**MAXIMIZE Your STEROIDS: ULTIMATE Anabolic SECRETS!**
07-16-2006 02:52 AM
07-16-2006 02:53 AM
Post a few studies showing that testosterone administration doesnt negatively affect lipids. I have posted t othe contrary.
Originally Posted by The Master
Please post something to back your claim that 'some steroids do not affect HPTA'.
Edit: sorry, did not see previous post about HPTA. It is important to note, however, that these patients had testicular failure.
07-16-2006 02:56 AM
Originally Posted by canadian champ
NOT ALL ANDROGENS CAUSE SHUTDOWN*
"Shutdown", is defined by a COMPLETE inhibition of the Pituitary/Testes, resulting in a TOTAL cessation of endogenous androgen production.
SOME androgens will only SUPPRESS endogenous androgen production, resulting in a DECREASED testosterone level, but not a complete shutdown. (Tbol, Var, Wistrol, EQ, Dianabol, masteron, proviron, halo, primo)
Very Androgenic/Progestenic/Estrogenic steroids(Tren, Deca, Drol, Test) cause a COMPLETE shutdown of endogenous hormone production.
The distinction between SUPRESSION and SHUTDOWN is utterly important, as steroids that cause LESS supression of endogenous hormones will allow for greater retention of gains upon ending the cycle, and a quicker, easier post cycle therapy.
Horm Metab Res. 1984 Sep;16(9):492-7.Related Articles, Links
Effect of non aromatizable androgens on LHRH and TRH responses in primary testicular failure.
Spitz IM, Margalioth EJ, Yeger Y, Livshin Y, Zylber-Haran E, Shilo S.
We have assessed the gonadotropin, TSH and PRL responses to the non aromatizable androgens, mesterolone and fluoxymestrone, in 27 patients with primary testicular failure. All patients were given a bolus of LHRH (100 micrograms) and TRH (200 micrograms) at zero time. Nine subjects received a further bolus of TRH at 30 mins. The latter were then given mesterolone 150 mg daily for 6 weeks. The remaining subjects received fluoxymesterone 5 mg daily for 4 weeks and 10 mg daily for 2 weeks. On the last day of the androgen administration, the subjects were re-challenged with LHRH and TRH according to the identical protocol. When compared to controls, the patients had normal circulating levels of testosterone, estradiol, PRL and thyroid hormones. However, basal LH, FSH and TSH levels, as well as gonadotropin responses to LHRH and TSH and PRL responses to TRH, were increased. Mesterolone administration produced no changes in steroids, thyroid hormones, gonadotropins nor PRL. There was, however, a reduction in the integrated and incremental TSH secretion after TRH. Fluoxymesterone administration was accompanied by a reduction in thyroid binding globulin (with associated decreases in T3 and increases in T3 resin uptake). The free T4 index was unaltered, which implies that thyroid function was unchanged. In addition, during fluoxymesterone administration, there was a reduction in testosterone, gonadotropins and LH response to LHRH. Basal TSH did not vary, but there was a reduction in the peak and integrated TSH response to TRH. PRL levels were unaltered during fluoxymesterone treatment.(ABSTRACT TRUNCATED AT 250 WORDS
07-16-2006 02:56 AM
I'm unclear why you came back after being made a fool the last time around. Bobo WILL ban you again. But for the sake of arguing I would like some proof of the following:
Originally Posted by The Master
1. Proof that lipid values will not be extremely poor if one follows you 3 on/1 off for AIs. I would like this in HUMAN MALES. As last time you did nothing but post studies of castrated rates you found on pubmed.
2. Proof that the front loading of EQ would not cause a significant rise in total serum blood levels fast enough to show its power in less than 12 weeks.
3. Proof that Primo builds muscle in a caloric deficit and more importantly proof that Tren does not do the same.
4. Proof the of superiority of AI's over serms when following a non-aromatizing steroid protocal. Seems like crushing estrogen that isn't even present would cause more problems then any extra benefits one might recieve.
If anyone wants to do more research on this guy look around for a guy called "The Mind of Ross."
07-16-2006 02:59 AM
Last time I checked, most of us did not have "primary testicular failure", so this really isnt relavent.
Originally Posted by The Master
07-16-2006 03:03 AM
Originally Posted by aspire210
This demonstrates your complete lack of understanding for scientific material.
07-16-2006 03:11 AM
1.) Aromasin has even been shown to exhibit a positive effect on blood lipids. You should be FINE using my protocol in my suggested DOSAGE.(12mgs ED)
Originally Posted by aspire210
2.) LOL--LEARN your CHEMISTRY buddy. With an Undeclynate ester, this is NOT POSSIBLE. You will however have ridiculous PEAK blood levels if you TRY this, and I would NOT SUGGEST it. Talk about BLOOD PRESSURE!
3.) You need PROOF that primo(Methenolone) builds muscle in a calorie defecit? LOL--everyone knows this, but I WILL dig up the study. And as for TREN; it has NOT been demonstrated, but--yes, I would agree that being 3 times more ANABOLIC than TEST and 4 times more androgenic, Tren could build muscle in a calorie defecit, so long as sufficient protein were present.
4.) SERMS do NOTHING to REDUCE ESTROGEN! Aromatase Inhibitors BLOCK the FORMATION of estrogen via inhibiting the ENZYME responsible for the CONVERSION of androgens to estrogens--AROMATASE. They also DRASTICALLY increase endogenous testosterone production, and even increase FREE test.
07-16-2006 03:46 AM
JornT, is that you?
07-16-2006 03:49 AM
ok, I appreciate debates, by why are you yelling?
You should also know that your use of HCG during PCT is suppressive in itself... you are mimicking LH, so in a sense taking a step out of the HPTA recovery... do you agree?
07-16-2006 03:53 AM
07-16-2006 03:54 AM
Originally Posted by Ubiquitous
HCG is used CLINICALLY to treat HYPGONADISM--and SECONDARY hypogonadism.
The problem with HCG is OVER-USE. This could potentially lead to a desensitization of your leydig cells to Lh/FSH signal.
I, however, CYCLE year-round.
07-16-2006 04:17 AM
I tried to keep this short butÖ.
Test prop is a good ester but most effective is not the term I would use. Requires more injections is not a benefit for most people, the trauma of injects add up. Scar tissue is a real concern. There really isnít such a thing as a stable blood level, what you mean here is that there is a very even release from the depot. Free test in the blood is only an indirect indicator of what is going on. If it was that important you could inject a long ester ED or EOD and get extremely even release of the hormones. The fact that youíre using prop for this type of dosing is irrelevant. Test base (suspension), acetate, benzoate, formate , and phenol propionate would all do the same. And again it comes at a cost. So does using any drug for that matter, they all have side affects. There is nothing for free. And HPTA recovery is only quicker because its out of your system quicker, running test prop or transdermal test for the last two weeks of your cycle will work just as well. Bulking and cutting are functions of your diet, not the drug you use. While some are better then others almost all will work for both.
AIs should not be run unless really needed. They hurt more then they help. Lipid profiles, ED problems and other side affects make these somewhat questionable for a lot of cycles let alone when youíre off. Off is off or should be.
All steroids shut you down, even if it does not affect all parts of the HPTA. It only has to shut down one part. AND I CANíT BELIEVE THAT YOU ARE ACTUALLY PERPOSING THAT A 17A METHYLATED STEROID CAN BE RAN LONGER THEN TEST. I am sorry that is just stupid.
Youíre partaully right on the EQ, it does take a while to kick in even when frontloading. However front loading DOES speed the things up by at least half. And EQ does shut you down and it has its own set of sides even if they are mild.
This no side affects business is getting old, primo does have sides, yes its nice but its mild and very expensive for what it does.
The first two reasons for spot injections (winny) working are things you donít want; they cause damage and scar tissue.
Sure you can stack two methylate steroids together. I mean, what has your liver done for you lately? Itís all over rated. But wouldnít moderation be just using one oral steroid and not pushing it?
You need estrogen. And the whole point of a SERM is that they allow estrogen to form. And no they do not affect the effectiveness of the AIs, ( I also thought that until someone showed me better info on that, sorry bro I canít think of your name) And there are dangerous? But running two orals steroids together is not?
07-16-2006 04:39 AM
Binging on Pure ****ing Rage
Originally Posted by Skye
I was waaaaaay too lazy to respond to this fella, but nice post. It might have been me, I posted a couple studies showing Novladex and Letro had no adverse effects on the pharmacokinetics of the other.
07-16-2006 05:59 AM
FIRST of all....
Originally Posted by Skye
It is impossible to achieve completely stable blood levels with long esters like Enanthate or cypionate. This is simple CHEMISTRY and the nature of esters. TONS of personal and ancedotal evidence ALL indicate that side-effects occur MUCH LESS FREQUENLTY when the PROPIONATE ester is administered.
Propionate will also allow for a quicker HPTA recovery because, as you mentioned, the ester clears the system faster. HOWEVER, this is not the ONLY reason....
REMEMBER--one can avoid total HPTA shutdown with propionate ester, by limiting cycle length to 2-6 weeks.* This CAN NOT be done with TEST SUSPENSION, becasue such a RAPID RELEASE triggers an IMMEDIATE negative feedback response, and PITUITARY INHIBITION occurs within a days. This makes PROP unique.
AND YES--PROP has virtually NO SIDE-EFFECTS.(relative to other test esters)
As for AROMATASE INHIBITORS--Most of thm are indeed, quite detrimental to blood lipid profiles. AROMASIN however, has been shown to even exhibit a POSITIVE effect on blood lipids*. using my PROTOCOLS is FINE.
NEXT--**NOT ALL STEROIDS CAUSE COMPLETE SHUTDOWN**!! This is a HUGE misconception! *The HPTA is NOT A SINGLE ENTITY!**
"The hypothalamic-pituitary-testicular axis (also HPTA) is a way of referring to the combined effects of the hypothalamus, pituitary gland, and gonads as if these individual endocrine glands were a single entity. Because these glands often behave in cooperation, physiologists and endocrinologists find it convenient and descriptive to speak of them as a single system.
You ADMIT that I am correct about EQ.
you admit that PRIMO is great.
You are WRONG about ESTROGEN being NEEDED! No male needs estrogen buddy. The REQUIRED amount of estrogen for healthy male function(glucose uptake, nutreint metabolism, bone/joint lubrication, cholesterol) is VERY MINIMAL. ALL BODYBUILDERS who are SERIOUS about maintaining MUSCLE will use an AI year round in the protocol I described above.
AND YES--Steroid HEPATOXICITY is WAAAAY OVERSTATED--FACT. Just look at SUPERDROL or PP. I have had many clients of mine run 17-aa for extended periods of time. SO LONG AS YOU MONITOR YOUR HEALTH and receieve REGULAR BLOOD TESTS, you are fine.
07-16-2006 07:11 AM
191cm, 98kg (6'3, 215lb)
Clomid and Nolvadex should not be used by bodybuilders.
Plain and simple:
* They are NOT NECESSARY
* Aromatase Inhibitors STOP estrogen production--SERM's do NOT.
* They DECREASE the effectiveness of AROMATASE INHIBITORS when administered together!
* They are Dangerous. (long-term)
* They do NOTHING to reduce estrogen.
* They cause a direct REBOUND effect upon cessation.
* Not worth it for it's effect on LH--testosterone production.
* Disturbs VISION PERMANENTLY!
Show me evidence that a SERM screws with an AI when used in PCT please?
Actually, by inhibiting the effects of estrogen in certain tissues (breast for instance with Nolva), they are combating the effects of estrogen.
Show me studies that show a redbound effect?
They have been clinically proven to increase natural testosterone production and testicular function.
Clomid is the only SERM that has shown to disturb vision, and that is after long term use (over 4 weeks).
07-16-2006 07:16 AM
Rationale for the Use of Aromasin with Tamoxifen During Post Cycle Therapy
(By Anthony Roberts)
Discussion of pharmaceutical agents below is presented for information only. Nothing here is meant to take the place of advice from a licensed health care practitioner. Consult a physician before taking any medication.
Aromasin (Exemestane) is one of those weird compounds that nobody really knows what to do with. What we generally hear about it makes it very uninterestingÖItís a third generation Aromatase Inhibitor (AI) just like Arimidex (Anastrozole) and Femera (Letrozole). Both of those two drugs are very efficient at stopping the conversion of androgens into estrogen, and since we have them, why bother with Aromasin? Itís a little harder to get than the other two commonly used aromatase inhibitors, because itís not in high demand, and thereís never been a readily apparent advantage to using it. And I meanÖlets face it: Itís awkward-sounding. Aromasin doesnít have much of a ring to it, and exemestane is even worse. Arimidex has a bunch of cool abbreviations ("A-dex" or just Ďdex) and even Letrozole is just "Letro" to most people. Whereís the cool nickname for
Aromasin/exemestane? A-Sin? E-Stane? It just doesnít work. Itís the black sheep of AIs. And why do we even need it when we have Letrozole, which is by far the most efficient AI for stopping aromatization (the process by which your body converts testosterone into estrogen)? Letro can reduce estrogen levels by 98% or greater; clinically a dose as low as 100mcgs has been shown to provide maximum aromatase inhibition (2)!
So why would we need any other AIs? Well, first of all, estrogen is necessary for healthy joints (3) as well as a healthy immune system (4). So getting rid of 98% of the estrogen in your body for an extended period of time may not be the best of ideas. This may be useful on an extreme cutting cycle, leading up to a bodybuilding contest, or if you are particularly prone to gyno, but certainly canít be used safely for extended periods of time without compromising your joints and immune system.
That leaves us with Arimidex, which isnít as potent as Letrozole, but at .5mgs/day will still get rid of around half (50%) of the estrogen in your body. Problem solved, right? Use Arimidex on your typical cycles, and if you are very prone to gyno or are getting ready for a contest, use Letro.
But what about Post Cycle Therapy (PCT)?
I think at this point most people are sold on the use of Nolvadex (Tamoxifen Citrate) instead of Clomid for post cycle therapy (PCT), since both compete estrogen at the receptor site, both increase serum test levels, and both drugs may also alter blood lipid profiles favorably [B](6). But since 20mgs of Tamoxifen is equal to 150mgs of clomid for purposes of testosterone elevation, FSH and LH, but Tamoxifen doesnít decrease the LH response to LHRH (6) I think most people agree to Nolvadexís superiority for PCT.[/B]
Aromasin with Nolvadex
Iíve always been in favor of using Nolvadex during PCT, along with an AI, because reducing estrogen levels has been positively correlated with an increase in testosterone (7) so in my mind, itís be beneficial to increase testosterone by as many mechanisms as possible while trying to recover your endogenous testosterone levels after a cycle. SO which AI do we use? Letro or A-dex? Well, why donít we just keep using whichever one we used during the cycle, and add in some Nolvadex? Unfortunately, Nolvadex will significantly reduce the blood plasma levels of both Letrozole as well as Arimidex (8). So if we choose to use one of them with our Nolvadex on PCT, weíre throwing away a bit of money as the Nolvadex will be reducing their effectiveness.
This, of course, is where Aromasin comes in, at 20-25mgs/day.
Aromasin, at that dose, will raise your testosterone levels by about 60%, and also help out your free to bound testosterone ratio by lowering levels of Sex Hormone Binding Globulin (SHBG), by about 20% (12)ÖSHBG is that nasty enzyme that binds to testosterone and renders it useless for building muscle. But what about using it along with Nolvadex for PCT?
Difference Between Type-I and Type-II Aromatase Inhibitors
To understand why Aromasin may be useful in conjunction with Nolvadex while both Letro and A-dex suffer reduced effectiveness, weíll need to first understand the differences between a Type-I and Type-II Aromatase Inhibitor. Type I inhibitors (like Aromasin) are actually steroidal compounds, while type II inhibitors (like Letro and A-dex) are non-steroidal drugs. Hence, androgenic side effects are very possible with Type-I AIs, and they should probably be avoided by women. Of course, there are some similarities between the two types of AIsÖboth type I & type II AIs mimic normal substrates (essentially androgens), allowing them to compete with the substrate for access to the binding site on the aromatase enzyme. After this binding, the next step is where things differ greatly for the two different types of AIís. In the case of a type-I AI, the noncompetitive inhibitor will bind, and the enzyme initiates a sequence of hydroxylation; this hydroxylation produces an unbreakable covalent bond between the inhibitor and the enzyme protein. Now, enzyme activity is permanently blocked; even if all unattached inhibitor is removed. Aromatase enzyme activity can only be restored by new enzyme synthesis. Now, on the other hand, competitive inhibitors, called type II AIís, reversibly bind to the active enzyme site, and one of two things can happen: 1.) either no enzyme activity is triggered or 2.) the enzyme is somehow triggered without effect. The type II inhibitor can now actually disassociate from the binding site, eventually allowing renewed competition between the inhibitor and the substrate for binding to the site. This means that the effectiveness of competitive aromatase inhibitors depends on the relative concentrations and affinities of both the inhibitor and the substrate, while this is not so for noncompetitive inhibitors. Aromasin is a type-I inhibitor, meaning that once it has done its job, and deactivated the aromatase enzyme, we donít need it anymore. Letrozole and Arimidex actually need to remain present to continue their effects. This is possibly why Nolvadex does not alter the pharmacokinetics of Aromasin (11).
Before we close the book on Aromasin, itís worth noting that you can (and should) still use one of the non-steroidal AIs during your cycle to reduce estrogen, if necessary. When you are ready for PCT, you can then switch over to Aromasin and still experience the full effects of an AI, since there is no cross-over tolerance experienced between steroidal and non-steroidal AIs (9). Since Aromasin is about 65% efficient at suppressing estrogen (10), itís certainly a very powerful agent, especially considering you wonít experience reduced effectiveness because of your concurrent use of Nolvadex or from any sort of tolerance developed by using other AIs on your cycle(9). There is also a decent amount of preclinical data suggesting that Aromasin has a beneficial effect on bone mineral metabolism that is not seen with non-steroidal agents, and it may also have beneficial effects on lipid metabolism that are not found in the non-steroidal Letro and A-dex (9).
Finally, as weíre going to be using Nolvadex for PCT anyway, and we ought to be using an AI with it for maximum recoveryÖI think Aromasin- considering itís compatibility with Nolvadex and beneficial effects on bone mineral content and lipid profile, has finally stopped being the black sheep of AIs and found a home in our cycles.
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[Clinical aspects of estrogen and bone metabolism] Clin Calcium. 2002 Sep;12(9):1246-51. Japanese.
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J Clin Endocrinol Metab. 2004 Mar;89(3):1174-80
.J Steroid Biochem Mol Biol. 2001 Dec;79(1-5):85-91.
The Oncologist, Vol. 9, No. 2, 126Ė136, April 2004
Zilembo N., Noberasco C., Bajetta E., Martinetti A., Mariani L., Orefici S. Endocrinological and clinical evaluation of exemestane, a new steroidal aromatase inhibitor. Br. J. Cancer, 72: 1007-1012, 1995
Clinical Cancer Research Vol. 10, 1943-1948, March 2004
The Journal of Clinical Endocrinology & Metabolism Vol. 88, No. 12 5951-5956
Copyright © 2003 by The Endocrine Society
07-16-2006 07:17 AM
Nolvadex and Clomid are NOT neccessitated--even if they CAN increase endogenous testosterone production.
They are inferior to HCG/AI's at that too.
07-16-2006 07:18 AM
Should Nolvadex be Avoided at All Cost?
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Winstrol - Oral versus Injectable by Anthony Roberts (June 2006)
Anabolic Steroid Induced Hypogonadism by Michael Scally, MD (April 2006)
Designing an Anabolic Steroid Cycle by Anthony Roberts (March 2006)
Should Nolvadex be Avoided at All Cost? by Dharkam (January 30, 2006)
Masteron As An Anti-Estrogen by Anthony Roberts (January 23, 2006)
Steroids and Red Blood Cells by William Llewellyn (January 3, 2006)
Post Cycle Therapy (PCT) by Anthony Roberts (November 14, 2005)
Testosterone for Women: Waiting for the Female Aphrodisiac by John Hoberman, PhD (August 14, 2005)
Anabolic Steroids and Suicide: A Brief Review of the Evidence by Jack Darkes, PhD (July 19, 2005)
Dopers in Uniform - Cops on Steroids by John Hoberman, PhD (May 22, 2005)
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Publication Date: January 30, 2006
Nolvadex is the trade name of a drug containing a molecule called Tamoxifen. Its primary use by male bodybuilders is to prevent gynecomastia (the growth of the breast tissue). It was introduced by steroid guru Dan Duchaine 25 years ago. After a quarter of century, it is time for an update about its use. What I am going to demonstrate is it is high time to eliminate Nolvadex from the bodybuilder's drug stacks.
A Little Bit of History
Back in the late 70's, more and more bodybuilders developed strange lumps around their mammary glands. At first, no one really took notice but more and more competitors grew a gynecomastia. In 1981, the M Olympia had a pretty serious gyno. This was shortly after the introduction of this new drug by Dan Duchaine. At the time, it was a pretty good idea as no one else could came up with a solution in order to prevent this growing problem. Nolvadex was popularised by Dan's first Underground Steroid Handbook. Dan even states that "this drug has a lot of potential but hasn't been used enough yet to find it". After more than 25 years of intensive usage, it is my opinion that it is time to forget about Nolvadex. Why? First, because newer and more effective drugs have been developed. Second, because it seems obvious that Nolvadex impairs muscle growth.
Nolvadex and Muscle Growth
After so many years of usage, it seems pretty clear that if Tamoxifen helps prevent the growth of the nipples, it also weakens the anabolic properties of steroids in a majority of bodybuilders. We are frequently said that this weakening effect is due to the anti-estrogenic action of Nolvadex. According to the fantasy, muscles require both testosterone and estrogens to grow at an optimal rate.
This belief is derived from the results of studies showing that without estrogens, testosterone alone possesses minimal anabolic properties. By increasing the density of androgen receptors, estrogens render the muscles much more sensitive to testosterone (1). This has been demonstrated in a very specific muscle called the levator ani. But this muscle does not reflect what happens in the muscles bodybuilders are interested in (2). Estrogens have even been shown to reduce muscle fiber size (3-4). I think this effect of estrogens is closer to what we experience on bodybuilders.
Another popular explanation of the weakening action of Nolvadex is provided by studies which have shown that it reduced the plasma level of IGF-1. I do not think this is a primary explanation.
What Nolvadex Truly Is
Most lifters assume Nolvadex is a pure estrogen antagonist (which would mean it prevents estrogens from acting on their receptors). As far as bodybuilding is concerned, this assumption is very wrong as Nolvadex is both an estrogen receptor agonist and an antagonist. It all depends upon the tissues. Along with the nipples, on which Nolvadex acts mainly as an antagonist, we are also interested by its behaviour on skeletal muscles, on the liver and on the fat cells.
Nolvadex has been shown to behave as estrogens in skeletal muscles (5). This is a very good thing for every athletes except bodybuilders. You see, estrogens protect muscle cells from the training-induced damages (5-6). It means that one can train more without damaging his muscles. Recovery will also be much faster. But for bodybuilders, the training-induced damages are a key ingredient to trigger growth. Nolvadex will therefore reduce the muscle building effects of resistance training.
As for the impact of Tamoxifen on IGF-1, it simply demonstrates another estrogen-like action of Nolvadex. By rendering the liver less sensitive to growth hormone (probably by reducing the liver density of GH receptors), estrogens and tamoxifen diminish the production of IGF-1. This action of estrogens explains why women produce less IGF-1 than men eventhough the have a higher GH level.
Nolvadex and Muscle Definition
Within 24 to 48 hours, Nolvadex is able to greatly increase muscular definition. As a result, bodybuilders assume Nolvadex will help them reduce their bodyfat level. But this rapid cutting action of Nolvadex is due to an anti-estrogenic action on water retention. Estrogens will make you hold water. Nolvadex will produce the opposite effect. But it says nothing about the impact of Tamoxifen on bodyfat. Depending upon your own production of estrogens and your estrogen receptor density on adipocytes, Nolvadex can act as an antagonist (which would help you lose fat) or an agonist. In that case, Nolvadex will make you fatter especially in the lower body area.
Conclusion: if the introduction of Nolvadex 25 years ago was a brilliant idea, times have changed. Very effective anti-aromatase drugs (such as Letrozole or Anastrazole) have been introduced. They will fight gynecomastia, help prevent the anti-anabolic actions of estrogens, fight fat and water retention. They will also boost natural testosterone production far more effectively than Nolvadex. So, it is up to you to decide whether you wish impair your rate of progression with an outdated drug or move on to the 21st century.
(1) Max SR. Androgen-estrogen synergy in rat levator ani muscle: glucose-6-phosphate dehydrogenase. Mol Cell Endocrinol. 1984 Dec;38(2-3):103-7.
(2) Rance NE, Max SR. Modulation of the cytosolic androgen receptor in striated muscle by sex steroids. Endocrinology. 1984 Sep;115(3):862-6.
(3) Kobori M, Yamamuro T. Effects of gonadectomy and estrogen administration on rat skeletal muscle. Clin Orthop Relat Res. 1989 Jun;(243):306-11.
(4) Suzuki S, Yamamuro T. Long-term effects of estrogen on rat skeletal muscle. Exp Neurol. 1985 Feb;87(2):291-9.
(5) Koot RW, Amelink GJ, Blankenstein MA, Bar PR. Tamoxifen and oestrogen both protect the rat muscle against physiological damage. J Steroid Biochem Mol Biol. 1991;40(4-6):689-95.
(6) Naessens G, De Slypere JP, Dijs H, Driessens M. Hypogonadism as a cause of recurrent muscle injury in a high level soccer player. A case report. Int J Sports Med. 1995 Aug;16(6):413-7.
07-16-2006 07:20 AM
BBC NEWS | Health | Bodybuilders' 'breast drug abuse'
Bodybuilders' 'breast drug abuse'
Some bodybuilders abuse the cancer drug tamoxifen to negate the breast-boosting effects of steroids, University of Glamorgan researchers found.
Steroids are derived from testosterone, but if levels of the male hormone are too high in the body, it is converted into oestrogen and men grow breasts.
A survey of 200 gym users found 22% took tamoxifen to reverse this effect.
Cancer experts expressed concern over the findings, published in the Journal of the Royal Society of Medicine.
The researchers compared the results of this survey, carried out last year, with one carried out in 2000 when just one to two per cent said they had taken tamoxifen.
They also found 11% of bodybuilders took human chorionic gonadotrophin to stimulate the testes, which wither due to excessive steroid use.
The researchers, from the University of Glamorgan's Health and Exercise Science Research Unit, say bodybuilders turn to steroids because they see themselves as too "weedy" - in a condition which is the opposite of anorexia.
But they are then forced to move on to using a ****tail of other drugs to counteract the effects of the steroids.
Professor Bruce Davies, who led the research, said: "Gym-goers are increasingly resorting to steroids and prescription drugs to counteract their altered body images.
"Sufferers of negative or heightened body image issues will go to extremes to meet their desired goals and doctors need to be more aware of the efforts 'bigorexics' will go to."
"Our results corroborate research undertaken in the US, that is, an increasing number of non-athletes are resorting to a combination of drugs with the sole intention of improving their physical appearance."
Professor Davies also warned bodybuilders were risking abscesses in their muscles, because they were injecting counterfeit drugs using aftershave rather than alcohol as a "sterilising" agent.
He called for the medical profession to recognise the needs of this group.
"There needs to be greater awareness of the psychological reasons of prescription drug and steroid abuse, and counselling and appropriate medical treatment made available."
Dr Kat Arney, cancer information officer at Cancer Research UK, said: "Tamoxifen is a potent and effective drug for treating breast cancer. Like all medication it can have side effects, so it should not be used without medical supervision.
"Bodybuilders who take tamoxifen or other inappropriate prescription drugs are gambling with their health."
07-16-2006 07:31 AM
nice post. my thoughts,
premise: Prop is the best Test-Ester.
CED59: I agree totally. If it allows for the most maintainable gains I don't know. Long Esters yield retainable gains usually. Based on the short'est' ester is best argument, we'd say that suspension gains would be more retainable. obviously, not the case
premise: EQ, need to be used 12 weeks.
CED59: I agree, but for a different reason however, you can frontload EQ 1000,1000,800 and it will be active at over 600mg in your body mid-way week 4.
premise: Some anabolic steroids don't shutdown HPTA.
CED59: Vague statement. Shutdown is dose dependent. Avoiding shutdown is possible though, that is correct.
premise: AI used year round.
CED59: I agree 95%. I don't get the estrogen sides but, if you are taking finasteride - I'd recommend it. Aromasin, ATD or 6oxo. not Letro or Adex! <-- bad news, in my opinion
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