Saw palmetto vs Testosterone

I know this is off topic, but I figure the ppl here know an awful lot
about testosterone.

If steroids reduce the body's own production of testosterone, will saw
palmetto increase it? If SP is blocking DHT will the body try to achieve
homeostasis by increasing testosterone production?

On Mon, 30 Oct 2006 20:09:08 GMT, eponymous cowherd <no@spam4me.com>
wrote:

>
>I know this is off topic, but I figure the ppl here know an awful lot
>about testosterone.
>
>If steroids reduce the body's own production of testosterone, will saw
>palmetto increase it? If SP is blocking DHT will the body try to achieve
>homeostasis by increasing testosterone production?

Two words: Tribulus Terrestris

BLink
--------------------------
"The worst thing about censorship is [redacted]"

Brian Link wrote:
> On Mon, 30 Oct 2006 20:09:08 GMT, eponymous cowherd <no@spam4me.com>
> wrote:
>
> >
> >I know this is off topic, but I figure the ppl here know an awful lot
> >about testosterone.
> >
> >If steroids reduce the body's own production of testosterone, will saw
> >palmetto increase it? If SP is blocking DHT will the body try to achieve
> >homeostasis by increasing testosterone production?
>
> Two words: Tribulus Terrestris
>
> BLink
> --------------------------
> "The worst thing about censorship is [redacted]"

Two words (for both)

"wasted money".

Brian, please show peer reviewed research to back your claim (implied)
that Tribulus Terrestris will boost test production. Hint: Muskley
Foulness ain't a peer reviewed journal.

In article <no-742B17.12090930102006@news.verizon.net>,
eponymous cowherd <no@spam4me.com> wrote:

> I know this is off topic, but I figure the ppl here know an awful lot
> about testosterone.
>
> If steroids reduce the body's own production of testosterone, will saw
> palmetto increase it? If SP is blocking DHT will the body try to achieve
> homeostasis by increasing testosterone production?

Saw palmetto does not block DHT, it (maybe) blocks 5-ar which prevents T
-> DHT. So, yes, it (maybe) increases T (and estrogen), but at the
expense of DHT. Your body may eventually decrease T production via
feedback, but I'm not sure this has been proven.

There's a study in dogs where they administered a 5-ar inhibitor and
antiaromatase and T when up 15 times or something (don't quote me, but
it went way up).

I say it's maybe a 5-ar inhibitor because there are some studies that
suggest that, but there are also studies showing it does nothing.
Specifically there's a study comparing it to finasteride showing saw
palmetto had no effect.

In article <nospam-B3A96C.20012430102006@newsclstr02.news.prodigy.com >,
Mary Brown <nospam@nospam.com> wrote:

> In article <no-742B17.12090930102006@news.verizon.net>,
> eponymous cowherd <no@spam4me.com> wrote:
>
> > I know this is off topic, but I figure the ppl here know an awful lot
> > about testosterone.
> >
> > If steroids reduce the body's own production of testosterone, will saw
> > palmetto increase it? If SP is blocking DHT will the body try to achieve
> > homeostasis by increasing testosterone production?
>
> Saw palmetto does not block DHT, it (maybe) blocks 5-ar which prevents T
> -> DHT. So, yes, it (maybe) increases T (and estrogen), but at the
> expense of DHT. Your body may eventually decrease T production via
> feedback, but I'm not sure this has been proven.
>
> There's a study in dogs where they administered a 5-ar inhibitor and
> antiaromatase and T when up 15 times or something (don't quote me, but
> it went way up).
>
> I say it's maybe a 5-ar inhibitor because there are some studies that
> suggest that, but there are also studies showing it does nothing.
> Specifically there's a study comparing it to finasteride showing saw
> palmetto had no effect.

T didn't increase 15 times, but 3 to 10 times.

Effect of dual inhibition of 5-alpha-reductase and aromatase on
spontaneously developed canine prostatic hypertrophy.

Suzuki K, Okazaki H, Ono Y, Kurokawa K, Suzuki T, Onuma E,Takanashi H,
Mamiya Y, Yamanaka H.
Prostate. 1998 Oct 1;37(2):70-6.*
Department of Urology, Gunma University School of Medicine, Maebashi,
Japan.

BACKGROUND: Our aim was to assess the effect of dual inhibition of
5-alpha-reductase and aromatase on prostate glands. METHODS: We
investigated the morphological changes in the prostate gland and the
changes in the hormonal environment after administration of finasteride
and arimidex to intact canine specimens. The study consisted of four
groups: a 5-alpha-reductase only group (5RI only, n = 5); a 5RI plus
aromatase-inhibitor combination group (5RI + ARI combination, n = 5); a
BPH control group (n = 3); and a castration control group (n = 3).
Finasteride (1 mg/kg/day) and the same dose of arimidex were orally
administered for 80 days. RESULTS: In the 5RI group, a significant
decrease in the serum dihydrotestosterone (DHT) level was found, and
prostatic volume was significantly decreased. However, significant
increases in serum testosterone (T) and DHT levels were observed, with a
concomitant increase in prostatic volume in the 5RI + ARI combination
group. Morphometric analysis showed that histopathological findings in
the 5RI + ARI combination group were similar to those in the BPH control
group. CONCLUSIONS: Dual inhibition of 5-alpha-reductase and aromatase
resulted in a significant increase in prostate volume, accompanied by a
3-10-fold increase in serum testosterone levels and a significant
increase in testicular volume.
http://pmid.us/9759700

"eponymous cowherd" <no@spam4me.com> schreef:

> I know this is off topic, but I figure the ppl here know an awful lot
> about testosterone.

What a weird assumption.

Just because we play with weights you figure we are a bunch of juice heads
?!?!?!

> If steroids reduce the body's own production of testosterone, will saw
> palmetto increase it?

Not really.

> If SP is blocking DHT will the body try to achieve
> homeostasis by increasing testosterone production?

Probably not. Even with finasteride production doesnt go up. There is
probably a higher THT ratio.
But thats not always a good thing. Many people who used a gram of test
together with finasteride will not do that for a second time.

Even if you have a tiny bit more T, gains will probaly be less.

----
Pete

"Mary Brown" <nospam@nospam.com> schreef:

> Saw palmetto does not block DHT...

It probably does.
Together with inhibtion of the 5-AR enzyme.

> it (maybe) blocks 5-ar...

Really?
To which receptor does the 5-AR bind again?

----
Pete

In article <no-742B17.12090930102006@news.verizon.net>, eponymous cowherd
<no@spam4me.com> wrote:

> I know this is off topic, but I figure the ppl here know an awful lot
> about testosterone.
>
> If steroids reduce the body's own production of testosterone, will saw
> palmetto increase it?

No.

>If SP is blocking DHT

That's far from proven in the manner you are thinking.


> will the body try to achieve
> homeostasis by increasing testosterone production?

No, though proscar will do that. It increases T by approx 15% in some
studies, which is not physiologically worthwhile really. SP appears to be
useful for BPH, and thats about it, and the machanism is more complex then
simple DHT blocking.

In article <rf6dk2l94f1148cbanie33i8v2i378d8ab@4ax.com>, Brian Link
<blink@visi.com> wrote:

> On Mon, 30 Oct 2006 20:09:08 GMT, eponymous cowherd <no@spam4me.com>
> wrote:
>
> >
> >I know this is off topic, but I figure the ppl here know an awful lot
> >about testosterone.
> >
> >If steroids reduce the body's own production of testosterone, will saw
> >palmetto increase it? If SP is blocking DHT will the body try to achieve
> >homeostasis by increasing testosterone production?
>
> Two words: Tribulus Terrestris

One word: worthless.

"Mary Brown" <nospam@nospam.com> schreef:

> Effect of dual inhibition of 5-alpha-reductase and aromatase on
> spontaneously developed canine prostatic hypertrophy.

> Suzuki K, Okazaki H, Ono Y, Kurokawa K, Suzuki T, Onuma E,Takanashi H,
> Mamiya Y, Yamanaka H.
> Prostate. 1998 Oct 1;37(2):70-6.
> Department of Urology, Gunma University School of Medicine, Maebashi,
> Japan.

Saw palmetto's primary therapeutic action is to inhibit 5-alpha reductase in
forming DHT and to a lesser extent, 3-alpha reductase, and to block the
action of DHT to receptors on prostate cells via 3-ketosteroid reductase.
Research has also shown an anti-inflammatory[5] and antiestrogenic[3, 6,7]
effect of Serenoa Repens. Use of saw palmetto in >patients with BPH results
in reduction in the size of the prostate.[5 ] With finasteride, however,
studies have shown that 6 to 12 months of >treatment with 5 mg of
finasteride daily can reduce prostate volume, DHT, and prostate-specific
antigen (PSA) levels by 50 percent.[8] Therefore, any patient placed on
finasteride must have a baseline PSA and digital rectal examination.The
mechanism of action mimics the pharmacologic action of finasteride, which
has recently been documented to be of little physiologic value compared with
a placebo or alpha blockers.[9] The purified extract of saw palmetto
contains 85% to 95% fatty acids and sterols. Unfortunately, there are many
forms of this extract on the market, containing additives and many
combinations of other herbs, vitamins, and minerals. Consequently the
consumer does not know exactly what he is purchasing. Saw palmetto has been
used in Europe for more than 20 years. Research there, however, has included
clinical studies showing its clinical urologic effects versus a placebo.
[10] Only one study measured the PSA levels prematurely after 3months "the
treatment did not significantly alter PSA concentrations in these
patients."[13] However 5-alpha reductase inhibitors will reduce the PSA
levels by average of 50% after 6-12 months of use, invalidating this study
on PSA. Consequently of most significance is the lack of well planned "long
term clinical studies" concerning the effects of saw palmetto on "lowering
the PSA" levels after 6-12 months! Any interference with PSA makes this test
useless as a diagnostic tool for prostate cancer.

In case you ask me for references;



References:
1. Weisser H., Tunn S., Behnke B., Krieg M.: Effects of the sabal serulata
extract IDS 89 and its subfractions on 5 alpha-reductase activity in human
benign prostatic hyperplasia. Prostate 1996; 28:300-306.

2. Lowe F., Ku J.: Phytotherapy in treatment of benign prostatic
hyperplasia: A critical review. Urology 1996; 48:12-20.

3. Carilla E., et al: Binding of Permixon, a new treatment for prostatic
benign hyperplasia, to the cytosolic androgen receptor in the rat prostate.
J. Steroid Biochem 1984; 20:521-523.

4. Sultan C., et al: inhibition of androgen metabolism and binding by a
liposterolic extract of serenoa repens B in human foreskin fibroblasts. J.
Steroid Biochem 1984; 20:515-519.

5. Di Silverio F., et al: Plant extracts in BPH. Minerva Urol Nefrol 1993;
45:143-149.

6. Di Silverio F., et a.: Evidence that Serenoa Repens extract displays
antiestrogenic activity in prostatic tissue of benign prostatic hypertrophy.
Eur. Urol 1992; 21:309-314.

7. Briley M., et al: Permixon, a new treatment for benign prostatic
hyperplasia, acts directly at the cytosolic androgen receptor in rat
>prostate. Br. J. Pharmacol 1983; 79:327.

8. Stoner E.: 5 Alpha-reductase inhibitors/finasteride. Prostate suppl.
1996; (6): 82-87.

9. Lepor H., Willford W.D., et al: The efficacy of terazosin, finasteride,
or both in benign prostatic hyperplasia. Veterans Administration Cooperative
Studies Benign Prostatic Hyperplasia Study Group. N. Engl. J. Med. 1996;
335:533-539.

10. Dreikorn K., Schonhofer PS: Status of phytotherapeutic drugs in
treatment of benign prostatic hyperplasia. Urologe A 1995 Mar; 34(2):
119-129.

11. Whitaker J.: The Prostate Report--Prevention and Healing, chapter 7, p
44. 1994, Phillips Publishing, Inc.

12. Stephenson R., et a.: "The fall in incidence of prostate carcinoma: On
the down side of a prostate specific antigen induced peak in
incidence"--Data from the Utah Cancer Registry. Cancer 1996; 77: 1342-1348.

13.Braeckman J.: The extract of sereona repens in the treatment of benign
prostatic hyperplasia: a multicenter open study.Current Therapeutic Research
(Vol. 55, No. 7,July, pp 776-785) 1994.

Any idiot can copy and paste these articles...

----

Pete

"Will Brink" <willbrink@comcast.net> schreef:

> No, though proscar will do that. It increases T by approx 15% in some
> studies, which is not physiologically worthwhile really. SP appears to be
> useful for BPH, and thats about it, and the machanism is more complex then
> simple DHT blocking.

(i will not even get into the role of estrogen wrt BPH...)

Will, when DHT enters the muscle cell, it doesnt seem to bind because its
quickly de-activated.

Yet, DHT seem to have, together with T, an anabolic effect. You get one of
those "non AR mediated" effects.

I guess the same is true for Anadrol and its metabolite mestanolone
(methyl-DHT)
(and i can only speculate why Deca works so well with Proviron...)

But... where, and what, are those effects ?!?!?!

I have been trying to figure this out for many years, but most people cant
give a statisfying answer.

----
Pete

In article <no-742B17.12090930102006@news.verizon.net>,
eponymous cowherd <no@spam4me.com> wrote:

> I know this is off topic, but I figure the ppl here know an awful lot
> about testosterone.
>
> If steroids reduce the body's own production of testosterone, will saw
> palmetto increase it? If SP is blocking DHT will the body try to achieve
> homeostasis by increasing testosterone production?


You may find these less-than-impressive studies on saw palmetto
interesting:


Comparison of finasteride (Proscar) and Serenoa repens (Permixon) in the
inhibition of 5-alpha reductase in healthy male volunteers.

Strauch G, Perles P, Vergult G, Gabriel M, Gibelin B, Cummings S,Malbecq
W, Malice MP.
Eur Urol. 1994;26(3):247-52.
Eclimed Pharmacologie Clinique, Hopital Universitaire Cochin, Paris,
France.

A total of 32 healthy male volunteers (age range 20-30 years) were
enrolled in a 1-week open, randomized, placebo-controlled study
comparing finasteride (Proscar), a 5 alpha-reductase inhibitor, with
Permixon, the plant extract of Serenoa repens. The objective of the
study was to evaluate the effect of single and multiple doses of the
drugs on the inhibition of 5 alpha-reductase as assessed by serum
dihydrotestosterone level determination. Following baseline measurements
on day 1, the subjects were randomized to finasteride 5 mg once a day (n
= 10), Permixon 80 mg x 2 twice a day (n = 11), or to placebo once a day
(n = 11) for 7 days. Serum testosterone and dihydrotestosterone levels,
were determined on day 1 (baseline and 12 h) and on days 2 (24 h), 3 (48
h), 4 (72 h), 6 (120 h), and 8 (168 h). After 12 h, a single dose of
finasteride 5 mg reduced the serum dihydrotestosterone level by 65% (p <
or = 0.01). The decreases ranged from -52 to -60% with multiple doses of
finasteride 5 mg once a day (p < or = 0.01). As in the placebo group,
there was no effect of Permixon on the serum dihydrotestosterone level.
No significant difference was detected between finasteride and Permixon
or between finasteride and placebo with respect to serum testosterone,
except on days 3 and 6, respectively (p < or = 0.05). However, the
corresponding serum testosterone levels remained within the normal
ranges. These data confirm the efficacy of finasteride as inhibitor of 5
alpha-reductase.(ABSTRACT TRUNCATED AT 250 WORDS)
http://pmid.us/7805711



Comparison of finasteride (Proscar), a 5 alpha reductase inhibitor, and
various commercial plant extracts in in vitro and in vivo 5 alpha
reductase inhibition.

Rhodes L, Primka RL, Berman C, Vergult G, Gabriel M, Pierre-Malice M,
Gibelin B.
Prostate. 1993;22(1):43-51.
Department of Biochemistry, Merck Research Laboratories, Rahway, New
Jersey.

Human prostate was used as a source of 5 alpha reductase. Compounds were
incubated with an enzyme preparation and [3H]testosterone.
[3H]-dihydrotestosterone production was measured to calculate 5 alpha
reductase activity. IC50 values (ng/ml) were finasteride = 1; Permixon =
5,600; Talso = 7,000; Strogen Forte = 31,000; Prostagutt = 40,000; and
Tadenan = 63,000. Bazoton and Harzol had no activity at concentrations
up to 500,000 ng/ml. In castrate rats stimulated with testosterone (T)
or dihydrotestosterone (DHT), finasteride, but not Permixon or Bazoton,
inhibited T stimulated prostate growth, while none of the three
compounds inhibited DHT stimulated growth. These results demonstrate
that finasteride inhibits 5 alpha reductase, while Permixon and Bazoton
have neither anti-androgen nor 5 alpha reductase inhibitory activity. In
addition, in a 7 day human clinical trial, finasteride, but not Permixon
or placebo, decreased serum DHT in men, further confirming the lack of 5
alpha reductase inhibition by Permixon. Finasteride and the plant
extracts listed above do not inhibit the binding of DHT to the rat
prostatic androgen receptor (concentrations to 100 micrograms/ml). Based
on these results, it is unlikely that these plant extracts would shrink
the prostate by inhibiting androgen action or 5 alpha reductase.
http://pmid.us/8381228



Saw palmetto for benign prostatic hyperplasia.

Bent S, Kane C, Shinohara K, Neuhaus J, Hudes ES, Goldberg H,Avins AL.
N Engl J Med. 2006 Feb 9;354(6):557-66.*
Osher Center for Integrative Medicine, Department of Medicine,
University of California, San Francisco, San Francisco, USA.

BACKGROUND: Saw palmetto is used by over 2 million men in the United
States for the treatment of benign prostatic hyperplasia and is commonly
recommended as an alternative to drugs approved by the Food and Drug
Administration. METHODS: In this double-blind trial, we randomly
assigned 225 men over the age of 49 years who had moderate-to-severe
symptoms of benign prostatic hyperplasia to one year of treatment with
saw palmetto extract (160 mg twice a day) or placebo. The primary
outcome measures were changes in the scores on the American Urological
Association Symptom Index (AUASI) and the maximal urinary flow rate.
Secondary outcome measures included changes in prostate size, residual
urinary volume after voiding, quality of life, laboratory values, and
the rate of reported adverse effects. RESULTS: There was no significant
difference between the saw palmetto and placebo groups in the change in
AUASI scores (mean difference, 0.04 point; 95 percent confidence
interval, -0.93 to 1.01), maximal urinary flow rate (mean difference,
0.43 ml per minute; 95 percent confidence interval, -0.52 to 1.38),
prostate size, residual volume after voiding, quality of life, or serum
prostate-specific antigen levels during the one-year study. The
incidence of side effects was similar in the two groups. CONCLUSIONS: In
this study, saw palmetto did not improve symptoms or objective measures
of benign prostatic hyperplasia. (ClinicalTrials.gov number,
NCT00037154.). Copyright 2006 Massachusetts Medical Society.
http://pmid.us/16467543



Serenoa repens extract for benign prostate hyperplasia: a randomized
controlled trial.

Willetts KE, Clements MS, Champion S, Ehsman S, Eden JA.
BJU Int. 2003 Aug;92(3):267-70.*
Natural Therapies Unit, Royal Hospital for Women, Randwick, Australia.

OBJECTIVE: To compare the effect of a Serenoa repens extract with
placebo for symptoms of benign prostatic hyperplasia (BPH). PATIENTS AND
METHODS: In a double-blind placebo-controlled randomized trial between
January 1999 and March 2000, 100 men with symptoms of BPH, aged < 80
years, with a maximum urinary flow rate of 5-15 mL/s for a voiding
volume of 150 mL, were randomly and equally allocated to 320 mg S.
repens extract or placebo (paraffin oil). The main outcome measures were
the International Prostate Symptom Score (IPSS), peak urinary flow rate,
and the Rosen International Index of Erectile Function (IIEF)
questionnaire. RESULTS: There was no significant difference between the
treatments over the 12 weeks of the study in the IPSS, peak urinary flow
rate or for the IIEF questionnaire. CONCLUSIONS: During the trial all
participants had some improvement in their symptoms of BPH but there was
no significant beneficial effect of this S. repens extract over placebo
in this 12-week trial.
http://pmid.us/12887481



A prospective, 1-year trial using saw palmetto versus finasteride in the
treatment of category III prostatitis/chronic pelvic pain syndrome.

Kaplan SA, Volpe MA, Te AE.
J Urol. 2004 Jan;171(1):284-8.
Department of Urology, College of Physicians and Surgeons, Columbia
University, New York.

PURPOSE: This study was designed to assess the safety and efficacy of
saw palmetto or finasteride in men with category III prostatitis/chronic
pelvic pain syndrome (CP/CPPS). MATERIALS AND METHODS: A prospective,
randomized, open label, 1-year study was designed to assess the safety
and efficacy of saw palmetto and finasteride in the treatment of men
diagnosed with CP/CPPS. Patients were randomized to finasteride (5 mg
once daily) or saw palmetto (325 mg daily) for 1 year. Patients were
evaluated using the National Institutes of Health Chronic Prostatitis
Symptom Index, individual domains (pain, urinary symptoms, quality of
life and mean pain score) and the American Urological Association
Symptom Score at baseline, 3, 6 and 12 months. RESULTS: A total of 64
consecutive men 24 to 58 years old (mean age 43.2) with a diagnosis of
CP/CPPS were equally randomized to the 2 treatment arms. All 64 men had
previously received antibiotics (duration of 3 to 93 weeks), 52 (82%)
had been on alpha-blockade. There were 61, 57 and 56 patients evaluable
at 3, 6 and 12 months, respectively. At 1 year mean total National
Institutes of Health Chronic Prostatitis Symptom Index score decreased
from 23.9 to 18.1 in the finasteride group (p <0.003), and from 24.7 to
24.6 in the saw palmetto arm (p = 0.41). In the finasteride arm the
quality of life and pain domains were significantly improved at 1 year;
however, urination was not. Adverse events included headache (3 cases)
in the saw palmetto group and decreased libido (2 cases) in the
finasteride group. At the end of the trial 13 of 32 (41%) and 21 of 32
(66%) opted to continue saw palmetto and finasteride, respectively.
CONCLUSIONS: CP/CPPS treated with saw palmetto had no appreciable
long-term improvement. In contrast, patients treated with finasteride
had significant and durable improvement in all various parameters except
voiding. Further studies are warranted to ascertain the mechanism and
reproducibility of these effects in a placebo controlled trial.
http://pmid.us/14665895

In article <4547779c$0$55713$dbd43001@news.wanadoo.nl>, "Pete"
<phoutstra@wanadoo.nl> wrote:

> "Will Brink" <willbrink@comcast.net> schreef:
>
> > No, though proscar will do that. It increases T by approx 15% in some
> > studies, which is not physiologically worthwhile really. SP appears to be
> > useful for BPH, and thats about it, and the machanism is more complex then
> > simple DHT blocking.
>
> (i will not even get into the role of estrogen wrt BPH...)
>
> Will, when DHT enters the muscle cell, it doesnt seem to bind because its
> quickly de-activated.
>
> Yet, DHT seem to have, together with T, an anabolic effect.

I dont think that's well documented, so it's guess work.

> You get one of
> those "non AR mediated" effects.

It's been theorized that it may be effects on things like agression and
motivation that DHT plays a part in vs direct anabolic effects which may
be non AR mediated. According to Pat:

"Tt is important to understand that even though testosterone is the active
androgen in muscle, and DHT exhibits relatively little direct anabolic
effects on muscle in men, DHT is still very important for the full
performance enhancement effects from testosterone. What I specifically
mean here are the effects of DHT on the central nervous system, which lead
to increased neurological efficiency (strength), and increased resistance
to psychological and physical stress - not to mention optimal sexual
function and libido."

Cont:

http://www.mesomorphosis.com/articles/arnold/dht.htm

>
> I guess the same is true for Anadrol and its metabolite mestanolone
> (methyl-DHT)

As far as I know, it was Bill Roberts who devided steroids into something
like class one and class two where he felt some AAS worked through non AR
mediated effects. I dont know if he has any follow up to that and I recall
Pat thought it was more or less BS. Cant tell you the right answer there.
It's not an area i have spent a lot of time on.

"Will Brink" <willbrink@comcast.net> schreef:

>> I guess the same is true for Anadrol and its metabolite mestanolone
>> (methyl-DHT)

> As far as I know, it was Bill Roberts who devided steroids into something
> like class one and class two where he felt some AAS worked through non AR
> mediated effects. I dont know if he has any follow up to that and I recall
> Pat thought it was more or less BS. Cant tell you the right answer there.
> It's not an area i have spent a lot of time on.

But do you know its true that both Deca and Primo have both a binding
affinity that is twice as strong then test, yet test, mg for mg, still gives
better results?

I always assumed that better binding is better, but then Bill pointed out
that both Dianabol and Anadrol have crappy binding. Yet the anabolic effects
are second to none.

I just want to figure out a few things before i start my last cycle.

I think i posted it before, but i will spare you the details. For now.

Anyway, the "workhorses" are still test, Deca, Dbol and Anadrol.
Besides Proviron i will probably add 20-25 mg Winstrol.

To optimize the others and reduce side effects.

----
Pete

French laboratory result. You can trust them as much as their anti-American
political purpose dictates. Just ask Lance Armstrong. This is how the French
say thanks for liberating them from the Nazis. Read
http://www.fuckfrance.com/ and enjoy.

"Mary Brown" <nospam@nospam.com> wrote in message
news:nospam-487B96.16405531102006@newsclstr02.news.prodigy.com ...
> In article <no-742B17.12090930102006@news.verizon.net>,
> eponymous cowherd <no@spam4me.com> wrote:
>
>> I know this is off topic, but I figure the ppl here know an awful lot
>> about testosterone.
>>
>> If steroids reduce the body's own production of testosterone, will saw
>> palmetto increase it? If SP is blocking DHT will the body try to achieve
>> homeostasis by increasing testosterone production?
>
>
> You may find these less-than-impressive studies on saw palmetto
> interesting:
>
>
> Comparison of finasteride (Proscar) and Serenoa repens (Permixon) in the
> inhibition of 5-alpha reductase in healthy male volunteers.
>
> Strauch G, Perles P, Vergult G, Gabriel M, Gibelin B, Cummings S,Malbecq
> W, Malice MP.
> Eur Urol. 1994;26(3):247-52.
> Eclimed Pharmacologie Clinique, Hopital Universitaire Cochin, Paris,
> France.
>
> A total of 32 healthy male volunteers (age range 20-30 years) were
> enrolled in a 1-week open, randomized, placebo-controlled study
> comparing finasteride (Proscar), a 5 alpha-reductase inhibitor, with
> Permixon, the plant extract of Serenoa repens. The objective of the
> study was to evaluate the effect of single and multiple doses of the
> drugs on the inhibition of 5 alpha-reductase as assessed by serum
> dihydrotestosterone level determination. Following baseline measurements
> on day 1, the subjects were randomized to finasteride 5 mg once a day (n
> = 10), Permixon 80 mg x 2 twice a day (n = 11), or to placebo once a day
> (n = 11) for 7 days. Serum testosterone and dihydrotestosterone levels,
> were determined on day 1 (baseline and 12 h) and on days 2 (24 h), 3 (48
> h), 4 (72 h), 6 (120 h), and 8 (168 h). After 12 h, a single dose of
> finasteride 5 mg reduced the serum dihydrotestosterone level by 65% (p <
> or = 0.01). The decreases ranged from -52 to -60% with multiple doses of
> finasteride 5 mg once a day (p < or = 0.01). As in the placebo group,
> there was no effect of Permixon on the serum dihydrotestosterone level.
> No significant difference was detected between finasteride and Permixon
> or between finasteride and placebo with respect to serum testosterone,
> except on days 3 and 6, respectively (p < or = 0.05). However, the
> corresponding serum testosterone levels remained within the normal
> ranges. These data confirm the efficacy of finasteride as inhibitor of 5
> alpha-reductase.(ABSTRACT TRUNCATED AT 250 WORDS)
> http://pmid.us/7805711
>
>
>
> Comparison of finasteride (Proscar), a 5 alpha reductase inhibitor, and
> various commercial plant extracts in in vitro and in vivo 5 alpha
> reductase inhibition.
>
> Rhodes L, Primka RL, Berman C, Vergult G, Gabriel M, Pierre-Malice M,
> Gibelin B.
> Prostate. 1993;22(1):43-51.
> Department of Biochemistry, Merck Research Laboratories, Rahway, New
> Jersey.
>
> Human prostate was used as a source of 5 alpha reductase. Compounds were
> incubated with an enzyme preparation and [3H]testosterone.
> [3H]-dihydrotestosterone production was measured to calculate 5 alpha
> reductase activity. IC50 values (ng/ml) were finasteride = 1; Permixon =
> 5,600; Talso = 7,000; Strogen Forte = 31,000; Prostagutt = 40,000; and
> Tadenan = 63,000. Bazoton and Harzol had no activity at concentrations
> up to 500,000 ng/ml. In castrate rats stimulated with testosterone (T)
> or dihydrotestosterone (DHT), finasteride, but not Permixon or Bazoton,
> inhibited T stimulated prostate growth, while none of the three
> compounds inhibited DHT stimulated growth. These results demonstrate
> that finasteride inhibits 5 alpha reductase, while Permixon and Bazoton
> have neither anti-androgen nor 5 alpha reductase inhibitory activity. In
> addition, in a 7 day human clinical trial, finasteride, but not Permixon
> or placebo, decreased serum DHT in men, further confirming the lack of 5
> alpha reductase inhibition by Permixon. Finasteride and the plant
> extracts listed above do not inhibit the binding of DHT to the rat
> prostatic androgen receptor (concentrations to 100 micrograms/ml). Based
> on these results, it is unlikely that these plant extracts would shrink
> the prostate by inhibiting androgen action or 5 alpha reductase.
> http://pmid.us/8381228
>
>
>
> Saw palmetto for benign prostatic hyperplasia.
>
> Bent S, Kane C, Shinohara K, Neuhaus J, Hudes ES, Goldberg H,Avins AL.
> N Engl J Med. 2006 Feb 9;354(6):557-66.
> Osher Center for Integrative Medicine, Department of Medicine,
> University of California, San Francisco, San Francisco, USA.
>
> BACKGROUND: Saw palmetto is used by over 2 million men in the United
> States for the treatment of benign prostatic hyperplasia and is commonly
> recommended as an alternative to drugs approved by the Food and Drug
> Administration. METHODS: In this double-blind trial, we randomly
> assigned 225 men over the age of 49 years who had moderate-to-severe
> symptoms of benign prostatic hyperplasia to one year of treatment with
> saw palmetto extract (160 mg twice a day) or placebo. The primary
> outcome measures were changes in the scores on the American Urological
> Association Symptom Index (AUASI) and the maximal urinary flow rate.
> Secondary outcome measures included changes in prostate size, residual
> urinary volume after voiding, quality of life, laboratory values, and
> the rate of reported adverse effects. RESULTS: There was no significant
> difference between the saw palmetto and placebo groups in the change in
> AUASI scores (mean difference, 0.04 point; 95 percent confidence
> interval, -0.93 to 1.01), maximal urinary flow rate (mean difference,
> 0.43 ml per minute; 95 percent confidence interval, -0.52 to 1.38),
> prostate size, residual volume after voiding, quality of life, or serum
> prostate-specific antigen levels during the one-year study. The
> incidence of side effects was similar in the two groups. CONCLUSIONS: In
> this study, saw palmetto did not improve symptoms or objective measures
> of benign prostatic hyperplasia. (ClinicalTrials.gov number,
> NCT00037154.). Copyright 2006 Massachusetts Medical Society.
> http://pmid.us/16467543
>
>
>
> Serenoa repens extract for benign prostate hyperplasia: a randomized
> controlled trial.
>
> Willetts KE, Clements MS, Champion S, Ehsman S, Eden JA.
> BJU Int. 2003 Aug;92(3):267-70.
> Natural Therapies Unit, Royal Hospital for Women, Randwick, Australia.
>
> OBJECTIVE: To compare the effect of a Serenoa repens extract with
> placebo for symptoms of benign prostatic hyperplasia (BPH). PATIENTS AND
> METHODS: In a double-blind placebo-controlled randomized trial between
> January 1999 and March 2000, 100 men with symptoms of BPH, aged < 80
> years, with a maximum urinary flow rate of 5-15 mL/s for a voiding
> volume of 150 mL, were randomly and equally allocated to 320 mg S.
> repens extract or placebo (paraffin oil). The main outcome measures were
> the International Prostate Symptom Score (IPSS), peak urinary flow rate,
> and the Rosen International Index of Erectile Function (IIEF)
> questionnaire. RESULTS: There was no significant difference between the
> treatments over the 12 weeks of the study in the IPSS, peak urinary flow
> rate or for the IIEF questionnaire. CONCLUSIONS: During the trial all
> participants had some improvement in their symptoms of BPH but there was
> no significant beneficial effect of this S. repens extract over placebo
> in this 12-week trial.
> http://pmid.us/12887481
>
>
>
> A prospective, 1-year trial using saw palmetto versus finasteride in the
> treatment of category III prostatitis/chronic pelvic pain syndrome.
>
> Kaplan SA, Volpe MA, Te AE.
> J Urol. 2004 Jan;171(1):284-8.
> Department of Urology, College of Physicians and Surgeons, Columbia
> University, New York.
>
> PURPOSE: This study was designed to assess the safety and efficacy of
> saw palmetto or finasteride in men with category III prostatitis/chronic
> pelvic pain syndrome (CP/CPPS). MATERIALS AND METHODS: A prospective,
> randomized, open label, 1-year study was designed to assess the safety
> and efficacy of saw palmetto and finasteride in the treatment of men
> diagnosed with CP/CPPS. Patients were randomized to finasteride (5 mg
> once daily) or saw palmetto (325 mg daily) for 1 year. Patients were
> evaluated using the National Institutes of Health Chronic Prostatitis
> Symptom Index, individual domains (pain, urinary symptoms, quality of
> life and mean pain score) and the American Urological Association
> Symptom Score at baseline, 3, 6 and 12 months. RESULTS: A total of 64
> consecutive men 24 to 58 years old (mean age 43.2) with a diagnosis of
> CP/CPPS were equally randomized to the 2 treatment arms. All 64 men had
> previously received antibiotics (duration of 3 to 93 weeks), 52 (82%)
> had been on alpha-blockade. There were 61, 57 and 56 patients evaluable
> at 3, 6 and 12 months, respectively. At 1 year mean total National
> Institutes of Health Chronic Prostatitis Symptom Index score decreased
> from 23.9 to 18.1 in the finasteride group (p <0.003), and from 24.7 to
> 24.6 in the saw palmetto arm (p = 0.41). In the finasteride arm the
> quality of life and pain domains were significantly improved at 1 year;
> however, urination was not. Adverse events included headache (3 cases)
> in the saw palmetto group and decreased libido (2 cases) in the
> finasteride group. At the end of the trial 13 of 32 (41%) and 21 of 32
> (66%) opted to continue saw palmetto and finasteride, respectively.
> CONCLUSIONS: CP/CPPS treated with saw palmetto had no appreciable
> long-term improvement. In contrast, patients treated with finasteride
> had significant and durable improvement in all various parameters except
> voiding. Further studies are warranted to ascertain the mechanism and
> reproducibility of these effects in a placebo controlled trial.
> http://pmid.us/14665895

In article <4548b336$0$211$dbd41001@news.wanadoo.nl>, "Pete"
<phoutstra@wanadoo.nl> wrote:

> "Will Brink" <willbrink@comcast.net> schreef:
>
> >> I guess the same is true for Anadrol and its metabolite mestanolone
> >> (methyl-DHT)
>
> > As far as I know, it was Bill Roberts who devided steroids into something
> > like class one and class two where he felt some AAS worked through non AR
> > mediated effects. I dont know if he has any follow up to that and I recall
> > Pat thought it was more or less BS. Cant tell you the right answer there.
> > It's not an area i have spent a lot of time on.
>
> But do you know its true that both Deca and Primo have both a binding
> affinity that is twice as strong then test, yet test, mg for mg, still gives
> better results?

Of course. T is more androgenic, some effects may be coming from T to E
conversion, increased agression and CNS, etc.

>
> I always assumed that better binding is better, but then Bill pointed out
> that both Dianabol and Anadrol have crappy binding. Yet the anabolic effects
> are second to none.

See above.

>
> I just want to figure out a few things before i start my last cycle.

> I think i posted it before, but i will spare you the details. For now.
>
> Anyway, the "workhorses" are still test, Deca, Dbol and Anadrol.
> Besides Proviron i will probably add 20-25 mg Winstrol.

That's all?! Pussy.
>
> To optimize the others and reduce side effects.
>
> ----
> Pete

"Will Brink" <willbrink@comcast.net> schreef:

>> But do you know its true that both Deca and Primo have both a binding
>> affinity that is twice as strong then test, yet test, mg for mg, still
>> gives
>> better results?

> Of course. T is more androgenic, some effects may be coming from T to E
> conversion, increased agression and CNS, etc.

I believe Robert said something similair.

>> I always assumed that better binding is better, but then Bill pointed out
>> that both Dianabol and Anadrol have crappy binding. Yet the anabolic
>> effects
>> are second to none.

> See above.

I understood that, but T has much better binding (according to Roberts) then
both Dbol and Anadrol.
And A-50 doesnt even convert, as it seems. Dianabol is more androgenic then
Deca, and has more conversion to E, but the binding, compared to T, is still
crappy.

Look at these posts from 6 years ago;

http://groups.google.nl/group/misc.f...ff90fee53c1690

So its true after all. Steroids can cause headaches. Its giving me one.

However, "testing" the stuff 4 1/2 years ago, a measly 30mg with some Deca,
was a *nice* experience.

When Lysis made the "observation" that, i quote;

"I have noticed an increased response of the shoulder girdle area
to methandrostenolone in particular, more so than other AAS."

This was a response by Bill;

"And interestingly, methandrostenolone (Dianabol) is one
of those steroids that oddly enough is very anabolic though
without binding well to the AR -- the mechanism of action
is not known."

Can all be found here;

http://groups.google.nl/group/misc.f...3ad50083058c83

And the headache gets worse.

>> Anyway, the "workhorses" are still test, Deca, Dbol and Anadrol.
>> Besides Proviron i will probably add 20-25 mg Winstrol.

> That's all?! Pussy.

I would like to stay in touch with my feminine side.

----
Pete

In article <4549d267$0$90688$dbd43001@news.wanadoo.nl>, "Pete"
<phoutstra@wanadoo.nl> wrote:

> "Will Brink" <willbrink@comcast.net> schreef:
>
> >> But do you know its true that both Deca and Primo have both a binding
> >> affinity that is twice as strong then test, yet test, mg for mg, still
> >> gives
> >> better results?
>
> > Of course. T is more androgenic, some effects may be coming from T to E
> > conversion, increased agression and CNS, etc.
>
> I believe Robert said something similair.
>
> >> I always assumed that better binding is better, but then Bill pointed out
> >> that both Dianabol and Anadrol have crappy binding. Yet the anabolic
> >> effects
> >> are second to none.
>
> > See above.
>
> I understood that, but T has much better binding (according to Roberts) then
> both Dbol and Anadrol.
> And A-50 doesnt even convert, as it seems. Dianabol is more androgenic then
> Deca, and has more conversion to E, but the binding, compared to T, is still
> crappy.

Which supports what we have been saying: it's clearly not a binding only
issue. A weak androgen that binds well will have less effects then a
strong androgen that does not bind as well, for reason that are unclear
but suggest other mechanisms, some of which are non AR mediated.

>
> Look at these posts from 6 years ago;
>
>
http://groups.google.nl/group/misc.f...ff90fee53c1690

Ahhh the good old days when there were really interesting threads by
interesting people and hard working funny trolls....

On Thu, 02 Nov 2006 09:46:57 -0500, willbrink@comcast.net (Will Brink)
wrote:

>In article <4549d267$0$90688$dbd43001@news.wanadoo.nl>, "Pete"
><phoutstra@wanadoo.nl> wrote:
>
>> "Will Brink" <willbrink@comcast.net> schreef:
>>
>> >> But do you know its true that both Deca and Primo have both a binding
>> >> affinity that is twice as strong then test, yet test, mg for mg, still
>> >> gives
>> >> better results?
>>
>> > Of course. T is more androgenic, some effects may be coming from T to E
>> > conversion, increased agression and CNS, etc.
>>
>> I believe Robert said something similair.
>>
>> >> I always assumed that better binding is better, but then Bill pointed out
>> >> that both Dianabol and Anadrol have crappy binding. Yet the anabolic
>> >> effects
>> >> are second to none.
>>
>> > See above.
>>
>> I understood that, but T has much better binding (according to Roberts) then
>> both Dbol and Anadrol.
>> And A-50 doesnt even convert, as it seems. Dianabol is more androgenic then
>> Deca, and has more conversion to E, but the binding, compared to T, is still
>> crappy.
>
>Which supports what we have been saying: it's clearly not a binding only
>issue. A weak androgen that binds well will have less effects then a
>strong androgen that does not bind as well, for reason that are unclear
>but suggest other mechanisms, some of which are non AR mediated.
>
>>
>> Look at these posts from 6 years ago;
>>
>>
>http://groups.google.nl/group/misc.f...ff90fee53c1690
>
>Ahhh the good old days when there were really interesting threads by
>interesting people and hard working funny trolls....

Ahhh, the rose tinted spectacles again Will; my main memory of that
era was John Williams, Lyle McDonald and Elzi Volk competing to see
who could profess to be the cleverest person on Earth, and you being
your usual irritating gun-toting fart self.

As for 'funny' "trolls", well we did have Robert Dorf (aka Bob Tokyo,
aka Bob Edo) who was a very droll "troll", but that was about it.

We mostly had nasty "trolls" like John Williams, Lyle McDonald and
Lysis, who were at each others' throats day in day out, with other
smaller nasty buggers (like yourself and Pat Styles) supporting one or
the other of the senior nasty "trolls".

Hobbes has continued to be good value, as has Cohen, with Art hiding
his potential value behind diffidence, and Se th always several weeks
behind.

The Group has been going along great for a long time, with some very
well-informed on-topic contributors, and a number of very amusing
contributions from the supporting cast.

The only person "trolling" at the moment is you Will, with this
further inept attempt! ;o)

"Charles" <jrh@msn.com> schreef:

>>Ahhh the good old days when there were really interesting threads by
>>interesting people and hard working funny trolls....

> We mostly had nasty "trolls" like John Williams, Lyle McDonald...

Why are you calling Lyle a troll?

The man knew a shitload about training and other items as well. I always got
along fine with Lyle.

> and Lysis, who were at each others' throats day in day out...

Lysis is a low life piece of shit who lives in the suer of Europe.

Thats lower than a troll.

> with other smaller nasty buggers (like yourself and Pat Styles) supporting
> one or
> the other of the senior nasty "trolls".

Got along fine with Styles as well. He had different ideas about training,
but we never had problems.

----
Pete

On Thu, 2 Nov 2006 16:58:25 +0100, "Pete" <phoutstra@wanadoo.nl>
wrote:

>"Charles" <jrh@msn.com> schreef:
>
>>>Ahhh the good old days when there were really interesting threads by
>>>interesting people and hard working funny trolls....
>
>> We mostly had nasty "trolls" like John Williams, Lyle McDonald...
>
>Why are you calling Lyle a troll?

Because he was a foul, self-abusing pervert, who would subject many
well-intentioned people to the most awfully vile personal attacks.

>
>The man knew a shitload about training and other items as well.

He certainly could be very helpful, but he was also particularly aware
of the commercial potentiality of what he was doing.

>I always got along fine with Lyle.

A great number of people didn't, including the other front runners JMW
and Elzi. But then the changing dynamics of that little grouping is
another story in itself.

>
>> and Lysis, who were at each others' throats day in day out...
>
>Lysis is a low life piece of shit who lives in the suer of Europe.

He certainly gave better than he got, to the discomfort of those
parading their personal lives for public perusal, while they were also
giving many other people a difficult time.

It appeared to those who were on the receiving end of *their*
nastiness, to be poetic justice! ;o)

>
>Thats lower than a troll.
>
>> with other smaller nasty buggers (like yourself and Pat Styles) supporting
>> one or
>> the other of the senior nasty "trolls".
>
>Got along fine with Styles as well. He had different ideas about training,
>but we never had problems.
>

Pat sadly took sides, as did many others, having weighed up which was
the best side to be on, forgetting the morality of proceedings, but
not wanting to end up as targets themselves - which was the *real*
alternative.

We have to remember also, that a number of them met socially in real
life, with resultant loyalties that made the Group prone to cliques
with a 'blind follow my leader' type mentality.