EGCG displaces estradiol from the estrogen receptor.

[OverMachoGrande]

[
Why not just take both? Finasteride and Beta-sitosterol are a very potent combination. Also why do you suggest not taking it every day? I take 1000+ mg every day in addition to finasteride with no sexual sides (not recommending this as a starting dosage). High estradiol was the only thing that has ever given me sexual sides. Lower your estradiol with grape seed extract (or ANY aromatase inhibitor) flaxseed/7HMR spruce lignans (enterlactone precursors- enterlactone prevents estrone (good estrogen) from converting to estradiol).



Everyone's endocrine system is different but IMO it's pretty damn hard to have sexual side effects with low estradiol.

Beta sitosterol is shown to drastically decrease serum estradiol too. I believe that estradiol is the real reason for male pattern baldness. Also soy lowers estradiol. I've read that the phytoestrogens in soy and beta-sitosterol itself has a very strong binding affinity to the estrogen/androgen receptor (SHBG).

 

[Bryan]

Beta sitosterol is shown to drastically decrease serum estradiol too.

Do you have a medical reference to support that claim, or is it just another one of your wild-*** theories?

 

[OverMachoGrande]

Do you have a medical reference to support that claim?

beta-Sitosterol, beta-Sitosterol Glucoside, and a Mixture of beta-Sitosterol and beta-Sitosterol Glucoside Modulate the Growth of Estrogen-Responsive Breast Cancer Cells In Vitro and in Ovariectomized Athymic Mice.
Ju YH, Clausen LM, Allred KF, Almada AL, Helferich WG.

Department of Food Science and Human Nutrition, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA. yhju@uiuc.edu

We hypothesized that the phytosterols beta-sitosterol (BSS), beta-sitosterol glucoside (BSSG), and Moducare (MC; BSS:BSSG = 99:1) could modulate the growth of estrogen-dependent human breast cancer cells in vitro and in vivo. The present study evaluated the estrogenic and antiestrogenic effects of BSS, BSSG, and MC (0.001 to 150 micromol/L) on the proliferation of Michigan Cancer Foundation 7 (MCF-7) cells in vitro. Both BSS (>1 micromol/L) and MC (>50 micromol/L) increased MCF-7 cell proliferation. Treatment with 150 micro mol/L of BSS and MC increased cell growth by 2.4 and 1.5 times, respectively, compared to the negative control (NC) group. However, BSSG had no effect at the concentrations tested. The effects of dietary BSS, BSSG, and MC on the growth of MCF-7 cells implanted in ovariectomized athymic mice were also evaluated. Estrogenic effects of the phytosterols were evaluated in the NC, BSS, BSSG, and MC treatment groups, and antiestrogenic effects were evaluated in the 17 beta-estradiol (E(2)), E(2) + BSS, E(2) + BSSG, and E(2) + MC treatment groups. Mice were treated with dietary BSS (9.8 g/kg AIN93G diet), BSSG (0.2 g/kg diet), or MC (10.0 g/kg diet) for 11 wk. Dietary BSS, BSSG, and MC did not stimulate MCF-7 tumor growth. However, dietary BSS, BSSG, and MC reduced E(2)-induced MCF-7 tumor growth by 38.9% (P < 0.05), 31.6% (P = 0.08), and 42.13% (P < 0.05), respectively. The dietary phytosterols lowered serum E(2) levels by 35.1, 30.2, and 36.5% in the E(2) + BSS, E(2) + BSSG, and E(2) + MC groups, respectively (P < 0.05), compared to that of the E(2) treatment group. Estrogen-responsive pS2 mRNA expression in tumors did not differ among groups, but expression of the antiapoptotic marker B-cell lymphoma/leukemia-2 (bcl-2) in tumors from the E(2) + MC group was downregulated, compared to that of the E(2) treatment group. In summary, BSS and MC stimulated MCF-7 cell growth in vitro. Although BSSG comprises only 1% of MC, BSSG made MC less estrogenic than BSS alone in vitro. However, dietary BSS and MC protected against E(2)-stimulated MCF-7 tumor growth and lowered circulating E(2) levels.

Autors: Young H. Ju, Laura M. Clausen, Kimberly F. Allred, Anthony L. Almada and William G. Helferich

Research Institute: Department of Food Science and Human Nutrition and Department of Animal Sciences, University of Illinois at Urbana-Champaign, Urbana (USA), Department of Physiology, University of Kentucky, Lexington (USA) and IMAGINutrition and MetaResponse Science, Laguna Niguel (USA)

Publication: Journal of Nutrition, 2004, 134:1145-1151

There are many plant sterols but the best known are beta-sitosterol, stigmasterol and campesterol. Plant sterols have many claimed health benefits. Studies show that plant sterols have a weak estrogenic effect and that they act as weak agonist for estrogen receptors. Plant sterols have a structure similar to that of cholesterol. Plant sterols can modulate the immune system and can replace cholesterol in the intestinal micelles, thereby reducing cholesterol absorption. Epidemiological studies also show that consumption of plant sterols reduces the risk of cancer of colon, prostate, ovary, stomach and breast.

The aim of this study was to investigate the estrogenic effects of the plant sterols beta-sitosterol, beta-sitosterol glucoside and Moducare (mixture of beta-sitosterol, beta-sitosterol glucoside). The test was carried out on estrogen dependent (this means that estrogen stimulates cancer growth) human breast cancer cells in vitro and in vivo.

First the effect of the plant sterols was determined in vitro on cancer cells. Only beta-sitosterol and Moducare increased cell growth. In the second test, the cancer cells were implanted in ovariectomized athymic mice and the estrogenic and anti-estrogenic effects of the plant sterols were determined. Dietary beta-sitosterol, beta-sitosterol glucoside and Moducare did not influence tumor growth, but they markedly reduced estradiol induced tumor growth and also reduced serum estradiol levels.[/color] The expression of the antiapoptotic marker B-cell lymphoma/leukaemia in tumours was downregulated.

The researchers concluded that beta-sitosterol and Moducare stimulated cancer cells in vitro and that dietary beta-sitosterol and Moducare protected against estrogen stimulated tumor growth. These findings suggest that beta-sitosterol could have potential benefits for women with a risk for estrogen-dependent breast cancer. However more studies are required to investigate the short and long term effects of plant sterols, their interactions with other drugs and their possible use as dietary supplements.

 

[Bryan]

In other words, you don't have any human studies to back that claim.

 

[baller234]

[
Why not just take both? Finasteride and Beta-sitosterol are a very potent combination. Also why do you suggest not taking it every day? I take 1000+ mg every day in addition to finasteride with no sexual sides (not recommending this as a starting dosage). High estradiol was the only thing that has ever given me sexual sides. Lower your estradiol with grape seed extract (or ANY aromatase inhibitor) flaxseed/7HMR spruce lignans (enterlactone precursors- enterlactone prevents estrone (good estrogen) from converting to estradiol).



Everyone's endocrine system is different but IMO it's pretty damn hard to have sexual side effects with low estradiol.

Beta sitosterol is shown to drastically decrease serum estradiol too. I believe that estradiol is the real reason for male pattern baldness. Also soy lowers estradiol. I've read that the phytoestrogens in soy and beta-sitosterol itself has a very strong binding affinity to the estrogen/androgen receptor (SHBG).

Well I have to disagree with you on this. Estradiol does not cause male pattern baldness (I'm basing this on my own personal experiences which I will get to.) I advocate lowering estradiol for overall well being, not hair growth. I think the main reason people get side effects on finasteride is because it increases estradiol. The only sexual side effect resulting from less DHT would be less nitric oxide production which can be easily remedied.

Alright now I'll tell you why DHT and not estradiol is the main driving force in male pattern baldness (at least in my case...). In the past I have taken very potent aromatase inhibitors (letrozole) to get rid of pubertal gyno. Letrozole has been shown to reduce estrogen by 98% so my estradiol would have been nonexistant. Well with the aromatase enzyme almost completely suppressed, alot more testosterone ends up converting to DHT via the 5ar enzyme. Needless to say I receded quite quickly during this time (this was actually when I became "aware" of my hair loss although i suspect it had been going on for some time albeit very slowly.)

However, while on high doses of Finasteride (5 mg) and Spironolacone (250 mg) my estradiol was undoubtedly quite high (I had painful breast growth). But guess what? I had great temple and hair line regrowth. So yes estradiol is not beneficial for a male's overall sense of well being but it IS beneficial for scalp hair and not just estradiol but all estrogens. Estriol and estrone are actually considered good estrogens and are beneficial for male health in addition to being beneficial for scalp hair.

 

[LewdBear]

In other words, you don't have any human studies to back that claim.

It's weird how his standards of evidence change when he's trying to support his own claims.

Mouse studies are good enough to support that claim that beta-sitosterol causes a "drastically decrease serum estradiol".

But beneficial effects of estradiol on Androgenetic Alopecia require human systemic studies. Because, you know, topical preparations must work differently for reasons unknown because they might be like ketoconazole or something.:jackit:

 

[OverMachoGrande]

It's weird how his standards of evidence change when he's trying to support his own claims.

Mouse studies are good enough to support that claim that beta-sitosterol causes a "drastically decrease serum estradiol".

I agree.

But beneficial effects of estradiol on Androgenetic Alopecia require human systemic studies. Because, you know, topical preparations must work differently for reasons unknown because they might be like ketoconazole or something.

It is interesting to note that ketoconazole is shown to displace estradiol from the estrogen receptor (SHBG).

 

[Bryan]

In other words, you don't have any human studies to back that claim.

It's weird how his standards of evidence change when he's trying to support his own claims.

How have my standards of evidence changed? Can you give me an example of that?

Mouse studies are good enough to support that claim that beta-sitosterol causes a "drastically decrease serum estradiol".

But beneficial effects of estradiol on Androgenetic Alopecia require human systemic studies. Because, you know, topical preparations must work differently for reasons unknown because they might be like ketoconazole or something.:jackit:

I have no idea what you're talking about here, or what point you're trying to make. Please explain.

 

[LewdBear]

How have my standards of evidence changed? Can you give me an example of that?

Not you; misterE.

I have no idea what you're talking about here, or what point you're trying to make. Please explain.

It was a reference to the other thread where he was asking for proof that estradiol had positive outcomes on hair growth in vivo.

From http://www.hairlosstalk.com/interact/viewtopic.php?f=11&t=57333&start=70 :

"I want to see some studies showing that 16-hydroxyestrogen and estradiol (very potent estrogens) stimulate human head hair growth in vivo; in the living body."

"You say topical... not systematic... If ketoconazole was systematic ,I would not be a strong advocate of ketoconalole!"

So in one case, only "human head hair growth" through systemic estradiol was acceptable evidence, but in contrast, rodent studies seem to be sufficient in this thread.

I still want to know why the German FPB topical estradiol studies weren't acceptable as evidence. It was never really answered, he just started talking about ketoconazole.

 

[Bryan]

Okay, thanks for the explanation, LewdBear. I thought you were talking about me, not misterE. After going back and re-reading your other post in the proper context, it now makes sense to me.

 

[Hoppi]

hehe people argue with misterE just like they argue with me! hehe ^_^


sorry I'm just playing, I'll get better stuck into this thread in a minute I think

 

[CCS]

I found this thread with a google search.

Bryan, I believe OP's research, but not his conclusions or explanations.

Yes, estrogen and finasteride would increase the number of androgen receptors. But that is not bad. It just shows the androgen receptors are not getting the androgens they are used to getting, and are trying to get more.

Same with Soy decreasing estrogen. The body senses it has more estrogen, so it makes less. That does not mean that the total estrogenic activity has decreased. Probably it increased.

...

Now are we sure that beta sis stimulates the estrogen receptor and blocks the androgen receptor? I'd like to see the studies for that. Depending on how they measured it, it might just do one of those but appear to do both.

I think estrogen is good for hair.

As for old men, just because their serum testosterone levels drop off does not mean their follicle DHT levels drop off. Every cell in the body is different. It takes castration DHT levels to overpower follicle 5ar2.

 

[CCS]

Is SHBG, and the androgen receptor, and the estrogen receptor, the same thing?

If keto displaces estrogen, that might not be a bad thing as long as the keto gives an estrogenic signal.

Have you guys considered topical beta sis?

Estrogen is not bad for general health. It is just bad when levels are too high in certain tissues, like breast tissue. Estrogen is great for building muscle and keeping tendons flexible.

Instead of consuming beta sis pills, why not grind them up and dissolve them in alcohol and pg and water and put it on your head?

Non-prescription, and maybe cheap, so you can make up for quality with quantity. The only possible problem is if it keeps longer binding estrogen from binding, and then is metabolized a few hours later, leaving the recepter open to DHT.

I'd still put egcg and beta sis in my shampoo. Maybe also some spironolactone pills.