Menthol chemical inhibits angiogeneis----bad news

[michael barry]

http://www.poseidonsciences.com/anti-inflammatory.html




I hated reading that. Damn. Im going to look into clove, rose hips and arnica to see if they do the same.

 

[powersam]

didn't bryan post a study a while back where the group using just an alcohol base with no other active ingredient showed regrowth?

 

[Jkkezh]

Seems like a lot of anti-androgens or anti-oxidants inhibit angiogenesis.

BTW Finasteride also inhibits angiogenesis......

There is definately some kind of relation

 

[bcapop]

Seems like a lot of anti-androgens or anti-oxidants inhibit angiogenesis.

BTW Finasteride also inhibits angiogenesis......

There is definately some kind of relation

Maybe that's why it's so hard to regrow new hair from Finasteride.

 

[Jkkezh]

Maybe that's why it's so hard to regrow new hair from Finasteride.

Indeed


Also: Minoxidil stimulates angiogenesis if I'm correct, that might also explain why finasteride and minoxidil work so well together.

SO what's the best way to stimulate angiogenesis besides minoxidil? (and increasing NO levels)

I know excercise can also stimulate angiogenesis so tom hagerty's scalp excercises, massages, scalp brushing, skin needling, christopher walken's hair pulling technique, they might all help a bit.

 

[bcapop]

Maybe that's why it's so hard to regrow new hair from Finasteride.

Indeed


Also: Minoxidil stimulates angiogenesis if I'm correct, that might also explain why finasteride and minoxidil work so well together.

SO what's the best way to stimulate angiogenesis besides minoxidil? (and increasing NO levels)

I know excercise can also stimulate angiogenesis so tom hagerty's scalp excercises, massages, scalp brushing, skin needling, christopher walken's hair pulling technique, they might all help a bit.

Adenosine increases angiogenesis safely and good according to the study done on humans. Red ginseng does the same only through another pathway.

 

[tino]

Seems like a lot of anti-androgens or anti-oxidants inhibit angiogenesis.

BTW Finasteride also inhibits angiogenesis......

There is definately some kind of relation

You mean that finasteride inhibits angiogenesis in prostatacancer cells?

 

[Jkkezh]

Yeah sorry should have mentioned that, it could be that finas doesn't inhibit angiogenesis in the scalp, but only in the prostate.

I assumed it might have similar effects on the scalp, but I haven't seen any studies about this.....

 

[tino]

Yeah sorry should have mentioned that, it could be that finas doesn't inhibit angiogenesis in the scalp, but only in the prostate.

I assumed it might have similar effects on the scalp, but I haven't seen any studies about this.....

prostatacancer cells do react compleatly in another way.Androgenes do induce growth there,and take away androgenes,inhibits growth.I have never read in more than 200 Studys about finasteride that it inhibits angiogenesis in scalp hair.It could be so that antiandrogenes inhibit angiogenesis in androgen sensitive body hair,for example chest hair.

 

[purecontrol]

Chocamine and cardio are the first ones that come to mind, do a google and search hard you will find many many more ie Hawthorn berry, bilberry, garlic, carnosine, vit. c ect ect.

 

[Jkkezh]

Yeah sorry should have mentioned that, it could be that finas doesn't inhibit angiogenesis in the scalp, but only in the prostate.

I assumed it might have similar effects on the scalp, but I haven't seen any studies about this.....

prostatacancer cells do react compleatly in another way.Androgenes do induce growth there,and take away androgenes,inhibits growth.I have never read in more than 200 Studys about finasteride that it inhibits angiogenesis in scalp hair.It could be so that antiandrogenes inhibit angiogenesis in androgen sensitive body hair,for example chest hair.

But the effect of finasteride on angiogenesis in the scalp has never been specifically studied, or has it? So we can't be sure

Using ELISA and reverse transcriptase-polymerase chain reaction, we investigated the role played by some steroids (estrogens, androgens, antiandrogens) in the modulation of vascular endothelial growth factor (VEGF) expression by DPC. The association of different treatments of DPC (5alpha-reductase inhibitor and androgen receptor antagonist) shows a great stimulation of VEGF and aromatase expression. Strong stimulation of VEGF protein and gene expression is observed in the presence of 17beta-estradiol. Also, the concentration-dependent inhibition of VEGF expression by DPC using the cytochrome-p-450-aromatase inhibitor, confirms the involvement of this estrogenic pathway in the regulation of VEGF expression in vitro.

http://www.nature.com/jidsp/journal/v4/ ... 0232a.html

Study about steroids and VEGF, I don't understand it fully ....maybe someone can link it to finasteride/anti-androgen use(?)

 

[Jkkezh]

The hair growth promoting effect of Asiasari radix extract and its molecular regulation

Results:

Among the tested plant extracts, the extract of Asiasari radix showed the most potent hair growth stimulation in C57BL/6 and C3H mice experiments. In addition, this extract markedly increased the protein synthesis in vibrissae follicle cultures and the proliferation of both HaCaT and human DP cells in vitro. Moreover, the A. radix extract induced the expression of VEGF in human DP cells that were cultured in vitro.

Conclusion:

These results suggest that the A. radix extract has hair growth-promoting potential, and that this effect may be due to its regulatory effects on both cell growth and growth factor gene expression.

from: http://linkinghub.elsevier.com/retrieve ... 110500023X

 

[tino]

Yeah sorry should have mentioned that, it could be that finas doesn't inhibit angiogenesis in the scalp, but only in the prostate.

I assumed it might have similar effects on the scalp, but I haven't seen any studies about this.....

prostatacancer cells do react compleatly in another way.Androgenes do induce growth there,and take away androgenes,inhibits growth.I have never read in more than 200 Studys about finasteride that it inhibits angiogenesis in scalp hair.It could be so that antiandrogenes inhibit angiogenesis in androgen sensitive body hair,for example chest hair.

But the effect of finasteride on angiogenesis in the scalp has never been specifically studied, or has it? So we can't be sure

Using ELISA and reverse transcriptase-polymerase chain reaction, we investigated the role played by some steroids (estrogens, androgens, antiandrogens) in the modulation of vascular endothelial growth factor (VEGF) expression by DPC. The association of different treatments of DPC (5alpha-reductase inhibitor and androgen receptor antagonist) shows a great stimulation of VEGF and aromatase expression. Strong stimulation of VEGF protein and gene expression is observed in the presence of 17beta-estradiol. Also, the concentration-dependent inhibition of VEGF expression by DPC using the cytochrome-p-450-aromatase inhibitor, confirms the involvement of this estrogenic pathway in the regulation of VEGF expression in vitro.

http://www.nature.com/jidsp/journal/v4/ ... 0232a.html

Study about steroids and VEGF, I don't understand it fully ....maybe someone can link it to finasteride/anti-androgen use(?)

That means that androgenes do may induce growth inhibition over inhibiting angiogenesis,and that antiandrogen treatment induced pro angiogenetic VEGF stimmulation (which leads to a better endothelial function),and armatase expression.It could be so that the direct VEGF stimmulation was induced over the aromatase expression induced by androgen inhibition.Estrogen is well known for VEGF Stimmulation.

 

[tino]

There is a very interesting point in this study.In the line of this investigation,Cyproteroneacetate,an antiandrogen which directly inhibits androgen action,was alone not able to induce VEGF upregulation.The autors think that maybe the fact that cyproteroneacetate cant induce Aromatase metabolism,is the reason for this failure.They think that a testosterone metabolism in the hair follicle has to be keep,because no testosterone,no aromatase activity.5-alpha-reductase inhibition does not touch the intercellulaer testosterone,and enabled so aromatase activity which may leads to VEGF upregulation.In this experiment,finasteride induced aromatase and VEGF upregulation.Some years ago i read a study about finasteride and the use in postmenopausal women.One Women,was almost completly bald.Every treatment failed,Androcur(cyproteroneacetate) and Minoxidil tonly finasteride was able to induce regrowth to her.My thoughts at that time,were identic whith the thoughts of the autors from the Finasteride/Angiogenesis Study.I told the people on my board,that a direct testosterone inhibition is maybe wrong,because it could be so,that the hair follicle needs testosterone for regrowth,which interacts positive whith growth factors like igf-1 and e2 when DHT is eliminated.I never seen big regrowth in women who use birth control pills,...the only thing i saw was a slower progression of their hair loss.


look at the pictures beyond.

http://www.alopezie.de/diskussion/fraue ... rid_2b.jpg


http://www.alopezie.de/cgi-bin/anyboard ... =2&gV=0&p=

 

[Jkkezh]

Thanks tino interesting indeed,

Our finding that finasteride stimulates VEGF and aromatase is very interesting and suggest two modes of action; finasteride may act like estrogen because it directly stimulates VEGF, or it acts via aromatase, because it also stimulates aromatase expression

So finasteride upregulates VEGF directly and via aromatase upregulation also (in vitro)

Btw: The full text pdf wasn't working for me before but now it is, here is the direct link.
http://www.nature.com/jidsp/journal/v4/ ... 40232a.pdf

 

[ram_in_md]

Does this mean that peppermint oil and water combo on the scalp is not a great idea. I have been regularly using that for about 15 days now.

 

[powersam]

Where did these knowledgeable and polite new posters suddenly appear from? Some very interesting info in this thread.

 

[Bryan]

There is a very interesting point in this study.In the line of this investigation,Cyproteroneacetate,an antiandrogen which directly inhibits androgen action,was alone not able to induce VEGF upregulation.The autors think that maybe the fact that cyproteroneacetate cant induce Aromatase metabolism,is the reason for this failure.They think that a testosterone metabolism in the hair follicle has to be keep,because no testosterone,no aromatase activity.5-alpha-reductase inhibition does not touch the intercellulaer testosterone,and enabled so aromatase activity which may leads to VEGF upregulation.In this experiment,finasteride induced aromatase and VEGF upregulation.Some years ago i read a study about finasteride and the use in postmenopausal women.One Women,was almost completly bald.Every treatment failed,Androcur(cyproteroneacetate) and Minoxidil tonly finasteride was able to induce regrowth to her.My thoughts at that time,were identic whith the thoughts of the autors from the Finasteride/Angiogenesis Study.I told the people on my board,that a direct testosterone inhibition is maybe wrong,because it could be so,that the hair follicle needs testosterone for regrowth,which interacts positive whith growth factors like igf-1 and e2 when DHT is eliminated.

When you say "a direct testosterone inhibition", are you referring to a suppression of the production of testosterone, as opposed to just a blocking of androgen receptors? To what degree does cyproterone acetate (when used in typical doses) reduce testosterone production?

Also, are you saying that you think that estrogen is SO important for the health of human scalp hair that the suppression of the production of testosterone possibly does more harm than good, by preventing (or reducing) the aromatization of testosterone into estrogen?

 

[tino]

There is a very interesting point in this study.In the line of this investigation,Cyproteroneacetate,an antiandrogen which directly inhibits androgen action,was alone not able to induce VEGF upregulation.The autors think that maybe the fact that cyproteroneacetate cant induce Aromatase metabolism,is the reason for this failure.They think that a testosterone metabolism in the hair follicle has to be keep,because no testosterone,no aromatase activity.5-alpha-reductase inhibition does not touch the intercellulaer testosterone,and enabled so aromatase activity which may leads to VEGF upregulation.In this experiment,finasteride induced aromatase and VEGF upregulation.Some years ago i read a study about finasteride and the use in postmenopausal women.One Women,was almost completly bald.Every treatment failed,Androcur(cyproteroneacetate) and Minoxidil tonly finasteride was able to induce regrowth to her.My thoughts at that time,were identic whith the thoughts of the autors from the Finasteride/Angiogenesis Study.I told the people on my board,that a direct testosterone inhibition is maybe wrong,because it could be so,that the hair follicle needs testosterone for regrowth,which interacts positive whith growth factors like igf-1 and e2 when DHT is eliminated.

When you say "a direct testosterone inhibition", are you referring to a suppression of the production of testosterone, as opposed to just a blocking of androgen receptors? To what degree does cyproterone acetate (when used in typical doses) reduce testosterone production?

Also, are you saying that you think that estrogen is SO important for the health of human scalp hair that the suppression of the production of testosterone possibly does more harm than good, by preventing (or reducing) the aromatization of testosterone into estrogen?

to my knowledge cyproteroneacetate blocks androgenes and androgene action in two ways.it is a steroidal antiandrogen,and drops serum testosterone alongside blocking AR.I have read some studys...they say that the risk of developing gyno is not so high when using androcur in men.That sounds like,that it also blocks aromatase activyty.In the line of this vitro study about VEGF etc,i think the receptor blocking induced the aromatase problem.


To the other point....yes,i think that dropping testosterone,and hence resulting aromatisation,is especially bad for hair REGROWTH.I know that testosterone keeps up serum igf-1,but i dont know for sure,if there is a testosterone modulated cellulaer metabolism in the same way.Im more sure,that missing estrogen in the cells,drops down the insulin and igf-1 RECEPTORS.I dont think that using oral or topical antiandrogenes which blocks testosterone action,cant stopp hair loss in cases with a REAL androgen dependet hair loss-receptor dependet male pattern baldness,or over systemic high androgen levels.But i don t think that this will lead to much regrowth.Almost every Study about Flutamide,Androcur etc in women whith high testo levels,shows only a slower progression of hair loss,but in the majority of cases,no regrowth.I can t evaluate that in men,because whith the exception of spironolactone,i have no studys.This one...or better one small study,one topical study,and one case report,do report regrowth.Another study showes a rise in endogen estrogen in men which use spironolactone orally.And the high risk of devoloping gyno under spironolactone is well known.All that speaks for a good aromatase activity in the tissues under spironolactone.If im right.....spironolactone works a little multifactorial,it inhibits skin DHT may more well than it blocks AR-or do i be mistaken?

 

[Bryan]

to my knowledge cyproteroneacetate blocks androgenes and androgene action in two ways.it is a steroidal antiandrogen,and drops serum testosterone alongside blocking AR.I have read some studys...they say that the risk of developing gyno is not so high when using androcur in men.That sounds like,that it also blocks aromatase activyty.In the line of this vitro study about VEGF etc,i think the receptor blocking induced the aromatase problem.

But we know that people with CAIS (Complete Androgen Insensitivity Syndrome) have luxuriant scalp hair growth, despite having non-functional androgen receptors. In their specific case, having no androgen-stimulated aromatase activity (even though there's no lack of the testosterone substrate) is not a problem for the health of their scalp hair.

I am specifically interested in the LEVEL of the reduction of testosterone (T) production, when using cyproterone acetate at typical doses. I would be surprised if that level of T reduction is really all that significant. Do you have any information on that?

To the other point....yes,i think that dropping testosterone,and hence resulting aromatisation,is especially bad for hair REGROWTH.I know that testosterone keeps up serum igf-1,but i dont know for sure,if there is a testosterone modulated cellulaer metabolism in the same way.Im more sure,that missing estrogen in the cells,drops down the insulin and igf-1 RECEPTORS.

How do you feel about those people out there who are still so convinced that estrogen is a negative factor in balding? They are big believers in the use of aromatase inhibitors for the purpose of (supposedly) fighting male pattern baldness!

I dont think that using oral or topical antiandrogenes which blocks testosterone action,cant stopp hair loss in cases with a REAL androgen dependet hair loss-receptor dependet male pattern baldness,or over systemic high androgen levels.But i don t think that this will lead to much regrowth.Almost every Study about Flutamide,Androcur etc in women whith high testo levels,shows only a slower progression of hair loss,but in the majority of cases,no regrowth.

I don't know about the effect of flutamide in women, but in men, flutamide RAISES the production of testosterone, it doesn't lower it. So at least you can't blame flutamide for reducing the substrate for aromatase, unlike with cyproterone.

I can t evaluate that in men,because whith the exception of spironolactone,i have no studys.This one...or better one small study,one topical study,and one case report,do report regrowth.Another study showes a rise in endogen estrogen in men which use spironolactone orally.And the high risk of devoloping gyno under spironolactone is well known.All that speaks for a good aromatase activity in the tissues under spironolactone.If im right.....spironolactone works a little multifactorial,it inhibits skin DHT may more well than it blocks AR-or do i be mistaken?

I've seen conflicting information on whether or not spironolactone is a 5a-reductase inhibitor. I've seen one study saying that it is, and another study saying that it isn't.