Cnn - Cotsarelis And Christiano Interview 10/18

[TJT]

It's because of sebaceous gland area enlarging that follows due to DHT (androgens) hitting on your androgen sensitive hair follicles. The sebaceous gland secretes the oil that is on your scalp, but due to the miniaturizing process it leads to increased secretion of the oil. That's why your scalp is so oily.

Here is a recent good study about that where they really looked at many men and performed a morphometric anlysis and they indeed found that in Androgenetic Alopecia patients the sebaceous gland area is really significantly larger than non-balding patients;

https://www.ncbi.nlm.nih.gov/pubmed/26147300

Got it; so Tsuji's solution will resolve both hair loss and oiliness in one shot!

 

[Swoop]

Got it; so Tsuji's solution will resolve both hair loss and oiliness in one shot!

 

[NewUser]

Indeed! He could give that mice a full coat. Not only that though. These are actually human cells growing in that mice. He simply took human cells and used the mice as a host to let the human hair follicle develop including all structures like sebaceous gland and APM. That's so damn different than using a mice itself as a drug model for Androgenetic Alopecia.

Christiano used mice to test jakinibs, and the results will likely lead to the first effective treatments for what were until recently several vexingly difficult to solve hairloss disorders: AA , AU and AT. His use of mice to grow a few straggly hairs doesn't seem to dawn on you just how important lab mice are for hair researchers, Tsuji included.

Youre not very big but you sure are stupid.

 

[InBeforeTheCure]

Orentreich did use vellus hair that were approximately 30-40um in diameter so these ain't exactly hardcore miniaturized hair follicles.

It says in the study that the hairs were more like 24 um in diameter on average, with some as thin as 10 um.

It's interesting too how while the vellus hairs grew, the terminal hairs actually shrunk until eventually both were the same size.

In my opinion that study indicates that mice might have some factor in their biological nature that might contribute to this or make this happen. This might mean that we simply haven't found that factor yet and that the possibility exists of a very good growth agent that might rapidly reverse vellus hair follicles to terminal ones. And the study you just have shown is relates to this too.

Mice can generate new follicles after wounding -- humans not so much. Since many of the same pathways involved in HF morphogenesis are also involved in HF cycling and regeneration, maybe some of those same pathways are responsible for the Krajcik/Orentreich results?

 

[Takeela370]

@Takeela370,

Weren't you the one that went into the AA forum to search if people with Androgenetic Alopecia had regrowth through hundreds of pages? Do you know how stupid that was? What did you expect, that they would regrow their hair? Deluded. You didn't have to search for that, you could have known that many years ago. Literally many years ago. I admire the effort though, but it's pretty damn dumb to search for that.

You can't refute any of my points while I did refute the statement of the CEO and did indeed show that tofacitinib exerts it's biological activity at the epidermis. That's all I need to know. Drugs have a certain way of working and If I can evaluate whether tofactinib saturates JAK3 enzyme orally at the hair follicle then I know enough; a topical won't work. Period. And it has been shown that tofactinib works at the epidermis which is non-vascularized. Perhaps you should do a bit of reading about pharmacology & pharmacokinetics.

Furthermore seeing from your posts you certainly don't display to have any knowledge of even basic hair follicle biology at all. Your post a week back where you posted showed incoherent rambling at best. There are countless people on this forum alone who I can name who have way better knowledge as you.

Your best argument is basically this: "yo guys you know we don't actually know if it won't work because it has never been tested!

I'll give you that though Takeela. You are right. Maybe we should do a clinical trial of platypus piss and elephant sh*t in a topical. After all it hasn't been tested dude! How do you know it won't work with 100%?

Lmao.

I didn't expect anything. No one was showing any pictures that had someone that had AA that had taken JAK inhibs and regrown in a horseshoe pattern that I could easily find. So I went through a thread on a forum. Why does that make me deluded? To find an answer to a question that many people were asking seems logical.

I did refute your points by quoting the new scientific journal article on JAK inhibitors. I bolded the main points for you. If PhD's in cell biology, who make hair biology, specifically, their expertise think it's worth exploring, then I'm just saying there's probably a reason. If a guy that has no actual research background, science degree, let alone a Ph.D in biochemistry or some related field, off a hair forum says there's a 100% chance something won't work, then I find evidence that makes multiple valid points why it will work (that's actually from the research that was just conducted on that molecule), then I'm going to say, "Eh, I don't think that's a 100% chance it won't work".

I honestly really don't want to go back and forth on this because you are set on the fact that you are right, and I'm set on the idea that, you could be right (lets not make this about right and wrong, lets say you had some valid points), but there are also some valid points that show maybe this could still work. And that's fine we're each entitled to our own opinions. Just stop claiming things are 100% fact when you're just making an educated guess.

You are very well read on many subjects pertaining to hair follicles, I have read many of yours and others posts here over the years (though I don't like to post... for obvious reasons). I think you are a wealth of knowledge for the community. So let's stop arguing with each other when our real focus should be helping educate each other, not tearing each other down.

 

[That Guy]

Let me know if I'm wrong, but doesn't Swoop actually have an education in biology or some such field? He's actually written articles on this site and sh*t.

Yet, here have some people with antisocial problems screaming about how he's an idiot forum poster...

 

[Beowulf]

Let me know if I'm wrong, but doesn't Swoop actually have an education in biology or some such field? He's actually written articles on this site and sh*t.

He's also a veteran who's even made and broken his own theories on hair loss.

...He's basically the guy that made me realise that forums actually were making serious contributions to ending hairloss.

 

[Armando Jose]

[QUOTE="TJT, post: 1381638, member: 127597"
I have DPA and I noticed that if I don't wash my hair for a day or more, the portion that is subject to hair loss becomes much more oily than the portion that is immune. Why is that? [/QUOTE]

I am not Swoop but I have something to introduce.
Immune areas are in contact, mainly in the night, with an absorbent surface. Is it your case?

 

[Trouse]

I'm not sure if I would describe the condition of my scalp as oily, it's kind of hard to tell. I would however, use that exact term for the skin on my forehead. It's odd because my skin is perfectly clear and looks quite healthy below the eyes, but the forehead has much worse texture and is susceptible to breakouts. Does this have anything to do with sebaceous glands? I mean there shouldn't be any follicles on that part of my face, right, so is this just a totally separate issue?

 

[TJT]

It's because of sebaceous gland area enlarging that follows due to DHT (androgens) hitting on your androgen sensitive hair follicles. The sebaceous gland secretes the oil that is on your scalp, but due to the miniaturizing process it leads to increased secretion of the oil. That's why your scalp is so oily.

Here is a recent good study about that where they really looked at many men and performed a morphometric anlysis and they indeed found that in Androgenetic Alopecia patients the sebaceous gland area is really significantly larger than non-balding patients;

https://www.ncbi.nlm.nih.gov/pubmed/26147300

Actually, one other thing, along with oiliness I also find the area prone to hair loss is the area that sweats during physical activity. Does the sweat gland area enlarge due to DHT hitting the androgen sensitive hair follicles too, or what's up with that?

 

[KO1]

Swooping, why are you so bullish on Tsuji? I don't think that science is really fully understood? Is there something that gives you confidence he will be able to grow hair in humans?

 

[Swoop]

Mice can generate new follicles after wounding -- humans not so much. Since many of the same pathways involved in HF morphogenesis are also involved in HF cycling and regeneration, maybe some of those same pathways are responsible for the Krajcik/Orentreich results?

Regarding the diameter, thanks I stand corrected. That's impressive. Yes, It does seem to indicate that these little buggers have something that we do not know about? I would really like to see that study repeated!

@Takeela370, ok all good. Let's just leave it at this.

Actually, one other thing, along with oiliness I also find the area prone to hair loss is the area that sweats during physical activity. Does the sweat gland area enlarge due to DHT hitting the androgen sensitive hair follicles too, or what's up with that?

Here is a study that might answer your question; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1281456/

"Thus sebum has three thermoregulatory roles. At higher temperatures sebum acts as a surfactant for eccrine secretions. whilst in hot conditions the internally generated fluid, eccrine sweat, is encouraged to spread in a film across the skin and to be retained on the surface"

So it is maybe logical to assume since you would have increased sebum at your areas prone to hair loss, physical activity would maybe lead to a "hot condition" and the extra sebum would only encourage the sweat to stay on your skin longer instead of being repelled? Maybe a baldite head cools itself better in hot conditions, at least we have some advantage to being bald lol...

 

[Swoop]

Swooping, why are you so bullish on Tsuji? I don't think that science is really fully understood? Is there something that gives you confidence he will be able to grow hair in humans?

Check here; https://www.hairlosstalk.com/intera...air-research-team.100006/page-33#post-1359804

Bottom line is that observations actually do heavily support that (stem)cells of the hair follicle can induce a new hair follicle in humans, not only in mice. The hair follicle is unique in this.

Remember on baldtruthtaIk the conversation where Aardon Gardner said that either dermal sheath cells or dermal papilla cells can induce a new hair follicle? It can be that easy. Anyway;

- Jahoda implanted his dermal sheath cells in his wife and new hair follicles grew;
http://www.nature.com/nature/journal/v402/n6757/full/402033a0.html

- Study of Toscani that splitting hair follicles can induce new hair follicles and they regenerate; http://drcarloswesley.com/T/06082014.pdf

Which has been observed and confirmed by these doctors too;

(Dr. Karadeniz noted that in transection in the donor area hair follicles sometimes regenerated)


That splitting is done this way;

Basically separating the mesenchymal part and the epithelial part. Tsuji is going to use stem cells of both parts and put them together like you know. Mesenchymal and epithelial interactions are at the center of hair follicle cycling but also hair follicle creation.

So if they are able to culture these cells correctly then what reasons would I have to not be very optimistic about Tsuji?

Intercytex/aderans simply never even succeeded culturing these cells correctly. Paul Kemp (recent hairclone.me startup)

Paul: At this point we still don’t know. There are many different culturing options, including 3D culturing, that are available and through our research we intend to find the one that works the best. The technique’s used by Claire Higgins give us the tools to rapidly determine which system works best before we use the cells in the clinic.

 

[KO1]

Thanks, that said, how do you know his protocol will be successful? IOW, how do you know he has hit upon the right formula for culturing these cells? For example Aderans knew about culturing two cell types together - epithelial and mesenchymal (fibroblasts and keratinocytes) back in 2003. I have trouble seeing what is innovative here. (maybe the 3d culturing).

 

[KO1]

Here is an interview with Washenik way back when...
http://www.hairlosshelp.com/hair_cloning/cloning_interview_washenik.cfm

(Mods: It's not a link to the HLH forum, but to an interview only).

 

[Swoop]

Thanks, that said, how do you know his protocol will be successful? IOW, how do you know he has hit upon the right formula for culturing these cells? For example Aderans knew about culturing two cell types together - epithelial and mesenchymal (fibroblasts and keratinocytes) back in 2003. I have trouble seeing what is innovative here. (maybe the 3d culturing).

I don't. I trust them on their word. They said that they fixed the problem of the mesenchymal stem cells and are only left to fix the epithelial stem cell culturing problem.

As I may quote them;

"With respect to the development of the technology to cultivate mesenchymal stem cells, that is papilla cells, being applicable to human clinical trials, we are already in progress now for development. On the other hand, as for the technology to cultivate epithelial stem cells of follicles, it still remains a significant challenge globally. We are currently in the middle of research and development for this. Based on our recent research results, we finally have some prospects and expect this issue to be resolved in the near future."

I don't know how they even succeeded culturing these mesenchymal stem cells. Going from a 2D environment to a 3D environment retains more signature expression through culture but still isn't sufficient. There is more too it probably.

Anyway if they indeed are able to culture these two cells then I think we have pretty much solved to create hair follicles.

 

[Noisette]

I would like to share with you a new publication authored by Colin Jahoda, published on June 2016 and called " What Lies Beneath: Wnt/β-Catenin Signaling and Cell Fate in the Lower Dermis" .

Abstract:
" Dermal cell populations are markedly heterogeneous, and they have the capacity to differentiate into dynamic and complex dermal cell compartments. However, the regulatory processes that govern the establishment of each dermal subset remain unknown. Mastrogiannaki et al. provide evidence of Wnt/β-catenin signaling controlling adipogenic differentiation in the developing reticular dermis. They also show that overexpression of localized Wnt converts dermal adipose cells into a distinct fibroblast subtype, which leads to fibrosis and disrupted hair follicle cycling. These findings highlight the multifaceted roles of Wnt signaling in the normal development and pathology of skin, including the establishment of dermal identity. Further understanding of Wnt involvement and uncovering the roles of specific Wnt ligands could be useful for discovering new therapeutic targets in treating fibrosis-related disorders " .