Regrowth Versus Androgenetic Alopecia Prevention

[mulder]

The whole GTE being a very effective blocker of DHT triggered hair loss and an inhibitor of angiogenesis raises an obvious issue I never see discussed. Regrowth and preventing DHT loss can sometimes be competing goals. Am I right in thinking that growth of new follicles and stimulating existing follicles require androgens and aspects of the 'inflammatory' response??

Right now I have GTE in one of my shampoos (use 1-2 a week, ~ 3%) and put some GTE in my emu-jojoba hair oil (use once a day, ~0.5%). I also drink about 3 cups a day of the stuff. Do you guys think this is too much GTE exposure. Is possible to counteract the anti-angiogenesis effects of GTE and still have it be effective in combating DHT mediated loss?

 

[mulder]

So CCS, if you're worried about the anti-VEGF properties of GTE you should be dumping curcumin too...Resveratol is out too.

Supposedly borage oil encourages VEGF activity though...so does adenosine...

 

[Pete]

The whole GTE being a very effective blocker of DHT triggered hair loss and an inhibitor of angiogenesis raises an obvious issue I never see discussed. Regrowth and preventing DHT loss can sometimes be competing goals. Am I right in thinking that growth of new follicles and stimulating existing follicles require androgens and aspects of the 'inflammatory' response??

Right now I have GTE in one of my shampoos (use 1-2 a week, ~ 3%) and put some GTE in my emu-jojoba hair oil (use once a day, ~0.5%). I also drink about 3 cups a day of the stuff. Do you guys think this is too much GTE exposure. Is possible to counteract the anti-angiogenesis effects of GTE and still have it be effective in combating DHT mediated loss?

The 2 angles that you need to approach hairloss are:

1) slow DHT converion internally

2) reverse inflammation topically and increase bloodflow






Regards
Pete

 

[Bryan]

So CCS, if you're worried about the anti-VEGF properties of GTE you should be dumping curcumin too...Resveratol is out too.

I haven't seen the thread in which CCS complained about the alleged anti-VEGF properties of GTE, but it reminds me of similar concerns expressed on alt.baldspot in past years. I'll say the same thing here that I've said before: what if the alleged anti-VEGF properties of GTE are due simply to an antiandrogenic effect on body hair? That would make the question moot, when it comes to scalp hair.

 

[mulder]

The whole GTE being a very effective blocker of DHT triggered hair loss and an inhibitor of angiogenesis raises an obvious issue I never see discussed. Regrowth and preventing DHT loss can sometimes be competing goals. Am I right in thinking that growth of new follicles and stimulating existing follicles require androgens and aspects of the 'inflammatory' response??

Right now I have GTE in one of my shampoos (use 1-2 a week, ~ 3%) and put some GTE in my emu-jojoba hair oil (use once a day, ~0.5%). I also drink about 3 cups a day of the stuff. Do you guys think this is too much GTE exposure. Is possible to counteract the anti-angiogenesis effects of GTE and still have it be effective in combating DHT mediated loss?

The 2 angles that you need to approach hairloss are:

1) slow DHT converion internally

2) reverse inflammation topically and increase bloodflow






Regards
Pete

But surely that isn't it in terms of getting any regrowth. How about reversing fibrosis, or stimulating existing follicle growth, reviving dormant follicle, turning vellus into terminal, or even generating new follicles. Surely blocking scalp DHT, increasing blood flow, and reversing inflammation isn't all there is to it.

 

[mulder]

So CCS, if you're worried about the anti-VEGF properties of GTE you should be dumping curcumin too...Resveratol is out too.

I haven't seen the thread in which CCS complained about the alleged anti-VEGF properties of GTE, but it reminds me of similar concerns expressed on alt.baldspot in past years. I'll say the same thing here that I've said before: what if the alleged anti-VEGF properties of GTE are due simply to an antiandrogenic effect on body hair? That would make the question moot, when it comes to scalp hair.

Well looking at the studies on pubmed:

EGCG inhibited VEGF, VEGF-induced endothelial cell proliferation, migration and tube formation in the stomach.

Similar findings in vascular smooth muscle, bronchial, cervical, hepatoma, breast, head and neck carcinoma cells.

That seems pretty wide ranging...I think it's reasonable to expect similar effects of GTE on endothelial cells throughout the body.

Can anyone take a peak at this article:
http://www.ncbi.nlm.nih.gov/sites/entre ... d_RVDocSum
I don't have access right now. Looks like a good review.

I'm really starting to think adding a VEGF stimulant is a necessary part of a regrowth regimen. More adenosine and GLA. Any suggestions on where to get some adenosine?

 

[bcapop]

You need to:

-Inhibit 5AR and thereby lowering DHT Type 2.
-Reduce TGF-B12 to normal levels (pre-bald state).
-Inhibit caspase 3, 6 and 7.
-Increase Bcl-2, decrease Bax.
-Decrease the inhibitory factors.
-Increase the growth factors and stimulating the dermal papilla.

That's about it I think.

 

[Beethoven]

You need to:

-Inhibit 5AR and thereby lowering DHT Type 2.
-Reduce TGF-B12 to normal levels (pre-bald state).
-Inhibit caspase 3, 6 and 7.
-Increase Bcl-2, decrease Bax.
-Decrease the inhibitory factors.
-Increase the growth factors and stimulating the dermal papilla.

That's about it I think.

Suppose someone (me) is doing all your list, except for the first one (I mean DHT remain at normal levels). Do you think he (me again...) has any chance?

 

[bcapop]

You need to:

-Inhibit 5AR and thereby lowering DHT Type 2.
-Reduce TGF-B12 to normal levels (pre-bald state).
-Inhibit caspase 3, 6 and 7.
-Increase Bcl-2, decrease Bax.
-Decrease the inhibitory factors.
-Increase the growth factors and stimulating the dermal papilla.

That's about it I think.

Suppose someone (me) is doing all your list, except for the first one (I mean DHT remain at normal levels). Do you think he (me again...) has any chance?

Sure, but how on earth are you going to do that?

 

[Beethoven]

I can't do all, but I should try to do as many as I can, since I had sides even with topicals which reduce DHT/block receptors.
In that topical you made you seem to cover many aspects. Do you have any idea where the formulator of Elsom had gone? I was playing with it trying to decide what to go for, but now it's missing from their site.

 

[bcapop]

I can't do all, but I should try to do as many as I can, since I had sides even with topicals which reduce DHT/block receptors.
In that topical you made you seem to cover many aspects. Do you have any idea where the formulator of Elsom had gone? I was playing with it trying to decide what to go for, but now it's missing from their site.

http://www.the-formulator.com/

What are the ingredients of your topical?

 

[Beethoven]

I was thinking about most of the stuff you used, specially taurin and ginkgo, excluding the ones that inhibit 5ar. Price and amount are an issue since I'm already using many other stuff (foam, prox-n, applepoly, aminexil, tricosaccride & zanthin), and I'm also "diffuser" so I need enough amount to cover whole front half of the scalp. Another question(thanks for all your help btw!): your topical is cream or liquid?

 

[bcapop]

I was thinking about most of the stuff you used, specially taurin and ginkgo, excluding the ones that inhibit 5ar. Price and amount are an issue since I'm already using many other stuff (foam, prox-n, applepoly, aminexil, tricosaccride & zanthin), and I'm also "diffuser" so I need enough amount to cover whole front half of the scalp. Another question(thanks for all your help btw!): your topical is cream or liquid?

It's a serum, because it's thinner then a cream, but thicker then a liquid. If you're not going to inhibit 5AR, you should look into Amacha, since it's a powerfull TGF-B inhibiter. I would also add sodium pyruvate.

 

[chris55]

bcapop- What exactly does sodium pyruvate do for hairloss? I have heard great things about it but havent really come across any studies regarding it.

 

[bcapop]

Sodium pyruvate

"We recently reported that pyruvate inhibited translocation and activation of p53 caused by DNA damage due to oxidant injury (Lee YJ, Kang IJ, Bunger R, and Kang YH. Microvasc Res 66: 91-101, 2003); this was associated with increased expression of apoptosis-related bcl-2 and decreased expression of bax gene."

"Activation of caspase-3 and the cleavage of procaspase-6 and procaspase-7 were strongly inhibited by pyruvate but markedly enhanced by l-lactate and aminooxyacetate, implicating redox-related antiapoptotic mechanisms of pyruvate."

"In addition, H2O2 downregulated extracellular signal-regulated kinase (ERK1/2) and phosphorylated p38 mitogen-activated protein kinase (MAPK), effects that were fully reversed by pyruvate within 2 h."

"Collectively, these findings indicate that pyruvate can protect cellular glutathione, thus enhancing cellular antioxidant potential, and that enhanced antioxidant potential can desensitize NF-kappaB transactivation due to reactive oxygen species, suggesting possible metabolic redox relations to NF-kappaB. Furthermore, pyruvate blocked the p38 MAPK pathway and activated the ERK pathway in an apparently redox-sensitive manner, which may regulate expression of genes believed to prevent apoptosis and promote cell survival. Thus pyruvate may have therapeutic potential for reducing endothelial dysfunction and improving survival during oxidative stress."

“Pyruvat does very much for us. Especially the p38 MAPK pathway inhibtion is of extraordenary value for us. TGF-beta not only activates the SMAD pathway to signal to the nucleus. It also acitvates the TAK1 MAPK pathway and both pathways merge on DNA transcription level in the nucleus and the TAK1 pathway potentiates the actions of the SMADs synergistically (not bare addition), I can proof this with articles and will do so. So inhibition of the TAK1 p38 MAPK pathway will inhibit this synergism and the bare SMAD part will stay. But even if some signals manage to get through ... pyruvate also acts after transcription of the TGF-beta target genes has occured. TGF-beta causes apoptosis by generating ROS (reactive oxigen spezies), I have articles on that. But pyruvate can counteract ROS itself and by preventing glutathione from depletion (very likely it prevents glutathione from depletion because it scavenges the ROS itself (see link above)), thereby protecting the mitochondria from the attack of the ROS and thereby preventing release of cytochrome c and caspase activation and apoptosis.â€￾

The last one is a comment from Fred.