The "Big Three" Diseases Associated With M.P.B.

[OverMachoGrande]

The "Big Three" diseases associated with M.P.B. are: atherosclerosis/heart disease, B.P.H. /prostate cancer and insulin resistance/diabetes.

Now, when I think of the human heart, I try and choose a hormone associated with a healthy, strong, "athletic" type heart...I instantly think of testosterone; the hormone that keep you athletically inclined. Studies have shown that when L.D.L cholesterol is high, testosterone is low. Studies have also shown that vertex balding is a biological marker for atherosclerosis.

When I think of B.P.H. I think of estradiol, which is shown to play a huge role in the development of prostate enlargement (along with IGF-1). Estrogen also depresses testosterone and Human Growth Hormone, which can kill your physical endurance, personal confidence and sexual performance!

When I think of insulin resistance I think obviously of insulin and insulin-like growth factor 1. When levels of Insulin and "free"IGF-1 are high, S.H.B.G. is low and when that's low your sex hormones become unbalanced. "Free"IGF-1 has been shown to cause vertex balding.

Controlling these four hormones/proteins (Total testosterone {High}, "free" estradiol {Low}, "free" IGF-1 {Low} and S.H.B.G. {High}) is the key to M.P.B. in my honest opinion.

Q. "Well, how do I "control" these hormones?"

A. "By avoiding the risks and causes of the three diseases, which are atherosclerosis, insulin resistance, and prostate enlargement, one simple step would to remove dairy out of your diet because it itself could be a major contributor to all thee diseases. ‘Better be safe than sorry.’ My mom always told me.â€￾

 

[Bryan]

When I think of B.P.H. I think of estradiol, which is shown to play a huge role in the development of prostate enlargement...

See the study below (I've already cited it for you a number of times) which found that reducing estrogen with an aromatase inhibitor had no effect on BPH, compared to placebo:

Prostate. 1996 Oct;29(4):199-208. "Estrogen reduction by aromatase inhibition for benign prostatic hyperplasia: results of a double-blind, placebo-controlled, randomized clinical trial using two doses of the aromatase-inhibitor atamestane." Atamestane Study Group.
Radlmaier A, Eickenberg HU, Fletcher MS, Fourcade RO, Reis Santos JM, van Aubel OG, Bono AV.
Department of Clinical Development Oncology, Schering AG, Berlin, Germany.

BACKGROUND: The concept of estrogen withdrawal by an aromatase inhibitor in the treatment of benign prostatic hyperplasia (BPH) was assessed in a prospective, randomized, double-blind, placebo-controlled multicenter trial. METHODS: Two hundred and ninety-two patients with clinical symptoms of BPH were randomly allocated to one of the following treatments for 48 weeks: placebo or the selective aromatase inhibitor, atamestane, at a daily dose of 100 mg or 300 mg. Both doses of atamestane significantly reduced serum concentrations of estradiol and estrone, and produced a slight, dose-dependent, counter-regulatory increase in peripheral androgen concentration. RESULTS: Clinical symptoms improved during treatment in all three groups. Even after 48 weeks, the effect of active treatment did not exceed the effect seen with placebo. Overall tolerance of 100 mg atamestane was excellent, but 300 mg showed a slightly increased incidence of side effects compared with placebo. CONCLUSIONS: The conclusion from this study is that the reduction in estrogen concentration using the selective aromatase inhibitor atamestane has no effect on clinically established BPH.

 

[OverMachoGrande]

Prostate. 2008 Apr 1;68(5):508-16.
The proliferative effect of estradiol on human prostate stromal cells is mediated through activation of ERK.

Zhang Z, Duan L, Du X, Ma H, Park I, Lee C, Zhang J, Shi J.
Department of Biochemistry and Molecular Biology, College of Life Sciences, Nankai University, Tianjin, China.

BACKGROUND: Estrogen is involved in the development and progression of benign prostatic hyperplasia (BPH). It can stimulate proliferation of prostate stromal cells (PrSCs). However, the exact mechanism remains unclear. METHODS: We used the primary cultured human PrSCs and a prostate stromal cell line, WPMY-1, to examine the signaling pathways involved in estrogen-mediated proliferation of PrSCs. Cells were treated with 17beta-estradiol (E(2)) or BSA-E(2). Cell proliferation was assessed by the MTT assay and by cell counting. Western blot analysis was used to determine the status of activation of ERK1/2. RESULTS: Results indicated that both E(2) and BSA-E(2) stimulated proliferation of primary PrSCs and WPMY-1 cells. ERK was rapidly activated by E(2) and BSA-E(2). PD98059, which is a selective ERK inhibitor, significantly inhibited estrogen-induced cell proliferation. PrSCs expressed estrogen receptor alpha (ERalpha) and GPR30 but not ERbeta. Small hairpin RNA (shRNA) to ERalpha, but not to GPR30, blocked estrogen-mediated ERK activation and cell proliferation. CONCLUSIONS: The results indicated that estrogen could activate ERK pathway through the non-genomic ERalpha pathway, leading to proliferation of PrSCs. Prostate 68: 508-516, 2008. (c) 2008 Wiley-Liss, Inc.

 

[OverMachoGrande]

Estradiol Activates the Prostate Androgen Receptor and Prostate-specific Antigen Secretion through the Intermediacy of Sex Hormone-binding Globulin


Atif M. Nakhla, Nicholas A. Romas and William Rosner.

Abstract

These experiments were designed to examine the relationship between the effects of steroid hormones mediated by classic intracellular steroid hormone receptors and those mediated by a signaling system subserved at the plasma membrane by a receptor for sex hormone-binding globulin. It is known that unliganded sex hormone-binding globulin (SHBG) binds to a receptor (RSHBG) on prostate membranes. The RSHBG·SHBG complex is rapidly activated by estradiol to stimulate adenylate cyclase, with a resultant increase in intracellular cAMP. In this paper we examine the effect of this system on a prostate gene product known to be activated by androgens, prostate-specific antigen. In serum-free organ culture of human prostates, dihydrotestosterone caused an increase in prostate specific antigen secretion. This event was blocked by the anti-androgens cyproterone acetate and hydroxyflutamide. In the absence of androgens, estradiol added to prostate tissue, whose RSHBG was occupied by SHBG, reproduced the results seen with dihydrotestosterone. Neither estradiol alone nor SHBG alone duplicated these effects. The estradiol·SHBG-induced increase in prostate-specific antigen was not blocked by anti-estrogens, but was blocked both by anti-androgens and a steroid (2-methoxyestradiol) that prevents the binding of estradiol to SHBG. Furthermore, an inhibitor of protein kinase A prevented the estradiol·SHBG-induced increase in prostate-specific antigen but not that which followed dihydrotestosterone. These data indicate that there is a signaling system that amalgamates steroid-initiated intracellular events with steroid-dependent occurrences generated at the cell membrane and that the latter signaling system proceeds by a pathway that involves protein kinase A.

 

[OverMachoGrande]

...

 

[moxsom]

"Free"IGF-1 has been shown to cause vertex balding.

How many times do I have to explain cause and correlation to you? They are NOT the same thing.

Not to mention this thread is filled with assumptions. What is your background anyway? Do you have any experience in research?

 

[Hoppi]

I like some of your points but yes some do seem a little hazy. I dunno I like your general approach a lot though, it's really nice to see someone on here expressing some view, ANY view other than "Take finasteride Take finasteride Take finasteride Take finasteride!!" lol

It's great to look at the whole picture as well, and try to understand what, helps and doesn't help in the body, genetics aside.

It's quite funny really when you consider how much is backed up by stuff like this: http://en.wikipedia.org/wiki/Baldness_t ... _lifestyle and probably on "real" encyclopedias and whatever too but I don't feel I need to prove anything to anyone

But yeah, a good thread in principal but some more scientific citation would go down a treat

Also, I know you seem passionate about people being vegan but, I can't believe that's the only way to do this, surely people can have some meat and dairy in their diets and still be ok? There are other things to watch out for, surely?

 

[Shma]

Bryan always seems to rely on certain studies, even if there are ones about the same subject proving him wrong (except of the topical finasteride thing). And when those studies are shown, he simply doesn't post anything in those threads anymore. happens all the time.

but what the hell, we can't force him to post, right?

 

[OverMachoGrande]

Bryan always seems to rely on certain studies, even if there are ones about the same subject proving him wrong (except of the topical finasteride thing). And when those studies are shown, he simply doesn't post anything in those threads anymore. happens all the time.

Indeed. I believe that Brayn knows the "truth" about male pattern baldness...but keeps it secret for some reason. He seems to stay away from the S.H.B.G. topic and is also present on various acne web-sites.

 

[Bryan]

Bryan always seems to rely on certain studies, even if there are ones about the same subject proving him wrong (except of the topical finasteride thing). And when those studies are shown, he simply doesn't post anything in those threads anymore. happens all the time.

Really? Give me some examples of where I did that (should be very easy, if it "happens all the time"). I await your response with great interest.

 

[OverMachoGrande]

Bryan always seems to rely on certain studies, even if there are ones about the same subject proving him wrong (except of the topical finasteride thing). And when those studies are shown, he simply doesn't post anything in those threads anymore. happens all the time.

Really? Give me some examples of where I did that (should be very easy, if it "happens all the time"). I await your response with great interest.

I'll post one for Shma...what do you have to say about this Brayn?

Estradiol Activates the Prostate Androgen Receptor and Prostate-specific Antigen Secretion through the Intermediacy of Sex Hormone-binding Globulin


Atif M. Nakhla, Nicholas A. Romas and William Rosner.

Abstract

These experiments were designed to examine the relationship between the effects of steroid hormones mediated by classic intracellular steroid hormone receptors and those mediated by a signaling system subserved at the plasma membrane by a receptor for sex hormone-binding globulin. It is known that unliganded sex hormone-binding globulin (SHBG) binds to a receptor (RSHBG) on prostate membranes. The RSHBG·SHBG complex is rapidly activated by estradiol to stimulate adenylate cyclase, with a resultant increase in intracellular cAMP. In this paper we examine the effect of this system on a prostate gene product known to be activated by androgens, prostate-specific antigen. In serum-free organ culture of human prostates, dihydrotestosterone caused an increase in prostate specific antigen secretion. This event was blocked by the anti-androgens cyproterone acetate and hydroxyflutamide. In the absence of androgens, estradiol added to prostate tissue, whose RSHBG was occupied by SHBG, reproduced the results seen with dihydrotestosterone. Neither estradiol alone nor SHBG alone duplicated these effects. The estradiol·SHBG-induced increase in prostate-specific antigen was not blocked by anti-estrogens, but was blocked both by anti-androgens and a steroid (2-methoxyestradiol) that prevents the binding of estradiol to SHBG. Furthermore, an inhibitor of protein kinase A prevented the estradiol·SHBG-induced increase in prostate-specific antigen but not that which followed dihydrotestosterone. These data indicate that there is a signaling system that amalgamates steroid-initiated intracellular events with steroid-dependent occurrences generated at the cell membrane and that the latter signaling system proceeds by a pathway that involves protein kinase A.

http://www.jbc.org/content/272/11/6838.abstract

See the study below (I've already cited it for you a number of times) which found that reducing estrogen with an aromatase inhibitor had no effect on BPH, compared to placebo:

Prostate. 1996 Oct;29(4):199-208. "Estrogen reduction by aromatase inhibition for benign prostatic hyperplasia: results of a double-blind, placebo-controlled, randomized clinical trial using two doses of the aromatase-inhibitor atamestane." Atamestane Study Group.
Radlmaier A, Eickenberg HU, Fletcher MS, Fourcade RO, Reis Santos JM, van Aubel OG, Bono AV.
Department of Clinical Development Oncology, Schering AG, Berlin, Germany.

BACKGROUND: The concept of estrogen withdrawal by an aromatase inhibitor in the treatment of benign prostatic hyperplasia (BPH) was assessed in a prospective, randomized, double-blind, placebo-controlled multicenter trial. METHODS: Two hundred and ninety-two patients with clinical symptoms of BPH were randomly allocated to one of the following treatments for 48 weeks: placebo or the selective aromatase inhibitor, atamestane, at a daily dose of 100 mg or 300 mg. Both doses of atamestane significantly reduced serum concentrations of estradiol and estrone, and produced a slight, dose-dependent, counter-regulatory increase in peripheral androgen concentration. RESULTS: Clinical symptoms improved during treatment in all three groups. Even after 48 weeks, the effect of active treatment did not exceed the effect seen with placebo. Overall tolerance of 100 mg atamestane was excellent, but 300 mg showed a slightly increased incidence of side effects compared with placebo. CONCLUSIONS: The conclusion from this study is that the reduction in estrogen concentration using the selective aromatase inhibitor atamestane has no effect on clinically established BPH.

Does the study I posted above change your mind about estrogen? And if it doesn't please explain why in great detail.

 

[Bryan]

Does the study I posted above change your mind about estrogen?

No. Why would it? Does the study _I_ posted above change YOUR mind about estrogen?

Frankly, I don't think you have the wit to understand the important differences between those two studies.

 

[OverMachoGrande]

The study I posted showed that when estradiol binds with sex hormone binding globulin, it has the same effects as D.H.T., and that even thou an estrogen was causing a D.H.T. like effect, its effects were not inhibited by an anti-aromatse drug, but with an anti-androgen (like propecia) or an estrogen metabolite call 2-methoxyestradiol.

This study clearly shows that estradiol is the true culprit in prostate enlargement. And since prostate enlargement is associated with male pattern baldness, maybe estradiol is the true culprit in that as well.

How do like them apples?

 

[Bryan]

The study I posted showed that when estradiol binds with sex hormone binding globulin, it has the same effects as D.H.T.

ONLY IN PROSTATE CELLS, dumbbell!

and that even thou an estrogen was causing a D.H.T. like effect, its effects were not inhibited by an anti-aromatse drug, but with an anti-androgen (like propecia) or an estrogen metabolite call 2-methoxyestradiol.

They didn't say "anti-aromatase drug", dumbbell, they said ANTI-ESTROGEN. Don't you understand the difference between those two concepts?? Jesus Christ...

Giving an aromatase inhibitor will REDUCE or ELIMINATE the presence of estrogen; and doing that had no effect on BPH in the study I've posted for you numerous times. Estrogen can't have a "DHT-like effect" IF THERE IS NO ESTROGEN IN THE FIRST PLACE, dumbbell!

This study clearly shows that estradiol is the true culprit in prostate enlargement. And since prostate enlargement is associated with male pattern baldness, maybe estradiol is the true culprit in that as well.

You are so dumb and insipid, I can't believe it.

 

[OverMachoGrande]

Why so defensive...is this a sensitive subject for ya?

WHAT ABOUT THE ESTRADIOL STUCK TO SEX HORMONE BINDING GLOBULIN...DUMBBELL!

WHY DOES SEX HORMONE BINDING GLOBULIN HAVE A RECEPTOR...ANSWER ME THAT...DUMBBELL!

 

[OverMachoGrande]

Giving an aromatase inhibitor will REDUCE or ELIMINATE the presence of estrogen;

Not if estrogen is stuck to S.H.B.G.

An aromatase inhibitor just prevents "free" testosterone from converting to estrogen. It doesn't have any effect on estrogen that is already bound to S.H.B.G. that is why an aromatase inhibitor doesn't help B.P.H. or hairloss...but I suspect a estrogen receptor antagonist does!

 

[Bryan]

WHAT ABOUT THE ESTRADIOL STUCK TO SEX HORMONE BINDING GLOBULIN...DUMBBELL!

WHY DOES SEX HORMONE BINDING GLOBULIN HAVE A RECEPTOR...ANSWER ME THAT...DUMBBELL!

That happens ONLY IN THE PROSTATE, stupid! Why did you ignore the good advice I gave you earlier today in that other thread about SHBG and estrogen in the prostate?? Here it is again for you. READ IT, this time:

Rather than indulge in your usual flights of fancy, I suggest you try to prove (or at least find evidence) that it happens that way, in both sebaceous gland cells and hair follicle cells.

 

[treeshrew]

Bryan, don't feed the trolls. It's not worth your time.

Hey, misterE, no one cares about your studies.

I just did a study that proves propecia stops hair loss. You can come examine me if you want proof!

 

[OverMachoGrande]

Brayn, you didn't answer my question about the S.H.B.G.-receptor!

Why does S.H.B.G. have a receptor?
Surely you know...so tell me.

 

[Bryan]

Giving an aromatase inhibitor will REDUCE or ELIMINATE the presence of estrogen;

Not if estrogen is stuck to S.H.B.G.

An aromatase inhibitor just prevents "free" testosterone from converting to estrogen. It doesn't have any effect on estrogen that is already bound to S.H.B.G. that is why an aromatase inhibitor doesn't help B.P.H. or hairloss...

LOL!! Is THAT the best you can do, to try to explain why reducing estrogen for YEARS with an aromatase inhibitor doesn't affect BPH or hairloss?