Menthol chemical inhibits angiogeneis----bad news

[tino]

Tino: I always assumed this angiogenesis you are discussing occurred (in the context you're talking about it) in "damaged" cells, not healthy cells. (And I don't put male pattern baldness follicles and their cells in the "sick, damaged" category.) I could be wrong though. I can't remember what makes me think this but it has "stuck" in my mind now for quite a while.

There was something I read about a chemical called "T4" or "TB4", or some new novel drug where this type of problem occurred. The article went on to talk about other medications that act as anti-androgens and I can only remember saying to myself "oh, that's only a problem with 'damaged', 'sick' cells, not our male pattern baldness cells".

I just can't put my finger on the specific stuff I read to make me come to that conclusion. So I could be WRONG! :blush:

No,Angiogenesis is disturbed in damaged/degenerative,and or aged cells.See the studys about Estrogen use in aged women and Androgen deprivation i have postet.They report increased VEGF,and Vasculaer endothelial growth factor stimmulates Angiogenesis.Maybe it can rather be called premature aged cells in the line of male pattern baldness.But aging is kind of sick......a degenerative process.


i dont know which study you mean.

 

[Bryan]

Re: fulltext

I copyed it out,because i cant find a mechanism to upload files here.

Human Reproduction vol.8 no.ll pp.1807-1812, 1993
The effect of flutamide on pulsatile gonadotrophin
secretion in hyperandrogenaemic women
T.Sir-Petermann1, B.Rabenbauer and L.Wildt

Thanks for posting that, Tino. It does look like I was correct in what I said before: in normal women, not only is there no negative feedback mechanism for the control of androgen production, there is actually a positive feedback mechanism (or maybe one could call it a feed-FORWARD control). But even this study still doesn't explain WHY it works that way in normal women, it just verifies that it DOES work that way.

 

[tino]

Re: fulltext

I copyed it out,because i cant find a mechanism to upload files here.

Human Reproduction vol.8 no.ll pp.1807-1812, 1993
The effect of flutamide on pulsatile gonadotrophin
secretion in hyperandrogenaemic women
T.Sir-Petermann1, B.Rabenbauer and L.Wildt

Thanks for posting that, Tino. It does look like I was correct in what I said before: in normal women, not only is there no negative feedback mechanism for the control of androgen production, there is actually a positive feedback mechanism (or maybe one could call it a feed-FORWARD control). But even this study still doesn't explain WHY it works that way in normal women, it just verifies that it DOES work that way.[/quote]


Yes,i you may right.Im not so familear whith classical endocrinologie,especially not whith feedback loops.But there seems to be somthing in the brain,for example the influence from estrogen on the pulse frequency of LH.

 

[Old Baldy]

Ok Tino, maybe I'm just remembering incorrectly. male pattern baldness cells are somewhat "diseased" I guess.

 

[CCS]

When testosterone is no longer turned into DHT, some of the spared testosterone is turned into estrogen. Estrogen is good for your hair, and is probably why women's baldness is often reversible. Stopping DHT just stops further damage. Inhibiting 5ar so that more scalp estrogen is produced is what regrows some. Unfortunately, men never produce enough estrogen to regrow like women would, unless you use dut2.5mg per day, which can have side effects. That is what I like about topical 5ar1 inhibitors.

Sudden changes in estrogen levels cause sheds. It does not matter if it is up or down. That is just how the hair cycle works. When I read studies of high estrogen inhibiting hair growth, I ask two question:
1. Scalp hair or body hair?
2. For how long? Did they go past 6 months? Fluctuating estrogen levels cause sheds.

As long as you take finasteride daily, your hair gets used to the new estrogen levels and regrows some. For some guys, the initial change in estrogen levels gives them a finasteride shed. If you get off finasteride, the scalp estrogen levels drop again, and you get another shed. So if you got a shed, that means the drug could be working for you.

Castration probably lowers estrogen levels, but also androgen levels. My advice is to keep testosterone production up so your scalp can make estrogen. But you need to really inhibit 5ar1 and 2 in the scalp. Then, you need some androgen receptor blockers in the scalp to take care of the testosterone.

Polyol chinese Licorice extract, available from that korea company, is stronger at 5ar inhibiting than mint is, and is also the strongest androgen receptor blocker of those tested, and also mimics estrogen a little. Not sure which licorice it was, but one of them also inhibited angiogenesis, but it was only a little. The compound responsible for that was in low concentration. I think that makes it safer than GTE.

I recommend 2/3 licorice/ 1/3 apple poly as a topical, with some lavendar oil in there. Then nizoral, oral finasteride, and tri-amino copper peptides, for regrowing the most hair possible.

I'd like to know if any of these anti-oxidants have the same effect as the copper peptides. I kind of doubt it since the copper peptides work only in such low concentrations.

 

[tino]

Oh....i think you are on the right way!Your thoughts are exactly the same like mine.Whith the exception that im not sure about the necessary degree of AR blocking.This may depends on the degree of the miniaturisation.Im not sure if the rising testosterone due dual 5-a-r inhibition,is bad for men in every stage of male pattern baldness.Maybe not in early stages?

In fact ... high Estrogen may cause serve shedding.In my case too.As i started dutasteride and Oral spironolactone,a very bad chest gland inflammation correlated with a bad bad shedding phase.I thought im going bald in some months.And that yellow or lighter hair is reported on this board when substitute Dutasteride,is no fairy tail.My hair started to turn kind of yellow at the same time the chest gland inflammation and the DIFFUSE shed occured. But that colour change is possibly not due estrogen,but rather due the direct influence of DHT inhibition.I know that DHT can interact whith alpha-melanocyte-stimmulating hormone,for example in the nether regions.In puberty it induces the darker pigmentation there.But after some months,the shed stopped,and occured never again,and the lighter hair turned darker again.i could not notice any further temple redceeding anymore,but my hair turned to some kind of feminine quality-like women whith natural given thinner hair shafts.And i noticed that regrowth in every scalp skin part occured slower than whitout Medical hormonal influence.I could resolve that problem by using many antioxidants,Protein and Amino acids.But i still have the feeling,that something still runs a little bit slower in my scalp skin metabolic activitys.

I think that when you turn the low male estrogen levels to high,shedding occures just in the beginning.After some months,the systeme will arrange whith that new metabolism.



you wrote:Polyol chinese Licorice extract, available from that korea company, is stronger at 5ar inhibiting than mint is, and is also the strongest androgen receptor blocker of those tested, and also mimics estrogen a little.


Im not sure if estrogen mimetics,or Estrogens eccept E2 and Estrone are good for regrowth.


You wrote:Sudden changes in estrogen levels cause sheds. It does not matter if it is up or down. That is just how the hair cycle works. When I read studies of high estrogen inhibiting hair growth, I ask two question:
1. Scalp hair or body hair?
2. For how long? Did they go past 6 months? Fluctuating estrogen levels cause sheds.

could you specify that a little more?


Why only tri amino copper peptides,and what kind of effects do you mean?

 

[CCS]

estrogen changes, not estrogen levels, cause sheds. dutasteride and finasteride cause estrogen levels to change rapidly, which causes sheds. But 6 months later, after the follicle is used to the new level, hair growth continues. It is not your high level of estrogen that caused the shed. Moving to the new high level caused it. That is why pregnant women lose hair temporarily.

There are men who don't have 5ar1, and they have very thick hair. DHT is not needed for hair.

Women start losing hair at menopause, when their estrogen levels drop. Estrogen promotes scalp head hair and inhibits body hair. People think androgenic hair loss is non-reversible. That is true if all you do is stop further damage by stopping DHT. But I believe estrogen can reverse hair loss. Topically applied estrogen, without 5ar inhibitors, regrows as much hair as finasteride in 6 months. I think the reason the 2.5mg dutasteride group was the only group to regrow a lot of hair because 85% of 5ar1 was inhibited, so there was a lot more testosterone in the scalp to make estrogen from. I don't want to take dutasteride 2.5mg, but I think propecia combined with topical 5ar1 inhibitors will do the trick great.

Don't think of it as increasing testosterone levels. Testosterone production does not change. Just less testosterone in the scalp is turned to DHT, which is much more androgenic. So the higher scalp testosterone levels are GOOD, not bad. It is these higher levels that your follicles use to make estrogen from, locally.

the famous tri-amino copper peptides break down scar tissue and remodel the skin. But if their concentration is too high, they burn the skin. This is not the case with GTE and other cheap anti-oxidants.

 

[tino]

estrogen changes, not estrogen levels, cause sheds. dutasteride and finasteride cause estrogen levels to change rapidly, which causes sheds. But 6 months later, after the follicle is used to the new level, hair growth continues. It is not your high level of estrogen that caused the shed. Moving to the new high level caused it. That is why pregnant women lose hair temporarily.

i meaned the changes too.I became the problems,as the system was confronted whith a estrogen change.When the system sees that there is outcome of new life ,it increases more than only estrogen-the complete immunesystem.IGF-1,Melatonin,and alpha-MSH are also trimester dependet upregulated during pregnancy.Pregnancy is truly a paradise for hair growth.



There are men who don't have 5ar1, and they have very thick hair. DHT is not needed for hair.

you mean congenital 5-a-r-2 defects(mc ginley et.al)?I did not said that DHT is good for hair.

Women start losing hair at menopause, when their estrogen levels drop. Estrogen promotes scalp head hair and inhibits body hair. People think androgenic hair loss is non-reversible. That is true if all you do is stop further damage by stopping DHT. But I believe estrogen can reverse hair loss. Topically applied estrogen, without 5ar inhibitors, regrows as much hair as finasteride in 6 months. I think the reason the 2.5mg dutasteride group was the only group to regrow a lot of hair because 85% of 5ar1 was inhibited, so there was a lot more testosterone in the scalp to make estrogen from. I don't want to take dutasteride 2.5mg, but I think propecia combined with topical 5ar1 inhibitors will do the trick great.


I also belive that estrogen can reverse hair loss,it upregulates many growth factors,and their receptors.And i belive that some 5-a-r inhibitor non responders,in terms of regrowth,may have a genetic aromatase problem.To which Study do you reference,when you say that topically applied estrogen regrows as much hair as finasteride in 6 months?Yes it could be so that your point is the reason for the good response of the 2,5 mg group.I know experiments,which schowed that DHT injection inhibits Serum IGF-1.Inhibition would cause a contrarivise event.Its a pity that noone knows if IGF-1 levels arise under massive DHT inhibition.I would not recomend 1 mg Propecia.I have Data,that Aromatase activity,may arises as first,if you take dosages up to 2,5 or 5 mg in women.I will search them later.

Don't think of it as increasing testosterone levels. Testosterone production does not change. Just less testosterone in the scalp is turned to DHT, which is much more androgenic. So the higher scalp testosterone levels are GOOD, not bad. It is these higher levels that your follicles use to make estrogen from, locally.


I thought nothing else.In my case,i think that blocking Testo over spironolactone may induced a slower growth rate.But im not sure how very insufficient follicles interact whith higher testosterone.I tend to belive that its also there not bad.



the famous tri-amino copper peptides break down scar tissue and remodel the skin. But if their concentration is too high, they burn the skin. This is not the case with GTE and other cheap anti-oxidants.

But other antioxidants do other important things,for example increasing cAMP,inhibiting PKC(Vitamin E),supply glutathione,increase the igf-1,etc.Additional Aid for follicles in the regenerating phase,and protection from many bad influences.

 

[tino]

http://www.eje-online.org/cgi/reprint/147/4/467


Some ideas why only 5 mg induced the higher e2,are written in the conclusions.But there are conflicts whith other works.

 

[tino]

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.

This menthol...thing,inhibited the angiogenesis in a inflammed ear in mices.Im not sure if this is assignable to male pattern baldness.Some inflammatory diseases,or processes go on whith increased Angiogenesis.But male pattern baldness not.....in this case the angiogenesis is disturbed.Maybe this substances do only inhibit angiogenesis there where it is induced by inflammation.

http://www.ncbi.nlm.nih.gov/sites/entre ... d_RVDocSum

http://www.ncbi.nlm.nih.gov/sites/entre ... d_RVDocSum

 

[tino]

Re: estrogen and body hair

estrogen changes, not estrogen levels, cause sheds. dutasteride and finasteride cause estrogen levels to change rapidly, which causes sheds. But 6 months later, after the follicle is used to the new level, hair growth continues. It is not your high level of estrogen that caused the shed. Moving to the new high level caused it. That is why pregnant women lose hair temporarily.

There are men who don't have 5ar1, and they have very thick hair. DHT is not needed for hair.

Women start losing hair at menopause, when their estrogen levels drop. Estrogen promotes scalp head hair and inhibits body hair. People think androgenic hair loss is non-reversible. That is true if all you do is stop further damage by stopping DHT. But I believe estrogen can reverse hair loss. Topically applied estrogen, without 5ar inhibitors, regrows as much hair as finasteride in 6 months. I think the reason the 2.5mg dutasteride group was the only group to regrow a lot of hair because 85% of 5ar1 was inhibited, so there was a lot more testosterone in the scalp to make estrogen from. I don't want to take dutasteride 2.5mg, but I think propecia combined with topical 5ar1 inhibitors will do the trick great.

I knew that i was right somewhere that there is a evidence for Estrogen use,and an increase in body hair.Except of this application study,it seemed logical to me,because Estrogen supports VEGF,and density for IGF-1 and Insulin receptors.But Dr Umbreit reports there,that he watced it by long term use.Only older men were investigated there.I think it just growths body hair,when there is a age dependet decline for it.He also reported decreased scalp hair thinning.

Its indeed in german only.


http://www.kup.at/kup/pdf/435.pdf.


citation;Bei Langzeit-substitution nahm der männliche Körperbehaarungszustand zu,und das Kopfhaar fiel nicht mehr aus. Zu den gesundheitlichenVerbesserungen zählten haupt-sächlich die Leistungsfähigkeit,Verbesserung der Gelenks- undKnochenprobleme, die Verbesse-rung des Schlafes, die Antide-pressionswirkung, das Verschwin-den von Herzrhythmusstörungenund Stenokardien sowie dieVerringerung von Pollakisurien.Die größte Angst vor dieserSubstitutionstherapie wurde beiden Männern mit der schlechte-sten Ausgangs-Potenz beobachtet.Hier benahmen sich Ärzte undProfessoren nicht anders.HORMONEFÜR DIEVERLANG-SAMUNG DESALTERUNGS-PROZESSESBEIM MANN
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34J. MENOPAUSE 3/1999HORMONEFÜR DIEVERLANG-SAMUNG DESALTERUNGS-PROZESSESBEIM MANNHORMONEFÜR DIEVERLANG-SAMUNG DESALTERUNGS-PROZESSESBEIM MANN4. Yen SSC, De Vane GW, Czekala NM,Judd hair loss. Circulating gonadotropins,estrogens and androgens. ObstetGynecol 1975; 121: 496.5. Nieschlag E. Anabole Steroide undFortpflanzungsfunktion bei Bodybuil-dern. Dt Ärztebl 87 (45): A-3543.6. Zander J, Holzmann K. Zwischen-beziehungen zwischen zentralhypo-physärem System und ovariellen Steroi-den. In: Käser, Friedberg, Ober, Thomsen,Zander (eds). Gynäkologie und Geburts-hilfe. 1969; 272–3.7. Husmann F. Climacterium feminale.Kurt Pamminger, Leonberg, 1995.8. Simmer HH. Rückwirkung vonHormonen. Und: Einfluß der Nebennie-renrinden-Hormone. In: Käser, Friedberg,Ober, Thomsen, Zander (eds). Gynäkolo-gie und Geburtshilfe. 1969; 198; 199.9. Kuhl H. Östrogene gegen Artero-sklerose und Prostataleiden. Med Tribune1996; 14: 24–6.10. Vahlensieck jr W. Benigne Prostata-hyperplasie. Therapiewoche 1996; 33:1796–1802.11. Schweikert HU. Pathogenese derbenignen Prostatahyperplasie – Ansätzezur endokrinologischen Behandlung. 35.Symposion der Deutschen Gesellschaftfür Endokrinologie in Bonn – 23. 02.1991, Satellitenveranstaltung derDeutschen Gesellschaft für Endokrinolo-gie in Bonn: Östrogenproduktion beimMann. Schering.
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