[dinoiii]

Originally Posted by slow-mun

What about Trib and Nolvadex?

You know the only theoretic suggestion that I could contribute here is that trib does, to some degree, promote elevations in DHEA (which is thought to be an alternative mechanism of action of the herbal favorite).

No controlled campaigns have been designed to evaluate said effects to date that I am aware, so it remains theory at best. I may very well (and for the reasons stated above) not suggest patients to use them concurrently, but true rationale remains unsupported.


D_

[dinoiii]

Protodioscin from herbal plant Tribulus terrestris L improves the male sexual functions, probably via DHEA

A. Adimoelja and P. Ganeshan Adaikan
Airlangga University, Indonesia and National University of Singapore
in 6th Biennial Asian-Pacific Meeting on Impotence in Kuala Lumpur, Malaysia (1997)
Int. J. Impotence Research v9, supp 1 (1997)
SUMMARY

An interesting correlation of dehydroepiandrosterone-sulphate (DHEA-S) level with the incident of low sex drive and higher occurrence of impotence was discovered in studies with patients diagnosed with diabetes mellitus. To test further the relationship between DHEA-S and erectile dysfunction (ED), we conducted a clinical trial of 30 non-diabetic men with ED, 30 non-diabetic men without ED and 15 diabetic men with ED. These men are given extract of Tribulus terrestris (Libilov) at 3 x 250 mg / day for 3 weeks. The DHEA-S levels, as well as other blood and liver parameters were evaluated.

We found a significant increase of DHEA-S levels in diabetic and non-diabetic subjects after treatment, and a significant increase in the frequency of successful intercourse by 60% in both the diabetic and non-diabetic groups with or without ED.

INTRODUCTION

Tribulus terrestris L (TTL) is a herbal plant native to Bulgaria and China that has a long history as a powerful aphrodisiac and as a traditional medicine for treating male infertility (1,6). Recently, a chemical compound isolated from TTL called protodioscin (2) has been identified, purified and standardized as a phytochemical agent. In a multi-center, placebo-controlled, randomized, double-blind clinical trial, protodioscin proved to be an effective form of treatment for male infertility (2,6,7).

It is known that sufficient dehydroepiandrosterone (DHEA) in the epididymis is necessary for the maturation process of spermatozoa (5). Furthermore, it has been speculated that in some idiopathic oligoasthenoteratozoospermia, male infertility is due to the low concentration of DHEA in the epididymis. In another clinical trial protodioscin is proved to increase the serum DHEA level of infertile men, without any change in the level of testosterone and other androgens. It is also shown that liver and kidney functions do not change significantly by protodioscin (1,2,6,7). The study concludes that protodioscin in TTL could be the precursor of DHEA in patients with low serum level of this hormone. As TTL has been known for its aphrodisiac quality, speculations have been made that its mechanism of action involves the conversion of protodioscin to DHEA. In turn, DHEA may increase cell membrane integrity and functions (3,4), thereby resulting in better sexual performance and the general feeling of well-being.

MATERIALS AND METHODS

The incident of erectile dysfunction (ED) is five times greater in patients diagnosed with diabetes mellitus as compared to non-diabetic patients. The correlation of lowered DHEA-sulphate (DHEA-S) in the diabetic patients and the increased frequency of ED in these patients suggests that improvement in DHEA-S level may constitute a treatment for ED.

This trial evaluated the DHEA-S levels of 30 non-diabetic male patients diagnosed with ED, 30 non-diabetic patients without ED, and 15 diabetic patients without ED. The group of non-diabetics with ED as well as the group of diabetics with ED were treated with TTL 3 times daily for 3 weeks (Libilov, 250 mg). The serum DHEA-S, testosterone, FSH, LH, prolactin, cholesterol, triglyceride, creatinine, Hb, and glucose levels, as well as liver and kidney functions were evaluated before and after treatment. These parameters were statistically tested (t-test for paired samples) to determine their statistical significance.

Finally, questionnaires were distributed to all men with ED to determine whether there was any improvement in their sexual functions

RESULTS

There was a significant difference (p < 0.01) in the serum DHEA-S levels in the non-diabetic men (101.5 ± 14.3) as compared to the diabetic patients without ED (77.5 ± 28.7). There was also a significant difference (p < 0.01) in the DHEA levels of non-diabetic men without ED with those with ED (41.8 ± 22.6). Furthermore, there was a significant difference in the serum DHEA-S levels of the diabetic patients without ED as compared to those with ED (32.2 ± 22.6). These data were summarized in Table I below.

Parameter [DHEA-S] in µg/dl
without ED with ED
Non-diabetics 101.5 ± 14.3 41.8 ± 22.6
Diabetics 77.5 ± 28.7 32.2 ± 24.8

Table I. [DHEA-S] concentration in µg/dl of non-diabetics with and without ED, and diabetics with and without ED before treatment with TTL (Libilov).

After treatment with TTL (Libilov), there were significant increases in the serum DHEA-S levels in the diabetic patients with and without ED (Table II).

Parameter [DHEA-S] in µg/dl
Before Treatment After Treatment
Non-diabetics with ED 41.8 ± 22.6 77.6 ± 25.9
Diabetics with ED 32.2 ± 24.8 50.0 ± 32.0

Table II. [DHEA-S] concentration in µg/dl of non-diabetics and diabetics with ED before and after treatment with TTL (Libilov).

There were no significant differences observed in the hormone (testosterone, FSH, LH and prolactine), cholesterol, triglycerides, and Hb levels, as well as in the liver (SGPT, SGOT, Gamma GT) and kidney (creatinine and urea) functions before and after TTL treatment in all ED patients.

During treatment, there was a significant increase in the frequency of successful sexual intercourse in 60% of the ED patients. This effect was reported from day 10 of treatment and onwards by both the diabetic and non-diabetic ED patients.

CONCLUSION

TTL improved the sexual drive in 60% of the ED cases. As this improvement in sexual function is accompanied by a significant improvement in the DHEA levels of these patients, we surmised that the improvement in the sex drive of these patients were linked to the conversion of protodioscin, the active ingredient of the TTL extract, into DHEA-S.

The role of DHEA-S in general health and sense of well-being was suggested by its varying levels in patients diagnosed with diabetes as compared to normal men. Further correlation of DHEA with sexual functions was shown by its decreased level in those also diagnosed with ED.

Increasing the serum DHEA-S level, thus, should improve the sexual functions in patients diagnosed with ED. This hypothesis was directly supported by our clinical trial: treatment with TTL extract (Libilov) resulted in improvement in the frequency of successful sexual intercourse in men (diabetics and non-diabetics alike) diagnosed with ED. This improvement in sexual function was accompanied by an increased level of serum DHEA-S in these ED patients.

The mechanism of DHEA-S in improving the sexual functions of the treated patients is hypothesized to include improvement of cell membrane integrity and function at the cellular level, to improvement of circulation, health and sense of well-being that indirectly result in improved sex drive. Further research into the direct mechanism of the action of DHEA-S is warranted.

ACKNOWLEDGEMENTS

The authors wished to thank PT Teguhsindo Lestaritama, Jakarta, Indonesia for its support by providing the TTL extract Libilov (250 mg) for this clinical trial; Prodia Clinical Laboratory, Surabaya for its continual support in evaluating the biochemical parameters in this study; and Dr. I. Haryono, M.D. for the statistical evaluation of the data.

REFERENCES

Adimoelja, A. (1996) Sex Therapy in Asia. 4th Asian Conference of Sexology in Taipei, Taiwan.

Adimoelja, A., Suryaatmadja, S., Setiawan, L., and Tanojo, T. (1997) Protodioscin, the main active component in Tribulus terrestris L. may improve sperm function in subfertile males and increase the frequency of successful intercourse in men with erectile dysfunctions. VII National congress of Andrology in Bandung,Indonesia.

Dyner, T.S., et al. (1993) An open label dose escalation trial of oral DHEA tolerance and pharmacokinetics in patients with HIV-disease. J. AIDS 6(5): 459-465

Gaby, A.R. (1993) DHEA: The hormone that "does it all". Holistic Medicine 19-24

Hafez, E.S.E., and Prasad, M.R.N. (1976) Functional aspects of the epididymis. In Human Semen and Fertility Regulation in Men. (The CV Mosby Company) 31-41

Moeloek, N., Adimoelja, A., Tanojo, T., and Pangkahila, W. (1994) Trial of Tribulus terrestris (Libilov) on oligozoospermia. National Congress of Indonesian Association of Andrologs. Scientific Meeting VI in Manado (1994)

Setiawan, L., Adimoelja, A, and Hinting, A. (1996) Tribulus terrestris L improves sperm morphology and enhances sperm acrosome reaction in oligoasthenoteratozoospermia. J. Panca Sarjana Univ. Airlangga 5(2-3): 35-40.

[Hank Vangut]

Originally Posted by dinoiii

I ALWAYS ask for people to ask questions when they don't get something suggested however. Funny many may not ask, but will later suggest they have no idea what the hell I am talking about.

funny, i'm one of those who has not asked but later admitted i had no idea what you were saying.
i actually had to read this post three times to try and comprehend it.
but i think i understand most of what you are saying here.
and i'll ask more questions on the parts i don't quite get.

Originally Posted by dinoiii

Possibly, but I don't recommend DHEA in any event for many reasons - and I wouldn't be doing my job if I was merely offering experimental protocol to clients/patients now would I?

experimental because it has not been published in a medical document?
or experimental because you have never seen any lab results to prove benefitial or negative?

Swale perscribes dhea to a lot of his hpta patcients.
he also seems to get favorable lab results showing significant improvement from his patcients. probably not a controlled setting, but i wouldn't think he wouldn't keep experimenting w/dhea if it didn't show some signs of benefit to his patcients.

Originally Posted by dinoiii

Of course, cortisol is also LOW (contrary to the abuse of anti-cortisol agents due to lack of understanding of these pathways in the immediate post-cycle timeframe), but alas I digress...this is supplement advertising at its finest.

i think i understand you here.
you are saying dhea use for cortisol suppression in the early stages of pct is unnecessary since cort levels are initially low?
what about later on when cort levels begin to climb?

Originally Posted by dinoiii

Still, if you weigh out this adrenal compensation (ie. - supply of exogenous DHEA, et al) vs. estrogenic control (and the side effects that may result - ie. - gyno, et al), I would bet sacrificing the use of the SERM is NOT something many would be willing to become a test subject for.

i thought only excess dhea in your system has the potential to convert to estrogen.
if you are hpta suppressed with low dhea levels, wouldn't supplementing w/dhea (using only engough to bring levels up to normal) not directly translate to elevated estrogen levels?



thanks D.

[dinoiii]

Originally Posted by Hank Vangut

experimental because it has not been published in a medical document?

Nope, but experimental because a controlled setting has not established adequate rationale for me to consider changing what I too have found to work just find with said individuals.

or experimental because you have never seen any lab results to prove benefitial or negative?

Nothing is "proven" in science, merely "supported." But - sure there are no adequate labs comparatively supporting DHEA vs. placebo to merit people who didn't use DHEA would be any worse off.

Swale perscribes dhea to a lot of his hpta patcients.
he also seems to get favorable lab results showing significant improvement from his patcients. probably not a controlled setting, but i wouldn't think he wouldn't keep experimenting w/dhea if it didn't show some signs of benefit to his patcients.

I said that they DID have effects - just NOT on the HPTA directly - Indirectly at best through the HPAA. Now, we also acknowledged in the above that a hypOadrenal state would experience improved mood overall - hence even recovery in depressed patients, HOWEVER, the trade-off when comparing anti-E (provided you are going to resort to SERM use) isn't worth it.

i think i understand you here.
you are saying dhea use for cortisol suppression in the early stages of pct is unnecessary since cort levels are initially low?
what about later on when cort levels begin to climb?

Perhaps, because the protocol I'd employ is a reverse ramp with lowering the SERM while increasing the AI simultaneously. I know of no such studies suggesting interference between an AI and DHEA. Still, one could also suspect that the use of DHEA with adrenal recovery (about 2.5 weeks post-cycle in rather indiscriminate fashion verified by 24-hour urinary cortisol amongst a battery of challenge tests) would offer minimal in the realm of added benefit at that time also.

i thought only excess dhea in your system has the potential to convert to estrogen. if you are hpta suppressed with low dhea levels, wouldn't supplementing w/dhea (using only engough to bring levels up to normal) not directly translate to elevated estrogen levels?

Again, keep in mind this is an adrenal-predominate. The levels required and length of cycle for DHEA (especially for someone in an age less-than 65-70 years) has not nearly been scrutinized enough. In order to see significant effect, your oral dose has to be up there, but then consider blood sugar regulation, et al issues which would contribute to problems keeping gains into post-cycle as well.

This is so not as "easy" a science as coming up with the "one-size-fits-all" approach. The problem with this search is that it doesn't exist and a case-by-case basis is what we know best.

This is also, perhaps, one of the reasons these things will always be seen as problematic in any over-the-counter sense. And consumers/patients see the medical establishment as the "demon" rather than the industry because they're an easier conspiracy target. See, I agree that people should have the ability to take what they want, BUT I also am aware of an oath I signed to not watch people screw themselves up the process.



D_

[Xodus]

Originally Posted by dinoiii

Again, keep in mind this is an adrenal-predominate. The levels required and length of cycle for DHEA (especially for someone in an age less-than 65-70 years) has not nearly been scrutinized enough. In order to see significant effect, your oral dose has to be up there, but then consider blood sugar regulation, et al issues which would contribute to problems keeping gains into post-cycle as well.


D_

What about transdermal DHEA where you get closer to 30-40% availability vs. oral (~3%)?

[TheNoid]

Originally Posted by dinoiii

Mind you, my humor is pretty "raw" as I have been told, so you may not be dropping dead in laughter - but somewhere someone is laughing - probably me?!?

Usually just you and thesinner. And I guess me at your nerdly back and forth banter. lol jk

What's one of the sure-fire things we know about lipids during cycle? The quoted "deleterious" effects include: decreased HDL, increased LDL, increased Tot. Cholesterol, etc... However, knowing too that 99% of dyslipidemia is found at the level of the liver - meaning if we try and "treat" cholesterol issues, we are screwing up the fundamental endogenous correction factor put in place by the body to supply androgen substrate. IT IS THAT WAY FOR A REASON...high cholesterol is the origin of increased test - leave it alone, or you will have difficulty re-gaining control of endocrinologic balance -

Why then the recommendation of dyslipidemia modifying agents in your PCT series?

[dinoiii]

Originally Posted by Xodus

What about transdermal DHEA where you get closer to 30-40% availability vs. oral (~3%)?

No controlled setting under the same set of conditions unfortunately. Even the patent that exists for TD DHEA doesn't consider any condition that closely approximates post-cycle.


D_

[dinoiii]

Originally Posted by TheNoid

Usually just you and thesinner. And I guess me at your nerdly back and forth banter. lol jk

I get ole sinner over at my subforum too.

He brightens my day (I suppose the appropriate suggestion would be "no homo" inserted here, no?).

Why then the recommendation of dyslipidemia modifying agents in your PCT series?

Great question!

There are, for whatever reason, many people suffering from one of the inhereted five most clinically-significant dyslipidemia categorizations that opt to run cycles. For someone in this instance, keeping a close watch on said issues is and will forever be pertinent.

There are, also people that fall within the norm of the population that wind up clinically-affected in the aftermath of running a cycle. I am a fan of heavy niacin therapy through most cycles (keeping in mind the relatively distinct range of effective and lethal doses with C17-alkylated subset).

Few things this means: 1. an effective dose tends to fall over about an 800-1200mg mark for most people (I am aware this leaves wiggle room - most often in the case of volume of distribution adjustments), 2. hepatotoxic effects start cropping up at roughly 3 grams or so, 3. Concurrent run of suggestive hepatoprotective agents like SAMe and time differential dosing parameters. This too must be taken in stride as the primary derrangement is a HDL decrease. HDL's primary responsibility is to essentially remove LDL and Trigs from the system. If keeping HDL from dropping, LDL and Tot chol stay much closer to norm allowing for a more expedited course toward normal androgen precursor states. Directly lowering LDL is rarely my suggestion - hence my discussions on Red Yeast Rice and the lowly statin equivalents.



D_

[hardknock]

There are, for whatever reason, many people suffering from one of the inhereted five most clinically-significant dyslipidemia categorizations that opt to run cycles. For someone in this instance, keeping a close watch on said issues is and will forever be pertinent.

In saying that, are you saying that there are some people that have no apparent negative effects and are, basically, not affected by running cycles, no matter the toxicity of the "supp"?

[arizonanewbie]

Dinoiii, I think it is fantastic to have an actual medical professional dispensing careful analysis instead of the kind of anecdotes that are the usual stock in trade. But I have to add something here and pardon me if I offend. I understand that one of your paramount messages is that the science is often far more complicated and nuanced than people in the AAS culture assume. I also am not surprised to read in threads such as this that people have a hard time understanding your postings. I have to tell you, as a person with 5 years of post-BA education (including an MA in linguistics), your writing is often d@mn-near impenetrable. And I don't believe it is only because the science is complicated. Your sytax is sometimes hard to follow, like someone who learned German before English.

I feel frustrated because I know that buried in the text is the gem of biochemical knowledge that is going to save my testicles, but it is buried.

Nome sayn?

[dinoiii]

Originally Posted by hardknock

In saying that, are you saying that there are some people that have no apparent negative effects and are, basically, not affected by running cycles, no matter the toxicity of the "supp"?

I was actually referencing that someone with one of these disorders is actually further burdened by the addition of PH/PS/DeS/AAS.

In other words, they were already "screwed" and victims of their own pathology and the use of aides to keep these guys more in the normal range (whatever "normal" means) may be of benefit.

To the rest, probably no need for employment.


D_

[dinoiii]

Originally Posted by arizonanewbie

Dinoiii, I think it is fantastic to have an actual medical professional dispensing careful analysis instead of the kind of anecdotes that are the usual stock in trade. But I have to add something here and pardon me if I offend. I understand that one of your paramount messages is that the science is often far more complicated and nuanced than people in the AAS culture assume. I also am not surprised to read in threads such as this that people have a hard time understanding your postings. I have to tell you, as a person with 5 years of post-BA education (including an MA in linguistics), your writing is often d@mn-near impenetrable. And I don't believe it is only because the science is complicated. Your sytax is sometimes hard to follow, like someone who learned German before English.

I feel frustrated because I know that buried in the text is the gem of biochemical knowledge that is going to save my testicles, but it is buried.

Nome sayn?

I do see presence of the "feedback sandwhich" obviously suggesting you are a very educated individual with knowledge of how to critique.

-----------------------------------------------------------

[Aside to those reading along:

Feedback Sandwhich...
Positive Critique / Negative Critique / Positive Critique

In this case:
Medical Professional and analytic = Good
Syntax Sucks = Bad
Something will probably save my balls = Good]

-----------------------------------------------------------


In any event, I appreciate the critique and ask for people to question me as when I type 100s of things daily in this fashion, they must come out as relative stream-of-conscious posts fully entrenched with medical lingo. Still, if people don't ask, I presume all understood me loud and clear.


Now, I did address all of the above questions in turn. If there is something that still didn't make sense, please point it out.


D_