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    Default Anti-Estrogens and Aromatase Inhibitors

    Because of their ability to reduce risk of gynecomastia (abnormal growth of breast tissue in males) and enhance recovery of natural testosterone production after a cycle, use of anti-estrogens such as Clomid (clomiphene citrate) Cytadren (aminoglutethimide) has become popular in bodybuilding. Anti-estrogens also can reduce bloating associated with anabolic/androgenic steroid use, and may avoid health risks associated with elevated estrogen levels. Medically, the drugs are used not only for treatment of breast cancer but also for improvement of fertility in both men and women, and occasionally for increasing testosterone levels in men such as endurance athletes with low testosterone. There are two categories of anti-estrogens: aromatase inhibitors and receptor blockers. Both shall be considered here.
    Estrogens

    As with androgens, where any hormone that has the activity of testosterone is an androgen and therefore all anabolic steroids are androgens, any hormone that has the activity of estradiol, the principal female sex hormone, is an estrogen. The most active natural estrogens in humans are estradiol and estrone.
    These hormones are related to each other rather similarly to how the andro prohormones are related to each other. Just as androdiol has a hydroxy (or –ol) group at both the 3- and 17- positions, estradiol likewise has a hydroxy group at those positions. Estrone, like androstenedione, has keto (or –one, pronounced “oan”) groups at those positions.
    Estradiol is the most potent (effective per milligram) of the natural estrogens. It is produced either from testosterone via the aromatase enzyme, or from estrone via the estrogenic 17b-HSD enzyme.
    Estrone is less potent, but all this means is that one needs more of it to accomplish the same job. It is produced either from androstenedione via aromatase, or from estradiol via the same 17b-HSD enzyme working in reverse.
    From the standpoint of the bodybuilder using anabolic/androgenic steroids (AAS), if nothing is done about the situation, high estrogen levels can cause gynecomastia, will inhibit natural testosterone production, and will cause bloating. High estrogen levels also make it more difficult to lose fat, and tend to cause female pattern fat distribution even in males.
    Estradiol also has carcinogenic metabolites, and a liver problem sometimes associated with AAS use, hepatic cholestasis, is caused not by androgen but by an estrogen metabolite.
    It is also not unusual for bodybuilders to feel poorly on beginning a cycle of high dose testosterone without antiestrogens, and for this reason many have advocated starting with a low dose and building up. However, I strongly suspect that the real problem is estrogenic effect on mood, and the problem can be avoided with use of an aromatase inhibitor.
    Aromatizable Steroids

    Though most bodybuilders feel they know which steroids aromatize and which do not, sometimes the beliefs are in error. This is because progestogenic activity (activity like that of progesterone, another female hormone) is easily mistaken for estrogenic activity. Both hormones can cause bloating, and both can cause gyno. So AAS which are capable of activating not only the androgen receptor but also the progesterone receptor are often mistakenly assumed to aromatize. (Note: these androgens do not “convert to progesterone” but rather are themselves, without any change needed, able to act on that receptor.)
    Nandrolone is proven to be a progestin. This fact is of clear importance in bodybuilding, because while moderate Deca-only use actually lowers estrogen levels as a consequence of reducing natural testosterone levels and thus allowing the aromatase enzyme less substrate to work with, Deca nonetheless can cause gyno in some individuals. Furthermore, just as progesterone will to a point increase sex drive in women, and then often decrease it as levels get too high, high levels of progestogenic steroids can kill sex drive in male bodybuilders, though there is a great deal of individual variability as to what is too much.
    Incidentally, this progestogenic activity also inhibits LH production, and contrary to common belief, even small amounts of Deca are quite inhibitory, approximately as much so as the same amount of testosterone.
    What relevance does this have to an article on antiestrogens? Well, antiestrogens can do nothing about these side effects of Deca.
    The same appears to be true of oxymetholone (Anadrol)and of norethandrolone (Nilevar).
    Methenolone (Primobolan), stanozolol (Winstrol), dromostanolone (Masteron), oxandrolone(Anavar), mesterolone (Proviron), stenbolone (Anatrofin), trenbolone, and DHT do not aromatize, and thus, antiestrogens are not relevant to these AAS either.
    The steroids where aromatization is of particular concern are testosterone, methandrostenolone (Dianabol), boldenone (Equipoise), and to some extent fluoxymesterone (Halotestin). However the latter is usually used in doses low enough that aromatization is not an issue.
    Among the prohormones, androstenedione is the principal offender with regard to aromatization, being readily converted to estrone. With androdiol, only that small portion which converts to testosterone can be converted further to estradiol, and that will occur only in the same percentage that other testosterone converts to estradiol.
    Norandrodiol cannot convert directly to estrogen, and even after conversion to nandrolone is not readily converted to estrogen.
    Norandrostenedione can be converted to estrone by aromatase, but is a very poor substrate for that enzyme. It can actually act as a competitive inhibitor, blocking better substrates such as androstenedione or testosterone. It is possible then, though unproven, that norandrostenedione might have some value as an aromatase inhibitor in bodybuilding. I do think, however, that the pharmaceuticals designed for the purpose should be assumed to be better choices.
    Aromatase Inhibitors

    (Author Note – May 2011: Years back, aromatase inhibitors such as Arimidex and letrozole were much more expensive than Cytadren and much less available, so in the past Cytadren was often used as an aromatase inhibitor. That use is today obsolete.)
    The most commonly used aromatase inhibitor in bodybuilding is aminoglutethimide (Cytadren). This drug also inhibits an enzyme (desmolase) necessary for synthesis of cortisol, but fortunately, aromatase can be inhibited with levels of drug that cause only limited inhibition of desmolase.
    Contrary to popular belief, it is generally not desirable to inhibit cortisol production. Doing so will likely lead to joint problems, and furthermore once the inhibition ends, the price of above-normal cortisol production must usually be paid.
    For an average male, a dose of 250 mg/day (one tablet) appears optimal. The half-life is 8 hours, so the drug is better taken in divided doses. The best plan seems to be to take half a tablet on arising, and quarter tabs six and twelve hours later. This keeps levels generally fairly constant, but allows a small drop in the hours shortly before arising, which is then compensated for by the higher dose on arising. With this scheme, inhibition of cortisol production is generally too low to be noticed, and generally there is no rebound effect on discontinuance. However it is not a bad idea nonetheless to taper off, first omitting the midday quarter tab dose for a few days, then omitting both quarter tab doses, then reducing the initial dose to one quarter tab, and then ending completely. A week is sufficient for the taper.
    Some people suffer a degree of lethargy or sedation from aminoglutethimide, even at this low dose, but most do not.
    Anastrozole (Arimidex) is a superior aromatase inhibitor which does not have the above side effects. It is, however, very expensive. With moderate doses of testosterone it seems that 1 mg/day is sufficient, and some have claimed half a tab to be sufficient. I do not have blood test data to verify that, however.
    Receptor Blockers

    Clomiphene (Clomid) and tamoxifen (Nolvadex) are the most popular drugs of this class. They are more precisely referred to as “selective estrogen receptor modulators.” This is because their mode of action is not so simple as merely blocking the estrogen receptor. Estrogen receptors require not only hormone but also activation of regions of the receptor called AF-1 and AF-2. AF-1, to be activated, requires phosphorylation, while AF-2 can be activated by any of a number of cofactors, such as IGF-1.
    As it happens, clomiphene and tamoxifen are estrogen receptor antagonists (blockers) in cells that depend on activation of the AF-2 region, while in cells which activate AF-1, these compounds are estrogens.
    In some cells these drugs activate one of the types of estrogen receptor (ERa) but are antagonists of the other type (ERb).
    The result is that these compounds are antiestrogenic in breast tissue, fat tissue, and in the hypothalamus, which is what we want in bodybuilding, but are estrogenic in bone tissue and with respect to favorable effect on blood lipid profile, both of which are, again, desirable. They also appear to have some estrogenic effect on mood, though this may be in only parts of the brain (the matter is not studied.)
    Cyclofenil is a similar drug to the above two. Clomiphene will do everything that the other two will do, but for some unknown reason, has been found more effective than tamoxifen both medically and in bodybuilding for increasing LH production.
    Raloxifene (Evista) is a new selective estrogen receptor modulator that, for women, has the advantage of being an antiestrogen in the uterus, whereas clomiphene and tamoxifen are estrogens in that tissue. For this reason, the latter two drugs can promote uterine cancer, while raloxifene actually should help prevent it, and is therefore a superior drug for women. It is not known how effective it may be in increasing LH production.
    While on high dose androgens it is impossible to maintain LH production in any case, and clomiphene can do no good in that regard. As androgen levels return to normal, however, a dose of 50 mg/day of clomiphene if estrogen levels are reasonable, or 100 mg/day if estrogen levels are high, is usually effective in restoring natural testosterone production.
    Because the drug has a long half-life, when one takes 50 mg/day the amount in the system is not only the 50 mg just taken, but also approximately another 250 mg from previous days. Thus, to immediately arrive at the therapeutic level, one would take 300 mg (50 mg six times) on the first day, and then continue with 50 mg/day.
    A small percentage of individuals suffer vision problems from use of clomiphene, which is generally reversible upon discontinuance. These persons, of course, should not use the drug after discovering the problem.
    It also must be pointed out that these are prescription drugs, and should be obtained and used only by precription with medical advice, though the selective estrogen receptor modulators have excellent safety records.
    After a cycle, it is reasonable to continue clomiphene use until at least four weeks after the last injection of long acting ester, or at least two weeks after the last use of an oral, or until natural testosterone production is clearly back to normal, whichever comes last.
    Conclusion

    Other than acne and accelerated hair loss, the two most common problems of AAS use are gynecomastia and difficulty in recovering natural testosterone production. Antiestrogenic drugs can effectively address both problems and are safe for most individuals. Ideally, if aromatizable drugs are used, the problem is corrected at the source by limiting production of estrogen by using an aromatase inhibitor. However, it is also effective to use a selective estrogen receptor modulator such as Clomid. The latter drug is also of particular use in helping to restore natural testosterone production after a cycle.
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    Author: Ben Presser
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    good basics for the newbies! Solid read
    Author: Ben Presser
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    Just made this a STICKY Post so those needing information on Aromatase Inhibitors

    Visit Us @ https://www.musclechemadvancedsupps.com/ for all your PCT Needs! As in Pre Cycle Therapy , Present Cycle Therapy , and Post Cycle Therapy, all of them as important as the other!
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    good read, was just going through some old post and read it.
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    all that you read here is only for entertainment purposes.

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    Good info. I do Muscle Chemistry Nolva Bloat, a-dex and anti-p. 10 mg of the nolva everyday, .5 a-dex 2 times per week. and anti-p for the tren. All work great! Side note also endure Gw for the tren also.
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    Quote Originally Posted by dpile View Post
    Good info. I do Muscle Chemistry Nolva Bloat, a-dex and anti-p. 10 mg of the nolva everyday, .5 a-dex 2 times per week. and anti-p for the tren. All work great! Side note also endure Gw for the tren also.
    Im a big believer in using Nolvadex during my cycle at dosages like your running. I never felt that it hindered my gains like a lot of guys say they are worried about.

    Do you honestly feel the cardarine helps with tren ? I havent tried it together, as I rarely use tren ace anymore. But thinking maybe next time ill add in some gw 501516 (cardarine) aka endurobol gw from Sarm Sciences lol, for those who are like what the fuck are they talking about
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    Quote Originally Posted by Presser View Post
    Im a big believer in using Nolvadex during my cycle at dosages like your running. I never felt that it hindered my gains like a lot of guys say they are worried about.

    Do you honestly feel the cardarine helps with tren ? I havent tried it together, as I rarely use tren ace anymore. But thinking maybe next time ill add in some gw 501516 (cardarine) aka endurobol gw from Sarm Sciences lol, for those who are like what the fuck are they talking about
    i see you prefer nolva to clomid on cycle, and clomid is used more for pct. so what is the difference for each ones use. just wondering. i've read of guys using clo on cycle, and i'm using it as well.
    just curious because both are serms and both attach to the estrogen receptors. am i missing something here or is it preference of which a person chooses to use.
    i also use the a-dex 0.5mg twice a week and prami the same.
    all that you read here is only for entertainment purposes.

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    clomid is more to jump start your natural test production again, nolvadex is simply an anti-estrogen by way of competing with free floating (already present estrogen) to attach to the receptor site.
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    I dont know where it came about in recent years that they are inner changable or of a personal prefrence. Theyre used for two totaLLY DIFFERENT THINGS , unless some new discovery was made that im not aware of
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    Clomid, Nolvadex and Testosterone Stimulation
    By William Llewellyn


    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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    for the record, when i think anti-estrogen im grabbing nolvadex, and when i think stimulate natural testosterone production, i grab clomid, and i think that is pretty universal regardless of each of them sharing the others properties or being in same family. I know i wouldnt use clomid as an anti - estrogen
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    Quote Originally Posted by Presser View Post
    for the record, when i think anti-estrogen im grabbing nolvadex, and when i think stimulate natural testosterone production, i grab clomid, and i think that is pretty universal regardless of each of them sharing the others properties or being in same family. I know i wouldnt use clomid as an anti - estrogen
    thanks, just a bit confused and still learning.
    all that you read here is only for entertainment purposes.

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    Quote Originally Posted by Presser View Post
    Im a big believer in using Nolvadex during my cycle at dosages like your running. I never felt that it hindered my gains like a lot of guys say they are worried about.

    Do you honestly feel the cardarine helps with tren ? I havent tried it together, as I rarely use tren ace anymore. But thinking maybe next time ill add in some gw 501516 (cardarine) aka endurobol gw from Sarm Sciences lol, for those who are like what the fuck are they talking about
    I always felt like NOLVA hindering gains was over hyped BS.
     

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    As did I! Like i said it never hindered my gains, at least not that i know of!
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    I've used it the last 2 tren runs. First tren run I would be out of breath just drying off from a shower. Cutting the grass was horrible. Last 2 runs with GW, CARDIO WAS NOT AN ISSUE AT ALL. Right now I JUST GOT SOME FROM THE MC STORE, It works great.

    - - - Updated - - -

    I love tren and feel like I need GW with it. I hope I can keep getting it. GW and anti-p I feel are a must with tren.
     

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    Quote Originally Posted by Ashop View Post
    I always felt like NOLVA hindering gains was over hyped BS.
    From everything Ive witnessed AIs, unless blood levels ate constantly monitored, are what will hinder gains and cause all types of other problems. Guys are just picking a dose. IE. 1 mg arimidex a day with test with absolutly no idea if this is too much for their body. If it happens to be the estrogen will go so low good luck. The best way to use AIs is to strictly monitor levels until you know what your body needs and what will not crash your e. These AIs are no fuckin joke. Arimidex was relesed in 1998 and was so damn strong I remember i had a small gyno ptoblem getting ready for s contest. Couldnt get rid of it. 1 mg Arimidex a day 2 weeks and it was totally gone. A drug like Letro, forget it, its so strong. Its the reason I dont care anymore if a little gyno pops up. 3-5 days of letro and all gynl is gone, totally. So, honestly, this topic, because of letrozolole, has become entirely unimportant to me.
    Use Noveldex or like was said clomid none of this needs to be worried about because neither lower estrogen.
    Precontest AIs are incredible if used correctly but otherwise id stick to SERMS or a very low dose of AI with a SERM.
    BTW good article.

    Sent from my LM-Q710(FGN) using Tapatalk
     

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    Sorry a little late with the reply. I just had surgery but back rolling now. I feel it works with the cardio. Tren makes me winded just drying off after a shower. The GW MAKES THAT PART WAY BETTER. It also helps with the bloods.
     

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