Replicel

[UK_]

Gutted what NW stage are you?

[MackJames]

so far the only sulfasalazine case i know of is from a user on HLH who claimed to regrow his full frontal hair line whilst on it.

Benaxoprofen also inhibits 5-LOX (in addition to cox 2) which im not sure sulfsalazine does. And its this combination that reveres mpb, Loreal have a patent on this.
Im only aware of Sulfsalazine inhibitting cox-2, which IMO should be enough to stop balding.

Do you notice an increase in nail growth since being on it?

I've noticed no increase in nail growth. I need to make a correction; I've been on the drug since mid 09 but took a few months off while my wife and I were attempting to conceive. Hypospermia can be a side effect of sulfsalazine use and my Doctor suggested I go off the medication in case my sperm count had been lowered.

I also inject immune suppressing biologics for my arthritis. So if there are any theories out there that suppressing the immune system may help hair loss; Im sorry to report that I haven't found that to be true, at least in my case.

[UK_]

I've noticed no increase in nail growth. I need to make a correction; I've been on the drug since mid 09 but took a few months off while my wife and I were attempting to conceive. Hypospermia can be a side effect of sulfsalazine use and my Doctor suggested I go off the medication in case my sperm count had been lowered.

I also inject immune suppressing biologics for my arthritis. So if there are any theories out there that suppressing the immune system may help hair loss; Im sorry to report that I haven't found that to be true, at least in my case.

Or maybe if you took no medication or no immune system suppressants you would still be the same as you are today?

You cant rule that out.

What we need is a therapy that can physically show de novo hair follicle formation, this will not come from some NSAID or drug already released for another condition - a baldness cure would be all over the front pages.

[MackJames]

Or maybe if you took no medication or no immune system suppressants you would still be the same as you are today?

You cant rule that out.

What we need is a therapy that can physically show de novo hair follicle formation, this will not come from some NSAID or drug already released for another condition - a baldness cure would be all over the front pages.

You can't rule anything out, I guess. At this point Id wager to guess it's not effective for hair loss.

As far as where I would be had I remained med free, it is hard to say. I didnt notice thinning until I turned 32, around the time I started taking these medications. I have a pic on here somewhere to give an indication of my hair loss.

I wouldn't go so far as to draw any associations between the two but I am fairly certain i can conclude at the very least the meds haven't made an appreciable difference On the condition of my hair.

[UK_]

They can grow lungs hearts and kidneys but not hair follicles.

I am just glad Replicel are happy themselves to go ahead with a Phase 2 - this time they will be aiming for efficacy - so phase 2 will be the trial to determine if it will be effective or not.

The perfect treatment would be a combination of everything we are all looking at, something that addresses the need for the correct signals (HSC) and something that can actually induce de novo follicle formation (Replicel/Aderans).

http://dermatology.jwatch.org/cgi/co...ull/2012/720/2

Wnts can be used to signal and autologous cell therapy to induce formation of new growth.

DKK-1 inhibits the Wnt signaling pathway and, consequently, stem cell division. Stem cells generate hair and also produce the elongated hair follicles of the anagen phase. In the anagen-to-catagen transition, stem cells stop replenishing apoptotic hair bulb epithelial cells, leading to cessation of hair growth and involution of the hair follicle.

Consequently, MPB (impact of DHT) leading to an overexpression of DKK-1 forcing more hairs into catagen and inducing apoptosis of outer root sheath keratinocytes and also blocking wnt signalling preventing stem cell division.

Now where does PGD2 & COX-2 fit in?

[UK_]

One of the hardest form of cells to create using stem cells are functioning nerve cells (in search of neurogenesis), most of the time you need to use totipotent embryonic stem cells - my point is that if totipotent stem cells are required to form nerve cells, then this study elucidates the power of wnt proteins as it proves they can be used in the process of neurogenesis:

http://www.plosone.org/article/info%...l.pone.0040843

[2020]

"DKK-1 inhibits the Wnt signaling pathway"

if so then what's the point of injecting wnt like HSC does?

[gutted]

Gutted what NW stage are you?

im nw 2. The only areas i need regrowth is hairline/temples and a bit more density in the frontal region.

[UK_]

"DKK-1 inhibits the Wnt signaling pathway"

if so then what's the point of injecting wnt like HSC does?

The point is that WNT signalling will cause stem cells to proliferate which is what you need for hair to grow, hence why Histogen were able to destroy all the naysayers and create 2 years of hair growth that nobody else has ever accomplished - please name one person on a forum who has accomplished such a feat?

I also do not deny that DKK-1 is also associated with MPB, but there may be other factors at play regarding the division of stem cells required for hair growth:

"Dickkopf-1 (DKK-1) protein have been found in biopsies of scalp skin in male pattern alopecia."

^^^Sounds a lot like PGD2 study, but not as many people care - I wonder why?

[gutted]

Consequently, MPB (impact of DHT) leading to an overexpression of DKK-1 forcing more hairs into catagen and inducing apoptosis of outer root sheath keratinocytes and also blocking wnt signalling preventing stem cell division.

Now where does PGD2 & COX-2 fit in?

simply -
excess dht/androgens/5alpha?? -> over expression of cox 2 -> automatic over expression of pgd2 etc - > hair thinning - > dormancy and mild fibrosis -> baldness -> full fibrosis.

obviously there are many many other ezymes and protiens in the pathway that will be affected through negative feedback mechanisms.