broadly blocking inflammation that contribute to the "itch" of male pattern baldness.
  • Wounding and growth stimulates work by stimulating stem cells to make new hairs to replace dead ones.
  • Stem cell therapies might be useful also for generating new hairs where old ones have died.
But what this also suggests is there is no singular "cure" for hair loss and that is why none has materialized. The only way to "cure" male pattern baldness would be to replace the galea with muscle so that the hair over top can move more naturally/freely and escape the mechanical stresses that trigger its degradation. That's impossible of course. So we must be pragmatic and attack the problem from the angles we can (as listed above).

Retrograde and DUPA are pretty rare. I could only speculate on their differences. Probably if you did a scalp MRI in retrograde you might see some unusual features to the shape of their occipital muscles or galea, but I don't know for sure. I presume in DUPA, the way the hair attaches to the dermis and underlying connective tissue is more "rigid" all over the scalp just like it is for normal men over the galea, so all the hair on the head is afflicted.

i wish you started going bald 10 years ago man
 

IdealForehead

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Or alternatively, to "cure" male pattern hair loss, you would have to study in detail in ways that no one has ever done before why some men's scalps do not upregulate their androgen sensitivity genes in response to galeal tension and mechanical stress, and try to develop a therapy that somehow recreates that resistance to galeal mechanical stress in balding men.

Probably what happens in men who are resistant to male pattern hair loss is some combination of the following:
  • There is something unique about their hair follicle genetics, where the androgenic sensitivity genes that are upregulated in balding men due to galeal stress are not expressed in response to the same mechanical pressures.
  • There is something unique about the connective tissue that links their hair follicles to the galea that prevents mechanical stress from being transduced to the hair follicle.
But both possibilities would not be easily replicated in non-balding men. These are likely genetically programmed differences like eye color or height. In hundreds of years, perhaps the genetics responsible will be understood and we can program future children to be free from these problems. But we cannot change the fundamental genetics of our hair follicles or the basic mechanical features of our scalp dermis in the way that we would need with current technology.

So again, we must approach the problem from a more practical standpoint of intervening in the inflammatory cascade at the varying levels we have the capacity to. Fighting hair loss will always then be a lifelong struggle, and those of us who are prone to it (ie. most men) must do our best to find the agents we can tolerate best and work most effectively for us.

Alternatively, a "cure" could be developed through technologies of hair multiplication, where if you have infinite follicles and infinite time and money, you can just keep getting tens of thousands of hair transplants every 10-20 years or so. But the scalp fibrosis and scarring from doing so would be prohibitive, as well as risks of these stem cell therapies generating cancer, so even if money was not an issue, this would not be wise without still using an ongoing conventional hair loss treatment to stop the loss of the new hairs once they are placed.
 

Ollie

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@IdealForehead in regards to Tsuji not working, what if the process involved transplanting the cells into a skin graft from a non androgen sensitive area taken from the recipient until the hair grows in the lab then transplanting to the persons scalp ?
 

IdealForehead

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@IdealForehead in regards to Tsuji not working, what if the process involved transplanting the cells into a skin graft from a non androgen sensitive area taken from the recipient until the hair grows in the lab then transplanting to the persons scalp ?

That would be interesting and it is unknown whether that would work but we can develop an informed perspective by considering the facts as we know them.

In theory the holy grail of hair loss treatment is not actually to do hair cloning and then transplant those hairs one by one, but rather to grow an entire lawn of healthy new scalp and hair and transplant that as one big unit. ie. If you can grow an entire lawn of 20 cm x 30 cm new scalp in a lab with perfect hair density, you can very easily then "cut" this lawn into a nice shape, excise the balding scalp completely, and replace it with the new lawn.

This could provide absolute perfect density with only a scar to deal with around the edges (which could be treated with lasers or camouflaged with small transplants).

But what would happen if you actually did this? Almost certainly, unfortunately, Androgenetic Alopecia would start again in time, as the dermis and connective tissue under the new scalp lawn would inevitably fuse to the galea, just like the natural scalp did. Then the same mechanical stresses from the galea would re-exert themselves over the years, upregulating androgen sensitivity genes in the hairs that overlie the galea, and eventually leading to the miniaturization and demise of those hairs in turn.

So unfortunately that approach would likely not solve the problem either. Also sorry, @sunchyme1 , but what this suggests is this is basically an unsolvable problem in a permanent sense and no "one time cure" will exist in our lifetime. We can hope for new anti-androgens, new stem cell therapies, etc. But hair loss will always be a lifelong battle as long as you choose to fight it.
 
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