NOLVADEX: inhibits muscle growth!

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    NOLVADEX: inhibits muscle growth!


    Heres an article I found, please read it THEN respond!

    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 popularized 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 even though 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.

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    source?
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    Honestly from all I've read I don't know why you'd ever use nolva anyway when clomid seems to have lower risks long term and actually helps with restart as well as preventing gyno... Unless you can't handle being a little moody for a while.
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    shock to the "swear by Nolva" community. nice post.
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    so letro is better than nolva, clomid, AND torem? according to this?
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    Quote Originally Posted by ShockCollar View Post
    so letro is better than nolva, clomid, AND torem? according to this?
    I'm not an expert by any means but I believe letrozole is an Aromatase Inhibitor (AI), and an extremely potent one at that, while the others you mentioned are Selective Estrogen Receptor Modulators (SERMs) so the mechanism of action would be different. An AI will decrease the amount of aromatase enzyme thereby having an effect on how much testosterone is converted to estrogen. This causes an endogenous increase in test (in addition to the reduction in estrogen mentioned) via the HPTA negative feedback loop. A SERM on the other hand, acts on the estrogen receptors in your body (Nolva is very breast tissue specific I think) but does not, to my knowledge, decrease the amount of circulating estrogen to any great degree.

    Like I said, I'm not an expert, so if I've inadvertently got anything wrong in the above response, please feel free to correct me.
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    That is an interesting article. On one hand it does acknowledge that without Nolvadex bodybuilders where getting gyno post cycle and thats not good, so you could still conclude that during pct, nolva is better than nothing. No argument there, unless you're into having boobies (I love that word). On the other hand, the article admits that to "other athletes" Nolva would have a good effect on recovery. Isn't that our goal while in pct after a cycle? Sure gaining mass during pct would be awesome, but isn't maintaining and recovering on cycle mass our goal? It never really says that Nolva would cause catabolization as much as it implies that gains would be minimized. Am I right, or have I misread the thing?
    I'm with n8te, I would be curious to know who wrote that, what their sources were, and if they have any "vested interests", in Letro etc. Sure, there might be better options than nolva, but to completely throw it's use out the window when it has been used with success for 25 years is a bit much.
    Interesting though. Thanks Cantell.
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    This is pissing me off! I dont understand if taking an "AI" for pct would be better than a SERM!!!!!
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    Quote Originally Posted by Cantell View Post
    Heres an article I found, please read it THEN respond!

    Its primary use by male bodybuilders is to prevent gynecomastia (the growth of the breast tissue).
    No it's not!

    Clomid, Nolvadex, and Testosterone Stimulation
    by:
    William Llewellyn

    Editors Note: I am extremely pleased to have Bill Llewellyn contributing an article for us this week. For those who are unaware, he is the author of Anabolics 2000 and Anabolics 2002 and is one of the bodybuilding world's foremost experts on androgens and anabolics. He is also the President of Molecular Nutrition, one of the most innovative companies in this business. Along with Avant Labs and ErgoPharm, Molecular Nutrition is one of the few companies dedicated to putting forth only those products backed by legitimate research, rather than excessive hype and other such B.S. Two products, in particular, that deserve to be more well-known are Viritase, a potent anti-estrogen, and Boldione, a boldenone precursor. To find out more about these, and the rest of their products, I reccomend that you head over to their website -- but only after you have finsished reading big Mf'r and spent all of your money on our products, of course

    Now, on to the article:

    Introduction

    I have received a lot of heat lately about my preference for Nolvadex over Clomid, which I hold for all purposes of use (in the bodybuilding world anyway); as an anti-estrogen, an HDL (good) cholesterol-supporting drug, and as a testosterone-stimulating compound. Most people use Nolvadex to combat gynecomastia over Clomid anyway, so that is an easy sell. And for cholesterol, well, most bodybuilders unfortunately pay little attention to this important issue, so by way of disinterest, another easy opinion to discuss. But when it comes to using Nolvadex for increasing endogenous testosterone release, bodybuilders just do not want to hear it. They only seem to want Clomid. I can only guess that this is based on a long rooted misunderstanding of the actions of the two drugs. In this article I would therefore like to discuss the specifics for these two agents, and explain clearly the usefulness of Nolvadex for the specific purpose of increasing testosterone production.

    Clomid and Nolvadex

    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.

    Conclusion

    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.

    In next month's follow-up article I will be discussing the role anti-estrogens play in post-cycle testosterone recovery. Most specifically, I will be detailing what a proper post-cycle ancillary drug program looks like, and explain why anti-estrogens alone are not effective during this window of time.

    References:

    1. Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men. Vermeulen, Comhaire. Fertil and Steril 29 (1978) 320-7

    2. Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro. Adashi EY, Hsueh AJ, Bambino TH, Yen SS. Am J Physiol 1981 Feb;240(2):E125-30

    3. The effect of clomiphene citrate on sex hormone binding globulin in normospermic and oligozoospermic men. Adamopoulos, Kapolla et al. Int J Androl 4 (1981) 639-45
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    Nice... Great info
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    taking a ai right after a cycle its not a smart thing to do , the possibility of a estrogen rebound and delayed gyno is a big problem , a serm will not cause any of those problems so nolva its still a must on pct
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    Quote Originally Posted by Ninjo View Post
    I'm not an expert by any means but I believe letrozole is an Aromatase Inhibitor (AI), and an extremely potent one at that, while the others you mentioned are Selective Estrogen Receptor Modulators (SERMs) so the mechanism of action would be different. An AI will decrease the amount of aromatase enzyme thereby having an effect on how much testosterone is converted to estrogen. This causes an endogenous increase in test (in addition to the reduction in estrogen mentioned) via the HPTA negative feedback loop. A SERM on the other hand, acts on the estrogen receptors in your body (Nolva is very breast tissue specific I think) but does not, to my knowledge, decrease the amount of circulating estrogen to any great degree.

    Like I said, I'm not an expert, so if I've inadvertently got anything wrong in the above response, please feel free to correct me.
    your right. you have to nolva AFTER letro.
    letro = lots of test, no estro whatsoever.
    after cycle= estro rebound
    which is why you would use nolva.
    i guess people will start using clomiphene instead now after this article? O_o
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    Quote Originally Posted by nunes View Post
    taking a ai right after a cycle its not a smart thing to do , the possibility of a estrogen rebound and delayed gyno is a big problem , a serm will not cause any of those problems so nolva its still a must on pct
    aren't most people taking AI's such as letro DURING cycles? to have maximum T and minimum E?....
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    References. We don't need no stinkin references.
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    Quote Originally Posted by austin82388 View Post
    aren't most people taking AI's such as letro DURING cycles? to have maximum T and minimum E?....
    Only if your cycle includes a compound that aromatizes...test will aromatize so some type of an AI "on cycle" may be prudent...not sure if letro is a good "on cycle" choice however as it is extremely potent...reduces your body's estrogen by ~ 90% if memory serves me correctly
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    Quote Originally Posted by Ninjo View Post
    Only if your cycle includes a compound that aromatizes...test will aromatize so some type of an AI "on cycle" may be prudent...not sure if letro is a good "on cycle" choice however as it is extremely potent...reduces your body's estrogen by ~ 90% if memory serves me correctly
    Estrogen has intrinsic anabolic properties as well as lipid beneficial and promoting characteristics. Eliminating estrogen is not advisable UNLESS one is KNOWN to be an extreme aromatizer to supraphysiological levels of estrogen that are proven to cause gyno in you....not someone else.. Otherwise supraphysiological levels of testosterone are expected to have elevated levels of estrogen. AI's can be counter productive to the anabolism that elevated testosterone can produce.

    Quit believing the urban legends! Educate yourselves!
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    ^+1
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    b51 thanx for shining in man
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    nice info, thanks
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    thanks much. would an ai be best added in (ex. ptc assist) at the start of wk 4 of a 20/20/20/20 nolva ptc?
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    if anything id assume, serms would close the growth plates very quickly.
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    Quote Originally Posted by citystreets View Post
    if anything id assume, serms would close the growth plates very quickly.
    Depends on which SERM we ae discussing --those that act as agonists in bone would surely close the growth plates.
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    Quote Originally Posted by sethroberts View Post
    Depends on which SERM we ae discussing --those that act as agonists in bone would surely close the growth plates.
    dont they all have mixed properties?

    nolva clomid do,

    wouldnt it be any phyto estrogen as well that agonized the ERb?
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    well in that case, evista users be prepared to stop growing lol. Jeez med school is so much fun. I think ill do my electives research on steroids woohoo
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    do AI;s close plates as well?
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    Quote Originally Posted by crazyfool405 View Post
    dont they all have mixed properties?

    nolva clomid do,

    wouldnt it be any phyto estrogen as well that agonized the ERb?
    To a certain degree they all do, but, if the maximal response induced is less than your endogenous estrogen (in terms of your individual androgen/estrogen ratio) then it would not be likely to close growth plates.

    Raloxifene is a strong agonist in bone (someone else mentioned it as Evista) and will close growth plates(see abstract below). There is conflictng evidence for tamoxifen -- one study in rats resulted in closure of growth plates but the dose was quite high. AI's will not cause growth plate closure and in fact will increase final height (see abstract below).


    1. Endocrinology. 2003 Apr;144(4):1481-5. Links
    Raloxifene acts as an estrogen agonist on the rabbit growth plate.Nilsson O, Falk J, Ritzén EM, Baron J, Sävendahl L.
    Pediatric Endocrinology Unit, Department of Women and Child Health, Karolinska Institutet, SE-17176 Stockholm, Sweden. ola.nilsson@kbh.ki.se

    Estrogen treatment has been used to induce growth plate fusion, thereby reducing the final height in girls expected to achieve extreme tall stature. The treatment is effective, in terms of limiting final height, but concerns have been raised that it might also increase the risk for malignancies later in life. Raloxifene, a selective estrogen receptor modulator, has been shown to act as an estrogen agonist on bone density but as an estrogen antagonist on breast and uterine tissue. The effect of raloxifene treatment on growth plate fusion and final height is unknown. The aim of this study was to determine whether raloxifene would act as an estrogen agonist or antagonist on growth plate cartilage. Ovariectomized immature rabbits were treated for 4 wk with vehicle (controls), estradiol cypionate (E2), or raloxifene. Tibial growth velocity was decreased in both E2- (P < 0.001) and raloxifene-treated animals (P < 0.001), compared with controls. E2 and raloxifene treatment also decreased chondrocyte proliferation and the height of the proximal tibial growth plate. In addition, E2 and raloxifene hastened fusion of the distal tibial growth plate (P < 0.05) and decreased the number of proliferative and hypertrophic chondrocytes per column in the proximal tibial growth plate. As expected, the uterus was enlarged by estrogen, but not raloxifene, treatment. We conclude that raloxifene acts as an estrogen agonist on the growth plate, accelerating growth plate senescence and thus hastening epiphyseal fusion.


    2. Mol Cell Endocrinol. 2006 Jul 25;254-255:207-16. Links
    Use of aromatase inhibitors to increase final height.Dunkel L.
    Kuopio University Hospital, Kuopio, Finland. Leo.Dunkel@kuh.fi

    During puberty in both sexes, the mechanism involved in epiphyseal fusion is mediated by the action of estrogen through a cascade of events including proliferation, differentiation, and apoptosis of chondrocytes. The enzyme P450 aromatase catalyzes the aromatization of C19 androgens (androstenedione and testosterone) to C18 estrogens (estrone and estradiol). Inhibition of estrogen action by aromatase inhibitors (AIs) appears to decelerate the process of growth plate fusion, and thus AIs may be used therapeutically to increase adult height. The clinical experience with AIs in the pediatric setting is limited to testolactone, fadrozole, letrozole, and anastrozole. Testolactone, a nonselective steroidal AI, has been used successfully as an adjunct to antiandrogen and gonadotropin-releasing hormone analogue (GnRHa), therapy for children with familial male-limited precocious puberty (FMPP) and congenital adrenal hyperplasia (CAH), and with some success in girls with McCune-Albright syndrome. The limitations of testolactone include its relatively low potency and the need for frequent dosing. Results of a randomized placebo-controlled trial in boys with delayed puberty treated with letrozole, a selective nonsteroidal AI, found that boys treated with letrozole + testosterone experienced delayed bone maturation and good growth response and achieved an increase in predicted adult height. In this study, only minor differences in bone density were seen between the placebo and letrozole treatment groups, both of which were receiving concomitant testosterone therapy. No adverse effects on testis size or inhibin B concentration were noted. The therapeutic value of AIs in growth promotion now remains to be substantiated in future controlled clinical trials.
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    Quote Originally Posted by sethroberts View Post
    References. We don't need no stinkin references.
    Sure, we do!
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    nice studies

    evista (raloxifen) is usually givin to post menopausal women so citystreets comment really wasnt necessary.

    AIs lupron and gh are given to children with precotious puberty to block any further androgen production and keep growth plates open will still allowing some another growth fact ot help along the way.

    so in children i see more AI use then SERM use
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    why do doctors only prescribe clomid to restart the htpa? and not novla?

    This article makes me only want to touch nolva.
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