Lithium Chloride

[Digidako]

I have 2kg of Lithium Chloride, and following SwissTemples (http://swisstemples.com/what-to-buy-and-use/) instruction to use at 10mg/ml I do not need this much.

If anyone is interested in some just PM me.

I also have 100g of Sulfasalazine that I would be willing to ship out in smaller quantities.

I have 2g of Finasteride (powder) and 500mg of Dutasteride also.

Going to add some 17a-Estradiol (0.5%) to my reg too.

I have no use for ALL of the product I have, and to avoid waste I'd be more than willing to help some of you guys out.
Let me know !!

- - - Updated - - -

**Also, I am experimenting with a 0.1% Tofacitnib solution**

Will report results.

 

[hellouser]

How did you get Sulfasalazine? I haven't seen any online pharmacy that sells and ships to Canada.

Having said that, I'm interested in Sulfa! PM with a price if you can, thanks!

 

[Digidako]

Regarding LiCl:

http://www.nature.com/jid/journal/v133/n8/full/jid2013132a.html

"...[FONT=museo_sans_500regular]In addition, it was found that agents, such as inhibitors of GSK3ß kinase, e.g., lithium chloride or similar small ions, which can mimic an effect of Wnt promoted signal transduction, e.g., inhibition of ß-catenin phosphorylation, e.g., by inhibition of GSK3ß kinase, or accumulation of ß-catenin, can regulate the ability of DP cells to promoter hair growth." - See more at: http://www.regrowth.com/hair-loss-f...se-lithium-chloride-wnt/#sthash.CPS8T424.dpuf[/FONT]

 

[Dench57]

Where did you get Tofa?

 

[kiwipilu]

I noticed Hellouser asked, but If you still have some sulfa left I would be interested. But first of all that would be more interestng to know where you get it ;p

 

[Solomon]

How did you get Sulfasalazine? I haven't seen any online pharmacy that sells and ships to Canada.

Having said that, I'm interested in Sulfa! PM with a price if you can, thanks!

Hey Hellouser!

Why are you interested in sulfa when you have seti? :\

 

[hellouser]

Hey Hellouser!

Why are you interested in sulfa when you have seti? :\

It upregulates PGE2 slightly, but also downregulates PGD2 (slightly).

 

[Swoop]

Tofa (0.1), sulfa, lithium chloride, alfatradiol..

All useless mate, complete bunk. At best you'll get minimal sh*t growth lol.

What I'm interested in though... What happened with your smoothened agonist experiment?

 

[kmm179]

Hellouser how is seti working for you?

 

[scar tissue]

Tofa (0.1), sulfa, lithium chloride, alfatradiol..

All useless mate, complete bunk. At best you'll get minimal sh*t growth lol.

Spoken like a guy who gave up and got a hair transplant.

 

[Hairloss23]

Spoken like a guy who gave up and got a hair transplant.

lmao

 

[Baldybald1]

Spoken like a guy who gave up and got a hair transplant.

Spoken like a guy who knows what he is talking about, go and look at his threads kid !

 

[kirklandism]

There has been no update by swisstemples on his regime.

 

[Digidako]

Tofa (0.1), sulfa, lithium chloride, alfatradiol..

All useless mate, complete bunk. At best you'll get minimal sh*t growth lol.

What I'm interested in though... What happened with your smoothened agonist experiment?

After further research, it's been shown that activation of smoothened is not sufficient enough to grow hair by itself, albeit still essential to stimulate anagen (Kishimoto, Burgeson, & Morgan, 2000; Fu & Hsu, 2013) (see attached)

(photo from Kishimoto et al., 2000)

It appears that hair follicle differentiation involves the participation and control of a multitude of signalling factors, each step dependent on the last. The photo above shows a control mouse (No Shh or Wnt-3a activity), a mouse with only Shh (and not Wnt3a activity), and a mouse that only demonstrates Wnt3a activity (absent of Shh). Wnt3A-only mice experienced 100% hair follicle induction, in comparison to Shh-only mice who demonstrated only 2% induction.

What can we deduce from this data ?

WNTs play a more influential influential role on HF differentiation compared to Shh-only mice.

I think a combination of a Dkk-1 (Prevents Wnt inactivation stimulating subsequent activation) + GSK-3B inhibitor (Prevents phosphorylation of B-Catenin) would positively stimulate the formation of Hair follicles. (Aside: Phosphorylation of B-Catenin renders it inactive, which we don't want.})

High levels B-Catenin is what want.

------------
My theory
------------
If androgens upregulate Dkk-1, Wnt becomes down-regulated. If Wnt is down-regulated, GSK-3B will remain bound to B-catenin which will cause subsequent down-regulation (of B-cat). If B-cat is down regulated, hair growth begins to cease and miniaturization occurs. This miniaturization continues until it begins to stop producing active hair follicles entirely.

I hypothesize that the Wnt pathway and prostaglandin pathways have a synergetic crosstalk, that is primarily dependent on Wnt. Wnt up-regulation (good) inhibits the bad prostaglandins (PGD) and up-regulates the good ones (PGF2a, PGE). This could be why some people don't see much success using one or the other, but swisstemples was able to achieve new growth with combination therapy.

I dont think that WNT and Prostaglandins, are going to become the magic cure. Though, I am confident that they both play an integral role in HF formation, and the subsequent growth of actual hair.

Obviously preventing androgen receptor activation would be necessary to PREVENT further hair loss, but WNT/Prostag has to be necessary for further growth.

Maybe Anti-androgens or AR antagonists might even be able to be avoided all together if my research is correct.

Hang in there boys, I'll pull through for ALL of us.

- - - Updated - - -

They may appear ineffective if used on their own, but I believe multi-targeted therapy will prove much more beneficial. Let the science speak for itself.

 

[Swoop]

@Digidako,

I don't take rodent models seriously. Especially if we try to use it as a "drug model" for androgenetic alopecia. It's totally useless and pretty much a established fact by now. In fact I have even asked this to 3 scientist from whom 2 top tier and they concur with that notion. Rodent models are perhaps interesting to study hair follicle cycling or processes like morphogenesis of hair follicles. However even that raises questions. In fact even if we go to this study which is released this week; http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0146791

They say the following;

In fact, this mouse study cannot be extrapolated to explain the behavior of human HFs. However, a similar mechanism may exist between follicular units during the HF cycle

And they are completely right about that and this is only about hair follicle cycling, not to mention Androgenetic Alopecia.

So when you present me data that a smoothened molecule grows hair better on mice than WNT then I don't extrapolate that to humans. Simply because rodent models are a terrible model for Androgenetic Alopecia. Unless you can show me data that involves smoothened agonist or SHH testing on humans. But to my knowledge such pathways have simply not been touched upon because of severe safety issues. I would take the stumptail macaque model more seriously too.

People have already tried what you think years ago by the way. At least with GSK3b inhibitors and DKK-1 antagonists. You are not the first one who thinks that way. By all means continue with your research though and good luck.

 

[hellouser]

@Digidako,

I don't take rodent models seriously. Especially if we try to use it as a "drug model" for androgenetic alopecia. It's totally useless and pretty much a established fact by now. In fact I have even asked this to 3 scientist from whom 2 top tier and they concur with that notion. Rodent models are perhaps interesting to study hair follicle cycling or processes like morphogenesis of hair follicles. However even that raises questions. In fact even if we go to this study which is released this week; http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0146791

They say the following;



And they are completely right about that and this is only about hair follicle cycling, not to mention Androgenetic Alopecia.

So when you present me data that a smoothened molecule grows hair better on mice than WNT then I don't extrapolate that to humans. Simply because rodent models are a terrible model for Androgenetic Alopecia. Unless you can show me data that involves smoothened agonist or SHH testing on humans. But to my knowledge such pathways have simply not been touched upon because of severe safety issues. I would take the stumptail macaque model more seriously too.

People have already tried what you think years ago by the way. At least with GSK3b inhibitors and DKK-1 antagonists. You are not the first one who thinks that way. By all means continue with your research though and good luck.

Perhaps it's time researchers we're given the possibility to conduct tests on humans?

Nah, who am I kidding, too much red tape and regulations to ever allow that.

 

[Norwood One]

The puzzle is fitting very nicely with prostaglandins and androgens, inflammation, growth factors. Probably even more so for researchers who have much more information than we do. Sounds very promising.

 

[Digidako]

it's more so just a matter of cost, but i'm willing to test it out on myself

- - - Updated - - -

@Digidako,

I don't take rodent models seriously. Especially if we try to use it as a "drug model" for androgenetic alopecia. It's totally useless and pretty much a established fact by now. In fact I have even asked this to 3 scientist from whom 2 top tier and they concur with that notion. Rodent models are perhaps interesting to study hair follicle cycling or processes like morphogenesis of hair follicles. However even that raises questions. In fact even if we go to this study which is released this week; http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0146791

They say the following;



And they are completely right about that and this is only about hair follicle cycling, not to mention Androgenetic Alopecia.

So when you present me data that a smoothened molecule grows hair better on mice than WNT then I don't extrapolate that to humans. Simply because rodent models are a terrible model for Androgenetic Alopecia. Unless you can show me data that involves smoothened agonist or SHH testing on humans. But to my knowledge such pathways have simply not been touched upon because of severe safety issues. I would take the stumptail macaque model more seriously too.

People have already tried what you think years ago by the way. At least with GSK3b inhibitors and DKK-1 antagonists. You are not the first one who thinks that way. By all means continue with your research though and good luck.

To each their own, but thanks !
Hows the RU58841 working out ?

- - - Updated - - -

Perhaps it's time researchers we're given the possibility to conduct tests on humans?

Nah, who am I kidding, too much red tape and regulations to ever allow that.

That's why there are guys like us on forums like these

 

[hellouser]

That's why there are guys like us on forums like these

The cell based treatments are far more promising. I'd rather try that out than topicals or pills. But yeah, I'll take what I can get.

 

[Digidako]

The cell based treatments are far more promising. I'd rather try that out than topicals or pills. But yeah, I'll take what I can get.

I completely agree, its more so a matter of procuring the resources needed for such treatments

- - - Updated - - -

But seriously I have 1kg of LiCl, which is about 1 000 000 mgs...
At 10mg/ml ED that is ~100 000 days worth equal to ~274 years.

I do not need 274 years worth of LiCl...