saw palmetto hinder gains??
- Thread starter *budd_2040
- Start date
simpllyhuge
New member
so what the consescs ? i stopped taking my straterra and i can focus enough to read this lol, can some one sum it up.
Here's a link to a paper written on DHT gel used as HRT:
http://www.endo-society.org/pubrelations/pressReleases/archives/2001/september_jcem.pdf
Blood tests revealed that increasing DHT decreased estrogen and had no negative effect on the prostate. In Europe, DHT gel is actually used to relieve prostate problems. More evidence that estrogen is the cause of prostate problems, not DHT.
I used to take Saw Palmetto all the time....Big mistake....
http://www.endo-society.org/pubrelations/pressReleases/archives/2001/september_jcem.pdf
Blood tests revealed that increasing DHT decreased estrogen and had no negative effect on the prostate. In Europe, DHT gel is actually used to relieve prostate problems. More evidence that estrogen is the cause of prostate problems, not DHT.
I used to take Saw Palmetto all the time....Big mistake....
*budd_2040
New member
bottom line though, regardless of what supposedly dht or estrogen does or doesnt do, saw palmetto is made for the prostate, and other supplements created to help the prostate include SP because of that reason
simpllyhuge
New member
i have had prostatitus for a while now, i started taking saw plametto at about a gram a day for like a week or 2 and my pee stream has improved so much that i can pee with no problem.
*budd_2040 said:
This is not correct. The point I'm trying to make as while drugs like SP or proscar are "made for the prostate", they are counter productive for bodybuilding as well as for the prostate. A lot of doc's and vets in this industry are waking up to the fact that estrogen could be the main cause of prostate problems, not DHT. SP may provide symptom relief, but will do nothing to shrink the prostate and in fact could make matters worse by increasing estrogen.
Another shorter article from T-mag entilted estrogen's dirty little secret.
http://www.t-mag.com/articles/171estro2.html
*budd_2040
New member
i bought some pygeum for my cycle..YOU ALL HAPPY?!?!
There is no problem taking SP before, during or after a cylce. It's effects are very weak at blocking DHT in the testes, and I think it's effects are being grossly overstated here. SP's effects are not enough to hinder gains at all or lower libido to any noticable degree. I use 320mg twice a day and it hasn't hindered my gains in 20 years. Nor have I ever had a problem with libido, especially on.
You're better off using SP and letting your anti-e worry about your E2 levels.
You're better off using SP and letting your anti-e worry about your E2 levels.
hhajdo
Community Veteran
Yes, SP is not a strong 5 alpha reductase inhibitor and would not significantly decrease plasma DHT (some studies show no change)...
It can definitely improve the symptoms of BPH, there are several reported mechanisms of action:
...."Preparations of saw palmetto, or sabal fruit (Serenoa repens, or Sabal serrulata), have been advocated for the symptomatic treatment of mild-to-moderate benign prostatic hyperplasia. Clinically evaluated products contain a liposterolic extract standardized to contain 70 to 95 percent free fatty acids; these preparations also include phytosterols (such as -sitosterol).29 The mechanisms for the reported benefit of saw palmetto in patients with benign prostatic hyperplasia remain to be clarified. Reported in vitro effects include inhibition of 5-reductase isoenzymes, inhibition of the binding of dihydrotestosterone to cytosolic androgen receptors in prostate cells, 1-adrenoceptor antagonism, interference with prolactin-receptor signal transduction, and antiinflammatory activity.29,81 In vivo studies have shown that saw palmetto decreases dihydrotestosterone levels and raises testosterone levels,82 has antiestrogenic activity,83 and increases apoptosis and reduces cell proliferation84 in prostatic tissue from patients with benign prostatic hyperplasia..."
from "Herbal Remedies"
Peter A.G.M. De Smet, Pharm.D., Ph.D
New England Journal of medicine
Volume 347:2046-2056 December 19, 2002
It can definitely improve the symptoms of BPH, there are several reported mechanisms of action:
...."Preparations of saw palmetto, or sabal fruit (Serenoa repens, or Sabal serrulata), have been advocated for the symptomatic treatment of mild-to-moderate benign prostatic hyperplasia. Clinically evaluated products contain a liposterolic extract standardized to contain 70 to 95 percent free fatty acids; these preparations also include phytosterols (such as -sitosterol).29 The mechanisms for the reported benefit of saw palmetto in patients with benign prostatic hyperplasia remain to be clarified. Reported in vitro effects include inhibition of 5-reductase isoenzymes, inhibition of the binding of dihydrotestosterone to cytosolic androgen receptors in prostate cells, 1-adrenoceptor antagonism, interference with prolactin-receptor signal transduction, and antiinflammatory activity.29,81 In vivo studies have shown that saw palmetto decreases dihydrotestosterone levels and raises testosterone levels,82 has antiestrogenic activity,83 and increases apoptosis and reduces cell proliferation84 in prostatic tissue from patients with benign prostatic hyperplasia..."
from "Herbal Remedies"
Peter A.G.M. De Smet, Pharm.D., Ph.D
New England Journal of medicine
Volume 347:2046-2056 December 19, 2002
hhajdo
Community Veteran
5 alpha reductase inhibitors are definitely not counterprodactive for prostate, they are frequently used to treat BPH, there are dozens of studies which show their effectivness...
It is definitely not true that estrogen is the main cause, both estrogens & androgens can cause BPH.
5 ar inhibitors alone can definitely improve BPH symptoms & decrease prostate volume, while aromatase inhibitors alone are not effective:
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.
It is definitely not true that estrogen is the main cause, both estrogens & androgens can cause BPH.
5 ar inhibitors alone can definitely improve BPH symptoms & decrease prostate volume, while aromatase inhibitors alone are not effective:
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.
hhajdo
Community Veteran
TESTinME said:
Here's a quote from that study:
"Plasma estradiol concentrations were un-changed by DHT treatment."
The E decrease is usually proportional to decrease of T, in this study no effect was noticed & you actually posted it as proof that DHT is an aromatase inhibitor ?
DHT can antagonize estrogen action but it seems that it's not a potent aromatase inhibitor in vivo.
Also, this doesn't prove that estrogen is the cause of prostate problems, the reseachers have speculated that DHT treatment didn't promote prostatic growth: "because of its in-ability to exhibit intraprostatic amplification"...
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