Has anyone used the following herbs?

[docj077]

So, I'm thinking about taking my hair loss battle in a different direction since I'm probably going to have to remove propecia from the battle. After doing some research I've discovered the the following herbs seem to be TGF-Beta inhibitors which is actually the next step once androgens bind and their complex transcribes the DNA.

So, I'm curious to know what others think or if anyone has used any of these:

1. Astragalus - Huang Qi

2. Angelica or A. Sinensis - Dang Gui

3. Ligustrum Lucideum - Found in AvaFlu

All are recommended for assistance with viral illness, cancer, and to assist the immune system during chemotherapy as they all impact the immune system and regulate its function. So, I'm thinking about trying one of these and seeing where it takes me. I'm pretty much convinced that DHT is needed in the male body and lowering it in any way is not beneficial.

I'm interested to hear any feedback or any thoughts on this one.

Sorry if this is supposed to be in the herbal treatment section. It just seems like nobody goes there and I think that inhibiting TGF-beta is the key to preventing its effects which are to inhibit proliferation of hair follicle cells and scarring through fibrosis.

 

[Guest]

I'm pretty much convinced that DHT is needed in the male body and lowering it in any way is not beneficial. .

not beneficial for what? for hair loss? you'd be wrong.

there are people in the dominican born without the ability to produce type II DHT. they are healthy.

 

[docj077]

I'm pretty much convinced that DHT is needed in the male body and lowering it in any way is not beneficial. .

not beneficial for what? for hair loss? you'd be wrong.

there are people in the dominican born without the ability to produce type II DHT. they are healthy.

Excuse me. I meant in my body with my genetics. Also, I was referring to the fact that it's not the androgens that cause the hair loss. It's their downstream effects that cause the hair loss.

 

[CCS]

who cares what he said about DHT. I agree he is wrong about DHT, but he has a good idea about the next part of the pathway.

Once androgens bind to the receptor, some other biochemical pipeline starts and makes some chemicals which I guess triggers fibrosis and attack by the immune system. Is that right?

So not only can we reduce androgen binding with dutasteride, we can inhibit the response of the androgens that make it through as well.

Please tell me more about this. If this is a well known process, and not needed, and we can know the herbs will interfere with it, then I want to add it to my regimen. Be warned though that many herbal tales are just tales.

Check out this site to see what evidence there is for various herbal claims.

http://www.pccnaturalmarkets.com/health ... samine.htm

I'm going to add Boswellia serrata to a topical because it may prevent local cells from sending off messages to the immune system to attack, and we know the immune system attacks hair follicles.
However, while the evidence for this is much stronger than for essential oils that i now think are rubbish, skinactives.com says http://skinactives.com/products/andrographis.htm this stuff is even better than the boswellia. So I will check that, again with the previous link as a starting point.

please check those herbals with the search engine in the first link and also elaborate more on this process for those of us who have not been paying attention to this biochemical pathway.

 

[CCS]

just saving this in case he edits it later. this is important stuff.

After doing some research I've discovered the the following herbs seem to be TGF-Beta inhibitors which is actually the next step once androgens bind and their complex transcribes the DNA.

1. Astragalus - Huang Qi

2. Angelica or A. Sinensis - Dang Gui

3. Ligustrum Lucideum - Found in AvaFlu

All are recommended for assistance with viral illness, cancer, and to assist the immune system during chemotherapy as they all impact the immune system and regulate its function. So, I'm thinking about trying one of these and seeing where it takes me.

I think that inhibiting TGF-beta is the key to preventing its effects which are to inhibit proliferation of hair follicle cells and scarring through fibrosis.

 

[CCS]

http://www.pccnaturalmarkets.com/health ... raphis.htm
http://www.pccnaturalmarkets.com/health ... agalus.htm
http://www.pccnaturalmarkets.com/health ... g_Quai.htm

 

[docj077]

Collegechemistry student.

I looked those herbs up that I was referring to and they don't have any scientific research to really back them up. Huang Qi (astragalus) and Ligustrum Lucidum both had immunomodulatory effects. They are listed as being used together for healthy immune function and cancer therapy.

Honestly, I really don't know if these would even work. I'm probably just throwing stones to try and create ripples in an ocean that's being ravaged by a hurricane.

I might just keep looking around and see if I can find better TGF-Beta antagonists. Something has to exist somewhere. I know that they already exist in the medical field for the treatment of various autoimmune and kidney related diseases.

Role of TGF-beta2 in the human hair cycle.Hibino T, Nishiyama T.
Shiseido Life Science Research Center, 2-12-1 Fukuura, Kanazawa-ku, Yokohama 236-8643, Japan. toshihiko.hibino@to.shiseido.co.jp

Male pattern baldness is the result of premature entry into catagen due to androgens. In order to prevent hair loss, it is important to understand two critical steps, i.e., the induction mechanism of premature entry and the regression process of catagen. At the initiation, dihydrotestosterone (DHT) stimulates synthesis of transforming growth factor-beta2 (TGF-beta2) in dermal papilla cells. TGF-beta2 suppresses proliferation of epithelial cells and stimulates synthesis of certain caspases. Then TGF-beta2 triggers the intrinsic caspase network and subsequently epithelial cells are eliminated through apoptotic cell death. TGF-beta antagonists are effective in preventing catagen-like morphological changes and in promoting elongation of hair follicles in vivo and in vitro. These lines of evidence strongly suggest the presence of a "catagen cascade" in male pattern baldness, involving: (1) the conversion of testosterone to DHT by type II 5-alpha-reductase; (2) the synthesis of TGF-beta2 in dermal papilla cells; and (3) the activation of the intrinsic caspase network. These sequential events contribute to the shortening of the human hair cycle. Copyright 2004 Japanese Society for Investigative Dermatology


I also found a study that says that Finasteride inhibits this process. I found that interesting.


Bascially, testosterone or DHT binding of the androgen receptor causes a conformational change in the receptor-androgen complex. This complex then bind to the DNA and begins transcription and translation of the TGF-beta gene. This gene these initiates the cascade that causes the follicular death and fibrosis.

Let me know if you find something better.

 

[docj077]

Also, to anyone reading this, don't go out an buy these herbs we're talking about. We're just trying to figure this thing out. They say that they have no side effects, but let's be sure first.

I'd rather have people healthy and bald, then have cancer and have a full head of hair.

 

[CCS]

to anyone who wants to try these herbs out:

you will probably waste $100 on a bunch of stuff that does nothing at all, like I did on saw palmetto and essential oils I bought.

I doubt they will hurt you if you don't concentrate them too much, but I guess there is that small posibility.

so don't be impulsive like me. save your money and wait for us to find the right herb.

 

[docj077]

I found a herb named Curcumin or Turmeric that has been used in studies to clearly demonstrate that it can inhibit any signaling pathway that involves TGF-beta. However, only pubmed like it. The herbal site you recommended to me gives it one star.

Also, this is in the kidney, but if this was made into a topical, it would be god-like.


Curcumin blocks multiple sites of the TGF-beta signaling cascade in renal cells.

Gaedeke J, Noble NA, Border WA.

Fibrosis Research Laboratory, Division of Nephrology, University of Utah, Salt Lake City, Utah, USA.

BACKGROUND: Over-expression of transforming growth factor-beta (TGF-beta) contributes greatly to fibrotic kidney disease. The activator protein-1 (AP-1) inhibitor curcumin, a polyphenolic compound derived from Curcuma longa, has been shown to reduce collagen accumulation in experimental pulmonary fibrosis. Here, we investigate curcumin's ability to modulate TGF-beta's profibrotic actions in vitro. METHODS: NRK49F rat renal fibroblasts were stimulated with TGF-beta (5 ng/mL), and the effects of curcumin on TGF-beta-regulated genes, TGF-beta receptors, and phosphorylated SMAD isoforms were analyzed by Northern blotting, enzyme-linked immunosorbent assay (ELISA), and Western blotting. The effects of c-jun depletion on TGF-beta-regulated gene and protein expression were analyzed with RNAi. RESULTS: When applied 30 minutes before TGF-beta, curcumin dose dependently and dramatically reduced TGF-beta-induced increases in plasminogen activator inhibitor-1 (PAI-1), TGF-beta1, fibronectin (FN) and collagen I (Col I) mRNA, and in PAI-1 and fibronectin protein. Prolonged curcumin treatment (>6 h) significantly reduced TGF-beta receptor type II levels and SMAD2/3 phosphorylation in response to added TGF-beta. Depletion of cellular c-jun levels with a RNAi method mimicked the effects of curcumin on expression of TGF-beta1, FN, and Col I, but not PAI-1. CONCLUSION: Curcumin blocks TGF-beta's profibrotic actions on renal fibroblasts through down-regulation of TbetaRII, and through partial inhibition of c-jun activity. These in vitro data suggest that curcumin might be an effective antifibrotic drug in the treatment of chronic kidney disease.

 

[CCS]

the curcumin also blocks 5ar.

as for the tumeric, it prevents skin cancer somehow. I think it is anti-angiogenic. micheal berry said the same thing about grean tea and says it may stop hairs from returning from telogen.

blood vessels grow up to meet the seedling follicle at the begining of anagen. I know this because I was going to have laser hair removal and I learned about this. I just am not sure this is the same kind of angiogenesis that cancer cells have. maybe different chemicals have differnet effects.

 

[docj077]

So, curcumin and tumeric aren't the same thing? I'm confused. I also found that selenite inhibits TGF-beta.

If it were possible to make a topical that inhibited TGF-beta we'd either have all our hair or have all our hair and be filthy rich.

 

[CCS]

I don't know if they are or are not. I just know I put tumeric root powder on my food. it is an indian spice, and very healthy and prevents skin cancer

 

[docj077]

Hmmm...so, have you noticed anything different about your hair or have you pretty much used that herb your entire life?

Otherwise, the only way this would work is if it's a topical and I have no idea how to do that.

 

[CCS]

if we know it works orally, then grind it up in water and PPG/ethanol, and dissolve what you can, and put it on your head.

might work, might not, but it is worth a try
hopefully we can mix it with other stuff so we don't have 10 different topicals
we just have to look into the herb more.

I have used it on and off, but never more than a month. I got a 4 inch cube of it for $3.50 at an indian food store. techproffesor will tell you all about it I'm sure.

i never noticed a difference. But i'll eat a lot more now. it is said to cure everything, so don't believe stuff unless you see it on pubmed or something.

 

[CCS]

remember all the hype saw palmetto gets for blocking DHT, and what BS that is. it does to a small extent, but not enough to be therapudic. I think pure oleic acid would be stronger. anyway, the herbs we look up online might be just as overhyped. so we need to be able to distinguish between the hype and what is real.

 

[docj077]

Here's what I've found.

Curcumin downregulated the expression of the TGF-beta receptor. This leads to a decreased potential for TGF-beta receptor activiation and the subsequent transcription of the TGF-beta gene within fibroblast cells. It only decreases TGF-betaII receptors and the main mechanism of action besides the decrease in TGF-beta receptors is thought to be caused by a decrease in the transcription factor c-jun and it's inhibition of nuclear factor KB.

30 minute curcumin treatment is required and the effect lasts 24 hours.

At 5.0 umol/L, curcumin reduces TGF-beta receptors by 50%. AT 10 umol/L it reduces them by 70%

What I've typed is the mechanism that is observed in the kidneys during the formation of disease causing fibrosis.

If this were to work in the hair, it would probably require a topical that stayed on for a while to make sure the TGF-beta receptor inhibitory effects were prolonged. Or, it would require extremely careful dosing.


Curcumin blocks multiple sites of the TGF-beta signaling cascade in renal cells.Gaedeke J, Noble NA, Border WA.
Fibrosis Research Laboratory, Division of Nephrology, University of Utah, Salt Lake City, Utah, USA.

BACKGROUND: Over-expression of transforming growth factor-beta (TGF-beta) contributes greatly to fibrotic kidney disease. The activator protein-1 (AP-1) inhibitor curcumin, a polyphenolic compound derived from Curcuma longa, has been shown to reduce collagen accumulation in experimental pulmonary fibrosis. Here, we investigate curcumin's ability to modulate TGF-beta's profibrotic actions in vitro. METHODS: NRK49F rat renal fibroblasts were stimulated with TGF-beta (5 ng/mL), and the effects of curcumin on TGF-beta-regulated genes, TGF-beta receptors, and phosphorylated SMAD isoforms were analyzed by Northern blotting, enzyme-linked immunosorbent assay (ELISA), and Western blotting. The effects of c-jun depletion on TGF-beta-regulated gene and protein expression were analyzed with RNAi. RESULTS: When applied 30 minutes before TGF-beta, curcumin dose dependently and dramatically reduced TGF-beta-induced increases in plasminogen activator inhibitor-1 (PAI-1), TGF-beta1, fibronectin (FN) and collagen I (Col I) mRNA, and in PAI-1 and fibronectin protein. Prolonged curcumin treatment (>6 h) significantly reduced TGF-beta receptor type II levels and SMAD2/3 phosphorylation in response to added TGF-beta. Depletion of cellular c-jun levels with a RNAi method mimicked the effects of curcumin on expression of TGF-beta1, FN, and Col I, but not PAI-1. CONCLUSION: Curcumin blocks TGF-beta's profibrotic actions on renal fibroblasts through down-regulation of TbetaRII, and through partial inhibition of c-jun activity. These in vitro data suggest that curcumin might be an effective antifibrotic drug in the treatment of chronic kidney disease.

 

[docj077]

I found this mentioned somewhere online:

"Turmeric is currently used in the formulation of some sun screens. Turmeric paste is used by Indian women to keep them free of superfluous hair."


However, I've also read that it's used to keep scalp hair healthy.

So, somehow it inhibits the growth of facial hair, but encourages the growth and health of scalp hair.

 

[CCS]

excellent work.

one of the compounds that can stop the next step of the pathway is curcumin, which is very cheap.

I'm still worried about the angiogenesis inhibition. they use it on their face to prevent hairs. And only need to use it 30 minutes a day I guess.

I'd feel a lot better knowing why they think it won't hurt scalp hair. Maybe it is because body hairs not only are deprived of androgens, but also get angiogeneis stopped, whereas the scalp hairs thrive in the abscence of the whole adrogen cascade, including the beta, and this makes up for the angiogenesis problems.

curcumin is very cheap and likely to do something. It would be nice if we knew only a small amount of angiogenesis inhibition would happen, or if we knew of another compound that would do the same good stuff without the same bad stuff, or if we knew that the mechanism for hair cycle angiogenesis is different enough from that of cancer so that the curcumin would not hurt the new hairs.

GTE is cheap and has curcumin in it and a bunch of other stuff that blocks 5ar and even one that blocks androgen receptors.

 

[docj077]

Here's the mechanism.



Curcumin inhibits hypoxia-inducible factor-1 by degrading aryl hydrocarbon receptor nuclear translocator: A mechanism of tumor growth inhibition.Choi H, Chun YS, Kim SW, Kim MS, Park JW.
Seoul National University College of Medicine.

Hypoxia-inducible factor-1 (HIF-1), a transcription factor comprised of HIF-1alpha and ARNT, plays a key role in cell survival and angiogenesis in hypoxic tumors, and many efforts have been made to develop anticancer agents that target HIF-1alpha. However, although ARNT is also required for HIF-1 activity, ARNT has been disregarded as a therapeutic target. Curcumin is a commonly used spice and coloring agent with a variety of beneficial biologic effects, which include tumor inhibition. In the present study, we tested the possibility that curcumin inhibits tumor growth by targeting HIF-1. The effects of curcumin on HIF-1 activity and expression were examined in cancer cell-lines and in xenografted tumors. We found that curcumin inhibits HIF-1 activity, and that this in turn down-regulates genes targeted by HIF-1. Moreover, of the two HIF-1 subunits, only ARNT was found to be destabilized by curcumin in several cancer cell types, and further, ARNT expression rescued HIF-1 repression by curcumin. We also found that curcumin stimulated the proteasomal degradation of ARNT via oxidation and ubiquitination processes. In mice bearing Hep3B hepatoma, curcumin retarded tumor growth and suppressed ARNT, erythropoietin, and vascular endothelial growth factor in tumors. These results suggest that the anticancer activity of curcumin is attributable to HIF-1 inactivation by ARNT degradation.