08-17-2005, 09:21 AM #1Associate Member
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- Oct 2001
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ultimate thread about natural test boosters/recoveries
What have you guys used in the past and at what doses....?
The three I can think of are:
Tribulus (1-4gs) daily
Tongkat Ali (Longjack, redkat, etc) ? daily
Avena Sativa ? daily
08-17-2005, 09:38 AM #2
Where is the ultimate thread about test boosters? I was expecting a good read or something.
08-18-2005, 04:39 PM #3
me too... BUMP for some info
08-18-2005, 05:16 PM #4
Originally Posted by juicy_brucy
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08-18-2005, 08:56 PM #5
This thread had real potential, too bad....
08-18-2005, 08:58 PM #6
08-19-2005, 10:11 AM #7Associate Member
Originally Posted by juicy_brucy
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08-19-2005, 10:25 AM #8Originally Posted by juicy_brucy
Me Too !
08-19-2005, 11:31 AM #9Originally Posted by juicy_brucy
08-19-2005, 11:31 AM #10
p.s. I dont believe in using natural test boosters. Seem's like too much of a rip-off.
08-19-2005, 11:31 AM #11
Ill start off then -
Test Boosters/ Support
Tribulus Terristris/horny goat weed - effective dose 500mg - 5g a day
Tongkat Ali/eurycoma longifolia/longjack - effective dose 500mg - 3g a day
Avena Sativa - 500mg - 5g a day
Yohimbe Bark extract (not yohimbine hcl) - effective dosage - 500mg- 3g a day
If every1 adds some info, then this may become a decent thread, ill post some articles and studies later, havent got time at the moment.
08-19-2005, 06:12 PM #12
Best Natural test booster
First well look at Tribulus this particular Suppliment is questionable although many take this root of a plant native to asia in terms of hopeing for test production The scientific evidence to back it up just isnt there.
I can say from personal experience that it does personally raise my libido but there is no way to really prove that it does this way by terms of raising LH hormone thus increasing testosterone production.Studies show that Tribulus acts as such a precursor to DHEA and the only real thing that can be determined is that it makes castrated rats really horny
But if you are going to use it in hopes of test production use it at a 5 Gram or higher dose to notice any significant effects.
Tongat Ali is a shrub tree that grows in maylasia which is mainly used as a male aphrodisiac which I will totally agree works for that purpose but is this because of a direct rise in Test levels again there is not enough scientific data to back this claim up
Take in 1-2 G doses
ZMA is next
Next we’ll take a look at ZMA, a combination of Zinc Monomethionine Aspartate (30mg), Magnesium Aspartate (450 mg) and Vitamin B-6 (10.5 mg). The theory behind ZMA is simple: zinc and magnesium are important in the production of steroids and B-6 is important in energy production, two things crucial to athletes. If you become deficient in any of the ingredients in ZMA you see a subsequent decrease in androgen production and performance in general--and there is evidence that a number of diets may be deficient in all three.
In vitro research clearly illustrates how supplementation with magnesium can decrease the amount of testosterone bound to human serum albumin, thus, increasing free testosterone.
Another interesting effect of both zinc and magnesium is their influence on cortisol secretion. A study conducted with oral dosages of zinc ranging from 25 mg to 50 mg showed an inhibitory affect on cortisol secretion over 240 minutes . This evidence suggests that ZMA supplementation could cause performance increases and an increase in testosterone via the decrease of the catabolic hormone cortisol.
From all of the research available today ZMA can offer a raise in testosterone to sunjects with deficient levels. But the likelihood of raising testosterone production above physiological maximums seems unlikely.So supplimenting with ZMA should be used IMO as more of a prevention method to ensure peak testosterone levels are maintained.
Then we are left with Androstenetrione.
Androstenetrione marketed by Ergopharm under 6-oxo works as a suicide inhibitor to aromatase. Aromatase is the enzyme responsible for converting Testosterone into Estrogen. Now the theory here is clear, reduce enough estrogen in the hypothalumus and the body will try and counteract this by producing more androgens which are the precursors to estrogen. This is the bodys only way at producing a high level of estrogen is to produce more testosterone in order to aromatase into estrogen.
But 6oxo is old news compared to the new legal ********* AIs mainly the ATD products these are found in Designer supps Rebound XT gasparis novedex xt and ALRIs ultra hotter. This is an extremely potent product and way better than 60x0
Now there is a new gem on the market that is currently on its beta testing phase it is called AcTivaTe and is being marketed by Designer Suppliments although this product does not directly increase Testosterone production it does increase actual useable test in the body by binding to SHBG to acheive more free test and therfore create an environment for enhanced muscle growth.
There are 4 proteins that testosterone can be bound to...they include:
OR the testosterone can be a free/unbound hormone.
Both free/unbound and albumin bound testosterone are biologically active, which is comprised of 33 to 54% of the total circulating testosterone. The SHBG is not availiable for physiological use, which is comprised of 44 to 65% of circulating testosterone.
Transcortin is a corticosteroid binding globulin and when bound to testosterone is a measure of estrogenicity.
Transferrin increase is associated with estrogen excess.
As you age, there is a decrease in synthesis of androgens by the Leydig cells in the testes and the zona reticularis of the adrenal cortex, with a increase in SHBG production by the liver.
What we primarly want to do is lower SHBG levels or prevent them from binding to testosterone and increase the free/unbound testosterone and the albumin bound testosterone.
Here is a graph showing how the product works
taken from Myostatin on *************
So Trib really has no scientific data to back up the claims of increased test production
ZMA should be used more as a prevention method to ensure that optimal levels of test are maintained.
And Androstenetrione shows the most promise for actually increasing ones test levels beyond normal parameters.
So the key palyers here are activaTe by Designer supps and either a traditional AI ie arimidex /femara/aromasin
or the legal OTC versions ie 6oxo or even better Rebound XT
The use of an AI will allow for higher than normal consentrations of testosterone production and the use of ActivaTe will make it so you can actually use more of the the increased testosterone for muscle building purposes!!!
08-20-2005, 02:24 AM #13
Thanks Bryan2. That's all anyone needs to know. One question though, how long can someone take an AI with ActivaTE and still be safe? (ie. not screwing up lipid profile, etc)
08-20-2005, 04:01 AM #14
Well as with everything the body tends to become adjusted to it and people loos results
As far as the lipid profile concerns some may not even see a change and some may who knows but either way I would limit cycles to 2 months and take a proportionate time off to get your body back into normal mode.
09-07-2005, 05:02 PM #15
I just tried that 6oxo. I really liked it. Felt like I got stronger. I tried Acetobolan by MuscleTech in the past but didn't really feel like I benefitted at all from it. Has anyone tried Anavol or any of the other NX mass supps ?
09-07-2005, 07:57 PM #16
Not really sure if these were mentioned but Fenugreek, maca and 200mg of dhea. I've heard good things running these in pct along with nolva and clomid.
09-08-2005, 09:17 PM #17
wow bryan... good post... i appreciate it man. i think i'm gonna get some activate now. thanx for giving me a reason to spend that loose change that is burning a hole in my pocket. ha ha
09-08-2005, 09:21 PM #18
Yeah only probl;em is they are waiting on the final version to be put out which will take them a while to source for raw materials
the reps estimate around a months timeframe from now
09-11-2005, 04:26 PM #19
Tribulus only works as an androgen and has no anabolic properties.
ZMA might work but not because of a debatable raise of testosterone , but because zinc lowers the affinity of cell-associated IGFBP's, and increases the affinity of the cell surface insulin -like growth factor-type 1 receptor (IGF-1R).
Zinc draws IGF-1 away from IGFBP's and makes it more available.
Nolvadex and HCG will help restore natural testosterone PCT, whereas clomid will not.
Femara/Aromasin and arimidex will not bring back natural testosterone in any way but will make estrogen-receptors more sensitive to estrogen for some months following discontinued use. Therefore (and for some other reasons) nolvadex is the better choice over femara/arimidex/aromasin to use as an estrogen blocker during a cycle.
09-11-2005, 04:33 PM #20Originally Posted by big'r
09-11-2005, 05:09 PM #21
sorry but your info is off big'r
09-11-2005, 05:09 PM #22
I don't think i have to get into the HCG part.
As for the nolvadex over clomid thing:
So which one should you use? Well personally, I'd have to say Nolvadex. Both as an on-cycle anti-estrogen and a post-cycle therapy. As an anti-estrogen its simply much stronger, demonstrated by the fact that better results are obtained with 20-40 mg than with 100-150 mg of clomid. For post-cycle, this plays a key role as well. It deactivates rebound estrogen much faster and more effective. But most importantly, Nolvadex has a direct influence on bringing back natural testosterone, where as clomid may actually have a slight negative influence. The reason being that Tamoxifen (as in Nolvadex) seems to increase the responsiveness of LH (luteinizing hormone) to GnRH (gonadtropin releasing hormone), whereas clomid seems to decrease the responsiveness a bit1.
Nolvadex has a few properties femara and the like don't have:
-Improves lipid profile.
-Actually does something against gyno, anti-a's do not prevent it.
-Will put less strain on the axis.
09-11-2005, 05:12 PM #23
Clomid still works to restore hpta i wouldnt use it.....but it does still work
09-11-2005, 05:13 PM #24
09-11-2005, 05:14 PM #25Originally Posted by bignatt
09-11-2005, 05:19 PM #26
in that article it even say that clomid works just that nolva is better which i totally agree on but to say that clomid doesnt work is just false
09-11-2005, 05:23 PM #27Originally Posted by bignatt
I meant in bringing back natural test bro. Not in blocking estrogen....
09-11-2005, 05:23 PM #28
I am not sure how Clomid and Nolvadex became so separated in the minds of bodybuilders. They certainly should not be. Clomid and Nolvadex are both anti-estrogens belonging to the same group of triphenylethylene compounds. They are structurally related and specifically classified as selective estrogen receptor modulators (SERMs) with mixed agonistic and antagonistic properties. This means that in certain tissues they can block the effects of estrogen, by altering the binding capacity of the receptor, while in others they can act as actual estrogens, activating the receptor. In men, both of these drugs act as anti-estrogens in their capacity to oppose the negative feedback of estrogens on the hypothalamus and stimulate the heightened release of GnRH (Gonadotropin Releasing Hormone). LH output by the pituitary will be increased as a result, which in turn can increase the level of testosterone by the testes. Both drugs do this, but for some reason bodybuilders persist in thinking that Clomid is the only drug good at stimulating testosterone. What you will find with a little investigation however is that not only is Nolvadex useful for the same purpose, it should actually be the preferred agent of the two.
Studies conducted in the late 1970's at the University of Ghent in Belgium make clear the advantages of using Nolvadex instead of Clomid for increasing testosterone levels (1). Here, researchers looked the effects of Nolvadex and Clomid on the endocrine profiles of normal men, as well as those suffering from low sperm counts (oligospermia). For our purposes, the results of these drugs on hormonally normal men are obviously the most relevant. What was found, just in the early parts of the study, was quite enlightening. Nolvadex, used for 10 days at a dosage of 20mg daily, increased serum testosterone levels to 142% of baseline, which was on par with the effect of 150mg of Clomid daily for the same duration (the testosterone increase was slightly, but not significantly, better for Clomid). We must remember though that this is the effect of three 50mg tablets of Clomid. With the price of both a 50mg Clomid and 20mg Nolvadex typically very similar, we are already seeing a cost vs. results discrepancy forming that strongly favors the Nolvadex side.
Pituitary Sensitivity to GnRH
But something more interesting is happening. Researchers were also conducting GnRH stimulation tests before and after various points of treatment with Nolvadex and Clomid, and the two drugs had markedly different results. These tests involved infusing patients with 100mcg of GnRH and measuring the output of pituitary LH in response. The focus of this test is to see how sensitive the pituitary is to Gonadotropin Releasing Hormone. The more sensitive the pituitary, the more LH will be released. The tests showed that after ten days of treatment with Nolvadex, pituitary sensitivity to GnRH increased slightly compared to pre-treated values. This is contrast to 10 days of treatment with 150mg Clomid, which was shown to consistently DECREASE pituitary sensitivity to GnRH (more LH was released before treatment). As the study with Nolvadex progresses to 6 weeks, pituitary sensitivity to GnRH was significantly higher than pre-treated or 10-day levels. At this point the same 20mg dosage was also raising testosterone and LH levels to an average of 183% and 172% of base values, respectively, which again is measurably higher than what was noted 10 days into therapy. Within 10 days of treatment Clomid is already exerting an effect that is causing the pituitary to become slightly desensitized to GnRH, while prolonged use of Nolvadex serves only to increase pituitary sensitivity to this hormone. That is not to say Clomid won't increase testosterone if taken for the same 6 week time period. Quite the opposite is true. But we are, however, noticing an advantage in Nolvadex.
The Estrogen Clomid
The above discrepancies are likely explained by differences in the estrogenic nature of the two compounds. The researchers' clearly support this theory when commenting in their paper, "The difference in response might be attributable to the weak intrinsic estrogenic effect of Clomid, which in this study manifested itself by an increase in transcortin and testosterone/estradiol-binding globulin [SHBG] levels; this increase was not observed after tamoxifen treatment". In reviewing other theories later in the paper, such as interference by increased androgen or estrogen levels, they persist in noting that increases in these hormones were similar with both drug treatments, and state that," …a role of the intrinsic estrogenic activity of Clomid which is practically absent in Tamoxifen seems the most probable explanation".
Although these two are related anti-estrogens, they appear to act very differently at different sites of action. Nolvadex seems to be strongly anti-estrogenic at both the hypothalamus and pituitary, which is in contrast to Clomid, which although a strong anti-estrogen at the hypothalamus, seems to exhibit weak estrogenic activity at the pituitary. To find further support for this we can look at an in-vitro animal study published in the American Journal of Physiology in February 1981 (2). This paper looks at the effects of Clomid and Nolvadex on the GnRH stimulated release of LH from cultured rat pituitary cells. In this paper, it was noted that incubating cells with Clomid had a direct estrogenic effect on cultured pituitary cell sensitivity, exerting a weaker but still significant effect compared to estradiol. Nolvadex on the other hand did not have any significant effect on LH response. Furthermore it mildly blocked the effects of estrogen when both were incubated in the same culture.
To summarize the above research succinctly, Nolvadex is the more purely anti-estrogenic of the two drugs, at least where the HPTA (Hypothalamic-Pituitary-Testicular Axis) is concerned. This fact enables Nolvadex to offer the male bodybuilder certain advantages over Clomid. This is especially true at times when we are looking to restore a balanced HPTA, and would not want to desensitize the pituitary to GnRH. This could perhaps slow recovery to some extent, as the pituitary would require higher amounts of hypothalamic GnRH in the presence of Clomid in order to get the same level of LH stimulation.
Nolvadex also seems preferred from long-term use, for those who find anti-estrogens effective enough at raising testosterone levels to warrant using as anabolics. Here Nolvadex would seem to provide a better and more stable increase in testosterone levels, and likely will offer a similar or greater effect than Clomid for considerably less money. The potential rise in SHBG levels with Clomid, supported by other research (3), is also cause for concern, as this might work to allow for comparably less free active testosterone compared to Nolvadex as well. Ultimately both drugs are effective anti-estrogens for the prevention of gyno and elevation of endogenous testosterone, however the above research provides enough evidence for me to choose Nolvadex every time.
bottom line is you need either one of them for postcycle therapy ideally both.like he said Nolvadex would seem to provide a better and more stable increase in testosterone levels, and likely will offer a similar or greater effect than Clomid for considerably less money.
oc Natl Acad Sci USA 76:4460-3
09-11-2005, 05:31 PM #29
Whoops. We're double-posting now. But here it comes for this thread:
The administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). However, whereas Clomid produced a decrease in the LH response to LH-releasing hormone (LHRH), no such effect was seen after the administration of tamoxifen. In fact, prolonged treatment (6 weeks) with tamoxifen significantly increased the LH response to LHRL. Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels. A significant increase in sperm density was observed only in subjects with oligospermia below 20 X 10(6)/ml and normal basal FSH levels. When basal FSH levels were increased or oligospermia was moderate (greater than 20 X 10(6)/ml); no effect on sperm density was seen. As sperm density increased, FSH levels decreased, suggesting an inhibin effect. Sperm motility was not improved by tamoxifen treatment. In five boys with delayed puberty, tamoxifen treatment appeared to activate the pituitary-gonadal axis and pubertal development.
09-11-2005, 05:37 PM #30
refer back to the other thread for my response
09-11-2005, 07:50 PM #31
Estrogen suppression in males: metabolic effects.
Mauras N, O'Brien KO, Klein KO, Hayes V.
Nemours Research Programs at the Nemours Children's Clinic, Jacksonville, Florida 32207, USA. email@example.com
We have shown that testosterone (T) deficiency per se is associated with marked catabolic effects on protein, calcium metabolism, and body composition in men independent of changes in GH or insulin -like growth factor I production. It is not clear,,however, whether estrogens have a major role in whole body anabolism in males. We investigated the metabolic effects of selective estrogen suppression in the male using a potent aromatase inhibitor, Arimidex (Anastrozole). First, a dose-response study of 12 males (mean age, 16.1 +/- 0.3 yr) was conducted, and blood withdrawn at baseline and after 10 days of oral Arimidex given as two different doses (either 0.5 or 1 mg) in random order with a 14-day washout in between. A sensitive estradiol (E2) assay showed an approximately 50% decrease in E2 concentrations with either of the two doses; hence, a 1-mg dose was selected for other studies. Subsequently, eight males (aged 15-22 yr; four adults and four late pubertal) had isotopic infusions of [(13)C]leucine and (42)Ca/(44)Ca, indirect calorimetry, dual energy x-ray absorptiometry, isokinetic dynamometry, and growth factors measurements performed before and after 10 weeks of daily doses of Arimidex. Contrary to the effects of T withdrawal, there were no significant changes in body composition (body mass index, fat mass, and fat-free mass) after estrogen suppression or in rates of protein synthesis or degradation; carbohydrate, lipid, or protein oxidation; muscle strength; calcium kinetics; or bone growth factors concentrations. However, E2 concentrations decreased 48% (P = 0.006), with no significant change in mean and peak GH concentrations, but with an 18% decrease in plasma insulin-like growth factor I concentrations. There was a 58% increase in serum T (P = 0.0001), sex hormone-binding globulin did not change, whereas LH and FSH concentrations increased (P < 0.02, both). Serum bone markers, osteocalcin and bone alkaline phosphatase concentrations, and rates of bone calcium deposition and resorption did not change. In conclusion, these data suggest that in the male 1) estrogens do not contribute significantly to the changes in body composition and protein synthesis observed with changing androgen levels; 2) estrogen is a main regulator of the gonadal-pituitary feedback for the gonadotropin axis; and 3) this level of aromatase inhibition does not negatively impact either kinetically measured rates of bone calcium turnover or indirect markers of bone calcium turnover, at least in the short term. Further studies will provide valuable information on whether timed aromatase inhibition can be useful in increasing the height potential of pubertal boys with profound growth retardation without the confounding negative effects of gonadal androgen suppression.
AIs work to increase testoserone product just as SERMS do. SERMs have the advantage over AIs in that they improve lipid levels wereas AIs "can" continue to hurt them.
Both work by sending a message to the HPTA that there is not enough estrogen wether it be by blocking the aromatise enzyme and not haveing total estrogen in the body, Or by having a synthetic weaker estrogen block the actual receptor and trick it into thinking the body doesnt have enough estrogen.
The body trys to produce more estrogen through raising testosterone levels in order for it to aromatase into estrogen
09-13-2005, 04:01 PM #32
Whoopsie, so my info was off afterall.
Sorry guys, but i get my info from dutch boards most of the time. I never read any info there about arimidex /femara helping to get the axis back up.
I did a thorough pubmed search regarding anastrozole/letrozole and LH and now definitely have to conclude you're right.
So thanx Bryan2 for the info and the link.
What they stated on my board was the following:
When on an cycle using AAS combined with an AI, the AI would drop your axis even more during and following your PCT.
The reason was that an AI would make your receptors more sensitive + you would get a temporary upregulation of estrogen receptors (because of the aromatase enzym). This would lead to more estrogen and less testosterone . The discussion was very interesting i'd have to say between 2 biochemists.
But none of them ever brought up the fact AI's would boost LH/FSH levels DURING a cycle.
In the light of this information i had to draw my conclusions. Convinced AI's would put pressure up the axis even more for at least 6 months following a cycle (this might possibly still be true), i concluded not to make AI's my friend. But i missed the point AI's would keep LH/FSH levels normal during a cycle.
09-13-2005, 05:41 PM #33
Well it wont help during aycle to keep your test levels in check once your shut down your shutdown no way around it.
But during PCT an AI will lead to a raise in test levels after exogenous hormones are ceased.
And using an AI does not really lead to an upregulation of estrogen receptors too much if even a noticable difference
The main problem is that after suppression of the aromatase enzyme for a long time or high percentage the body trys to make more aromatase enzyme because it realizes that it is being blocked.
So after discontinuing an AI abruptly the body will produce much more than normal ranges of aromatase enzyme causing excess estrogen leading to unwanted sides.
This is why one should always tapper down off of an AI.
AIs solo apart from exogenous androgens are a safe(minus the possible lipid effects) an effective way to raise test levels without any effect to the HPTA at all.
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