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    Clomid

    Currently on pct which includes nolva and clomid.This is my first time taking these two well ever since I started clomid Ive been seeing trails like Im tripping,this happens for the first couple minutes after I wake up in the middle of the night and also get foggy vision sometimes. Also gives me a diiferent feel of sight hard to explain but has anyone experienced any this with clomid?I ve read it can cause irreversible loss of sight so Im debating whether to continue with the just nolva been on clomid 19 days 50mg ed/ nolva 20mg ed for 32days so far.
    Last edited by bigrene; 09-23-2010 at 11:20 AM. Reason: forgot something

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    I've never heard about irreversible loss of sight. I do know at high dosages it messes with your vision but nothing permanent.

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    I started the nolva with hcg in case anyone was wondering why Ive been on nolva for a month and clomid 19 days. Next time I do hcg will be during cycle but I didnt so I did it at end and from what I heard is hcg and clomid doesnt go together.Also I was on pretty long so I kind of want to make sure i GET SUFFICIENT PCT.

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    Try throttling back the clomid and see how it treats ya. Clomid is nasty on your vision.

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    Yes, clomid will sometimes cause vision issues. You'll be fine.

    Why are you using nolva? It decreases your natural GH and IGF-1. That is the WORST thing you can do to yourself during PCT. Drop it NOW.

    You need clomid and aromasin. NOTHING ELSE.

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    Quote Originally Posted by CT View Post
    Why are you using nolva? It decreases your natural GH and IGF-1. That is the WORST thing you can do to yourself during PCT. Drop it NOW.

    oh jeez...

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    Quote Originally Posted by Du View Post
    oh jeez...
    haha,

    tru dat...thatbtrue dat.... check out ghrp-6 if you want to gain 10 plus lbs while on pct, run it with cjc-1295 OR Hexarelin....then cycle back to, if you are on it, hgh after the pct program.....pct for the pituitary, then a pct for the test axis...flip flopped.......aminooutpost.com cheap......the igf is good good shit btw

    clomid is not the best pct, but you are lucky to have it around Nolva is much better imao

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    Quote Originally Posted by barrym View Post
    haha,

    tru dat...thatbtrue dat.... check out ghrp-6 if you want to gain 10 plus lbs while on pct, run it with cjc-1295 OR Hexarelin....then cycle back to, if you are on it, hgh after the pct program.....pct for the pituitary, then a pct for the test axis...flip flopped.......aminooutpost.com cheap......the igf is good good shit btw

    clomid is not the best pct, but you are lucky to have it around Nolva is much better imao
    Why in your opinion is nolva better than clomid for PCT?

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    Quote Originally Posted by Du View Post
    oh jeez...

    Interesting read from William LLewelyn
    Estrogen is not the enemy

    Aromatizable Androgens and Anabolism:
    The Role of Estrogen in Muscle Growth
    by William Llewellyn


    Can estrogen work to augment muscle growth? Is this hormone always unwanted when we are taking anabolic steroids? Anecdotal reports from athletes suggest that the use of estrogen maintenance drugs such as tamoxifen (anti-estrogen) or aminoglutethimide (anti-aromatase) may slightly hinder muscle mass gains during steroid therapy. An explanation or even clarification for this observation has not been easy to come by. Here I would like to take a look at the comparative effectiveness of certain aromatizable and non-aromatizable drugs, as well as the possible mechanism in which estrogen can play a beneficial role to the athlete.

    The Androgen Receptor
    All anabolic/androgenic steroids promote muscle growth primarily via the cellular androgen receptor (abbreviated as AR in this article). The steroid attaches to and activates the androgen receptor, which ultimately gives the cell an order to increase protein synthesis. This process is well understood. But it has been suggested that other mechanisms may foster muscle growth during steroid therapy as well, which lie outside of the androgen receptor. One way this is evidenced is by the fact that steroids displaying a high affinity for the AR in muscle tissue do not always promote an equally high level of muscle growth. In other words, anabolic potency does not always correspond perfectly to receptor affinity. Clearly there are some disparities that lead into question whether or not the androgen receptor is the only thing at work concerning growth.

    Testosterone, Nandrolone and Methenolone
    Testosterone is without question one of the most effective steroids for building muscle mass available to athletes. However it does not have the highest affinity for the androgen receptor compared to some other steroids. For example, it has been shown that by eliminating the 19-methyl group (nandrolone) the affinity of the steroid for the androgen receptor is greatly enhanced[i]. Nandrolone thus displays approximately 2-3 times greater affinity for the androgen receptor compared to testosterone, yet its ability to promote muscle growth seems to be considerably lower than testosterone at an equal dosage. One discussed possibility for this occurrence is the reduced androgenic potency of nandrolone. While testosterone converts to the more active steroid dihydrotestosterone (3-4 times greater AR affinity) upon interaction with the 5-alpha reductase enzyme in various androgenic target tissues such as the skin, scalp, prostate, CNS and liver, nandrolone drops to a third of its original potency by converting to the weak steroid dihydronandrolone[ii]. However this action is very site specific, and in muscle tissue nandrolone dominates as the active form of the steroid. Therefore this explanation may not suffice.

    Nandrolone also differs from testosterone in its ability to be converted by the aromatase enzyme to estradiol (an active estrogen). In comparison, nandrolone aromatizes at approximately 20% of the rate testosterone does, and as such is not known as a very estrogenic steroid. It is likewise favored when reduced estrogenic side effects such as water retention, fat deposition and gynecomastia are desired. However athletes know that there is a trade off with the reduced tendency for nandrolone to promote side effects, in that it is a less anabolic steroid. With its known high affinity for the AR in muscle tissue, could this suggest that estrogen may also be a key mediator of muscle growth?

    When we look at Primobolan® (methenolone) we see a similar trend. Methenolone is at least as good a binder of the androgen receptor as testosterone. By some accounts it is on par with nandrolone[iii]. However it is known to be much weaker than both steroids at promoting muscle growth. We know that methenolone does not interact with 5-alpha reductase, and as such its affinity for the AR does not increase or decrease in androgen target tissues. This would logically seem like a more favorable trait for anabolism over the weakening we see with nandrolone. However methenolone is a markedly weaker anabolic, and requires relatively high doses to promote growth. This also brings into question the role of 5-alpha reductase in promoting an anabolic state. Perhaps the fact that Primobolan® is a non-aromatizable steroid is more relevant.

    Estrogen and GH/IGF-1
    To date the most common explanation for why anti-estrogens may be slightly counterproductive to growth in the sports literature has been the suggestion that estrogen plays a role in the production of growth hormone and IGF-1. IGF-1 (insulin like growth factor 1, formerly known as somatomedin C) is of course an anabolic product released primarily in the liver via GH stimulus. IGF-1 is responsible for the growth promoting effects (increased nitrogen retention, cell proliferation) we associate with growth hormone therapy. We do know that women have higher levels of growth hormone than men, and also that GH secretion varies over the course of the menstrual cycle in direct correlation with estrogen levels[iv]. Estrogen is likewise often looked at as a key trigger in the release of GH in women under normal physiological situations.

    It is also suggested that the aromatization of androgens to estrogens in men plays an important role in the release and production of GH and IGF-1. This was evidenced by a 1993 study of hypogonadal men, comparing the effects of testosterone replacement therapy on GH and IGF-1 levels with and without the addition of tamoxifen[v]. When the anti-estrogen tamoxifen was given, GH and IGF-1 levels were notably suppressed, while both values were elevated with the administration of testosterone enanthate alone. Another study has shown 300mg of testosterone enanthate weekly (which elevated estradiol levels) to cause a slight IGF-1 increase in normal men, whereas 300mg weekly of nandrolone decanoate (a poor substrate for aromatase that caused a lowering of estradiol levels in this study) would not elevate IGF-1 levels[vi]. Yet another study shows that GH and IGF-1 secretion is increased with testosterone administration on males with delayed puberty, while dihydrotestosterone (non-aromatizable) seems to suppress GH and IGF-1 secretion, presumably due to its strong anti-estrogenic/gonadotropin suppressing action[vii]. All of these studies seem to support a direct, estrogen-dependant mechanism for GH and/or IGF-1 release in men. It is difficult to say at this point just how important estrogen is to IGF-1 production as it relates to the promotion of anabolism in the steroid using athlete, however it remains an interesting subject to investigate.

    Glucose Utilization and Estrogen
    Estrogen may play an even more vital role in promoting an anabolic state by affecting glucose utilization in muscle tissue. This occurs via an altering the level of available glucose 6-phosphate dehydrogenase. G6PD is an important enzyme in the support anabolism, as it is directly tied to the use of glucose for muscle growth and recuperation[viii] [ix]. During the period of regeneration after skeletal muscle damage, levels of G6PD are shown to rise dramatically. G6PD enzyme plays a vital role in what is known as the pentose phosphate pathway, and as such this rise is believed to enhance the PPP related process in which nucleic acids and lipids are synthesized in cells; fostering the repair of muscle tissue.

    A 1980 study at the University of Maryland has shown that levels of glucose 6-phosphate dehydrogenase rise after administration of testosterone propionate, and further that the aromatization of testosterone to estradiol is directly responsible for this increase.[x] In this study neither dihydrotestosterone nor fluoxymesterone could mimic the affect of testosterone propionate on levels of G6PD, an affect that was also blocked by the addition of the potent anti-aromatase 4-hydroxyandrostenedione to testosterone. 17-beta estradiol administration caused a similar increase in G6PD, which was not noticed when its inactive estrogen isomer 17-alpha estradiol (unable to bind the estrogen receptor) was given. An anti-androgen could also not block the positive action of testosterone. This study provides one of the first palatable explanations for a direct and positive effect of estrogen on muscle tissue.

    What does this all mean?
    It is a long held belief among athletes that estrogen maintenance drugs can slightly hinder muscle gains during steroid therapy with a strong aromatizable steroid such as testosterone. Whether or not we have plausibly explained this remains to be seen, however the above evidence certainly does provide strong support for a direct and positive affect of estrogen on growth. Does this mean we should abandon estrogen maintenance drugs? I don’t think that should be the case. It is important to remember that estrogen can deliver many unwanted effects such as increased water retention, fat deposition and the development of female breast tissue when it becomes too active in the male body. Clearly if we plan a high-dose cycle with an aromatizable steroid, anti-estrogens will be an important inclusion. However we cannot ignore the suggestion of using estrogen maintenance drugs only when they are necessary to combat visible side effects during mild to moderately dosed cycles,especially if bulk is the ultimate goal of the athlete.


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    And the wheel goes round and round.... I've already responded to that. Search my posts.


    Edit: I'll save ya the hassle.

    Quote Originally Posted by Du View Post
    [/INDENT]

    If the idea of nolva being bad is what you got out of that article, I would suggest a re-read. Nowhere in there is there any comparison of Clomid vs Tamox, which is the topic of this discussion.

    This essay is supporting the idea of limited anti E's while on PCT; not of Clomid over Nolva.

    Quote Originally Posted by Du View Post
    Ha, I read too fast, sorry about that.

    My opinions, well... I guess I roundabout got to it in my last one; I still stand by Nolva over Clomid. The article itself really doesn't knock Nolva over Clomid, it simply suggests backing off the Anti E (whichever you may choose) unless you need it, as judged by physical appearance.

    Personally, unless I were able to get frequent (and I mean frequent) bloodwork to assess hormone levels, then I'd stick with avoiding gyno via use of an anti-.

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    Quote Originally Posted by Du View Post
    And the wheel goes round and round.... I've already responded to that. Search my posts.


    Edit: I'll save ya the hassle.

    Yeah, that's fine use whatever you want.

    My original post was stating that nolva decreases IGF-1 and GH. I never compared the two like your doing here, right?

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    Quote Originally Posted by CT View Post
    Yeah, that's fine use whatever you want.

    My original post was stating that nolva decreases IGF-1 and GH. I never compared the two like your doing here, right?

    Well, you said something to the effect of using Tamox is "the worst thing you can do to yourself post cycle. Use Clomid, aromasin, and nothing else."

    In doing so, you knock Tamox and support Clomid... hence, my reply.

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    Quote Originally Posted by CT View Post
    Why in your opinion is nolva better than clomid for PCT?

    opinion, and its just that...I feel..nolva/hcg OCT...clomid pct (but then why)...I know guys who will run a cycle for over a year...doing OCT the entire time...I think the future will be more a balance between peptide/igf/hgh/pituitary/test axis TO aas......in this case how effective or needed is a pct...when the results even with the doubted igf-2 lr3 is more of a leydig stimulus, and this is why folks are disappointed with the results..ITS NOT IGF-1.

    Here is an interesting read, couldnt find the other articles, but i am just defending my personal stance, not on a soap box to say one is bad, one is good, one is just superior to the other, imo

    Here is an article i found on the internet regarding the two compounds. You might have seen the post i made previously about my acne clearing, only to find out it comes back during PCT. After some research into this i found that the most liekly cause for this is the clomid. I foudn that i can reduce the acne by skipping on the clomid. Because i bought a shitload of nolva i will be using only this compound. What do you all think??

    Nolvadex vs. Clomid for PCT

    It seems like everyday questions concerning PCT pop up, and weather one should use either Clomid or nolva or a combo of both. I hope that this article written by BigCat may help to clear up some misconceptions.

    While practically similar compounds in structure, few people ever really consider Clomid and nolva to be similar. Its not just a common myth in steroid circles, but even in the medical community. This misconception originates from their completely different uses. Nolvadex is most commonly used for the treatment of breast cancer in women, while Clomid is generally considered a fertility aid. In bodybuilding circles, from day one, Clomid has generally been used as post-cycle therapy and Nolvadex as an anti-estrogen.

    But as I intend to demonstrate this is in essence the same. I believe the myth to have originated because nolva is clearly a more powerful anti-estrogen, and the people selling Clomid needed another angle to sell the stuff, so it was mostly used as a post-cycle aid. But few users really understand how Clomid (and also Nolvadex, logically) works to bring back natural testosterone in the body after the conclusion of a cycle of androgenic anabolic steroids. After a cycle is over, the level of androgens in the body drop drastically. The body compensates with an overproduction of estrogen to keep steroid levels up. Estrogen as well inhibits the production of natural testosterone, and in the period between the return of natural testosterone and the end of a cycle, a lot of mass is lost. So its in everybody's best interest to bring back natural test as soon as humanly possible. Clomid and Nolvadex will reduce the post-cycle estrogen, so that a steroid deficiency is constated and the hypothalamus is stimulated to regenerate natural testosterone production in the body. That's basically how the mechanism works, nothing more, nothing less.

    Both compounds are structurally alike, classified as triphenylethylenes. Nolvadex is clearly the stronger component of the two as it can achieve better results in decreasing overall estrogen with 20-40 mg a day, than Clomid can in doses of 100-150 mg a day. A noteworthy difference. Triphenylethylenes are very mild estrogens that do not exert a lot, if any activity at the estrogen receptor, but are still highly attracted to it. As such they will occupy the receptor and keep it from binding estrogens. This means they do not actively work to reduce estrogen in the body like Proviron, Viratase or arimidex would (by competing for the aromatase enzyme), but that it blocks the receptor so that any estrogen in the body is basically inert, because it has no receptor to bind to.

    This has advantages and disadvantages. The disadvantage is that when use is discontinued, the estrogen level is still the same and new problems will develop much sooner. The advantage is that it works much faster and has results sooner than with an aromatase blocker like Proviron or arimidex. Therefor, when problems such as gynocomastia occur during a cycle of steroids one will usually start 20 mg/day of nolva or 100 mg/day of Clomid straight away, in conjunction with some Proviron or arimidex. The proviron or arimidex will actively reduce estrogen while the Clomid or Nolvadex will solve your ongoing problem straight away. This way, when use is discontinued there is no immediate rebound.

    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.

    Another noteworthy fact about Nolvadex is that it acts more potently as an estrogen in the liver. As you remember, I mentioned that clomiphene and tamoxifen are basically weak estrogens. Well, tamoxifen is apparently still quite potent in the liver. This offers us the positive benefits of this hormone in the liver, while avoiding its negative effects elsewhere in the body. As such Nolvadex can have a very positive impact on negative cholesterol levels2 in the body, and therefore too should be considered a better choice than Clomid. It will not solve the problem of bad cholesterol levels during Steroid use, but will help to contain the problem to a larger degree.

    Another reason why I promote the use of Nolvadex over Clomid post-cycle (as if being 3-4 times stronger and having more of a direct effect on restoring natural test wasn't enough) is because it's a lot safer. Not just because it improves lipid profiles, but also because it simply doesn't have the intrinsic side-effects that Clomid has. Clomid causes more acne for sure, but that's mainly because you need to use a 3-4 times higher dose. But Clomid seems to also affect the eyesight. Long-term Clomid therapy causes irreversible changes in eyesight3 in users. Irreversible. For me that alone is reason enough to prefer Nolvadex.

    Lastly, one should be aware that use of these compounds can reduce the gains made on steroids. Nolvadex more so than Clomid, simply because it is stronger. Estrogen is responsible for a number of anabolic factors such as increasing growth hormone output, upgrading the androgen receptor and improving glucose utilization. This is why aromatizing steroids like testosterone are still best suited for maximum muscle gain. When reducing the estrogen levels, we therefore reduce the potential gains being made. For this reason one may opt to try Clomid during a cycle instead of Nolvadex. Although I would imagine that the problem that needed solved would be of more concern, in which case nolva remains the weapon of choice. It's a plain fact that there is a high correlation between gains and side-effects. Either you go for maximum gains and tolerate the side-effects, or you reduce the side-effects, and with it the gains. That's life, nothing is free.
     
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    THE EXCITING THING HERE IS THIS

    10 WEEK AAS CYCLE} YOU KNOW IT ALL=)...HGH IN MIX? LETRO, ARIM, HGC on cycle therapy

    10 WEEK PCT???} IGF-1 LR3, IGF-2 LR3 (HPTA) HCG, GHRP-6, GHRP-2, CJC-1295, FRAGMENTS, HEXARELIN, NOVLADEX/CLOMID.............HOLY SHIT THERE IS NO PCT, JUST AN AAS FLIP RECOVERY

    which 10 week cycle will i gain the most...each persons chemistry is different, as we have all learned, but this insures no ectomorphic hard gainer will be left in the cold, no age is out of the race. its a win win situation...thanks to PAULING, COREY AND JAMES D. WATSON

    Now someone needs to simply find the mutation code and administration for myostatin and it gets even sweeter=)

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    Quote Originally Posted by barrym View Post
    opinion, and its just that...I feel..nolva/hcg OCT...clomid pct (but then why)...I know guys who will run a cycle for over a year...doing OCT the entire time...I think the future will be more a balance between peptide/igf/hgh/pituitary/test axis TO aas......in this case how effective or needed is a pct...when the results even with the doubted igf-2 lr3 is more of a leydig stimulus, and this is why folks are disappointed with the results..ITS NOT IGF-1.

    Here is an interesting read, couldnt find the other articles, but i am just defending my personal stance, not on a soap box to say one is bad, one is good, one is just superior to the other, imo

    Here is an article i found on the internet regarding the two compounds. You might have seen the post i made previously about my acne clearing, only to find out it comes back during PCT. After some research into this i found that the most liekly cause for this is the clomid. I foudn that i can reduce the acne by skipping on the clomid. Because i bought a shitload of nolva i will be using only this compound. What do you all think??

    Nolvadex vs. Clomid for PCT

    It seems like everyday questions concerning PCT pop up, and weather one should use either Clomid or nolva or a combo of both. I hope that this article written by BigCat may help to clear up some misconceptions.

    While practically similar compounds in structure, few people ever really consider Clomid and nolva to be similar. Its not just a common myth in steroid circles, but even in the medical community. This misconception originates from their completely different uses. Nolvadex is most commonly used for the treatment of breast cancer in women, while Clomid is generally considered a fertility aid. In bodybuilding circles, from day one, Clomid has generally been used as post-cycle therapy and Nolvadex as an anti-estrogen.

    But as I intend to demonstrate this is in essence the same. I believe the myth to have originated because nolva is clearly a more powerful anti-estrogen, and the people selling Clomid needed another angle to sell the stuff, so it was mostly used as a post-cycle aid. But few users really understand how Clomid (and also Nolvadex, logically) works to bring back natural testosterone in the body after the conclusion of a cycle of androgenic anabolic steroids. After a cycle is over, the level of androgens in the body drop drastically. The body compensates with an overproduction of estrogen to keep steroid levels up. Estrogen as well inhibits the production of natural testosterone, and in the period between the return of natural testosterone and the end of a cycle, a lot of mass is lost. So its in everybody's best interest to bring back natural test as soon as humanly possible. Clomid and Nolvadex will reduce the post-cycle estrogen, so that a steroid deficiency is constated and the hypothalamus is stimulated to regenerate natural testosterone production in the body. That's basically how the mechanism works, nothing more, nothing less.

    Both compounds are structurally alike, classified as triphenylethylenes. Nolvadex is clearly the stronger component of the two as it can achieve better results in decreasing overall estrogen with 20-40 mg a day, than Clomid can in doses of 100-150 mg a day. A noteworthy difference. Triphenylethylenes are very mild estrogens that do not exert a lot, if any activity at the estrogen receptor, but are still highly attracted to it. As such they will occupy the receptor and keep it from binding estrogens. This means they do not actively work to reduce estrogen in the body like Proviron, Viratase or arimidex would (by competing for the aromatase enzyme), but that it blocks the receptor so that any estrogen in the body is basically inert, because it has no receptor to bind to.

    This has advantages and disadvantages. The disadvantage is that when use is discontinued, the estrogen level is still the same and new problems will develop much sooner. The advantage is that it works much faster and has results sooner than with an aromatase blocker like Proviron or arimidex. Therefor, when problems such as gynocomastia occur during a cycle of steroids one will usually start 20 mg/day of nolva or 100 mg/day of Clomid straight away, in conjunction with some Proviron or arimidex. The proviron or arimidex will actively reduce estrogen while the Clomid or Nolvadex will solve your ongoing problem straight away. This way, when use is discontinued there is no immediate rebound.

    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.

    Another noteworthy fact about Nolvadex is that it acts more potently as an estrogen in the liver. As you remember, I mentioned that clomiphene and tamoxifen are basically weak estrogens. Well, tamoxifen is apparently still quite potent in the liver. This offers us the positive benefits of this hormone in the liver, while avoiding its negative effects elsewhere in the body. As such Nolvadex can have a very positive impact on negative cholesterol levels2 in the body, and therefore too should be considered a better choice than Clomid. It will not solve the problem of bad cholesterol levels during Steroid use, but will help to contain the problem to a larger degree.

    Another reason why I promote the use of Nolvadex over Clomid post-cycle (as if being 3-4 times stronger and having more of a direct effect on restoring natural test wasn't enough) is because it's a lot safer. Not just because it improves lipid profiles, but also because it simply doesn't have the intrinsic side-effects that Clomid has. Clomid causes more acne for sure, but that's mainly because you need to use a 3-4 times higher dose. But Clomid seems to also affect the eyesight. Long-term Clomid therapy causes irreversible changes in eyesight3 in users. Irreversible. For me that alone is reason enough to prefer Nolvadex.

    Lastly, one should be aware that use of these compounds can reduce the gains made on steroids. Nolvadex more so than Clomid, simply because it is stronger. Estrogen is responsible for a number of anabolic factors such as increasing growth hormone output, upgrading the androgen receptor and improving glucose utilization. This is why aromatizing steroids like testosterone are still best suited for maximum muscle gain. When reducing the estrogen levels, we therefore reduce the potential gains being made. For this reason one may opt to try Clomid during a cycle instead of Nolvadex. Although I would imagine that the problem that needed solved would be of more concern, in which case nolva remains the weapon of choice. It's a plain fact that there is a high correlation between gains and side-effects. Either you go for maximum gains and tolerate the side-effects, or you reduce the side-effects, and with it the gains. That's life, nothing is free.
     
    Via……..pimpinUNIT…MESOMORPHISIS.COM


    Hahaha.... as I said, wheel goes round & round. Above, I posted my replies to the "clomid vs nolva" article. In the same thread, I posted the article by BigCat that you just posted.

    It's like deja vu, all over again.

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    no need for both, drop the clomid and rock nolva

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    Quote Originally Posted by Du View Post
    Hahaha.... as I said, wheel goes round & round. Above, I posted my replies to the "clomid vs nolva" article. In the same thread, I posted the article by BigCat that you just posted.

    It's like deja vu, all over again.

    haha yea, true.....if we needed to be right we would be taking estrogen

    .

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    i am on clomid right now actually, it works well, but not to well, which is fine for the moment, for me....novla is superior but is different, as the good books say

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    Quote Originally Posted by Du View Post
    Well, you said something to the effect of using Tamox is "the worst thing you can do to yourself post cycle. Use Clomid, aromasin, and nothing else."

    In doing so, you knock Tamox and support Clomid... hence, my reply.

    I said it's the worst thing during PCT becasue it lowers your natural GH and IGF-1 levels. Do you not think that is important while trying to recover from an AAS cycle?

    As for natural test recovey, I would still use clomid over nolva. Always.

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    Quote Originally Posted by CT View Post
    I said it's the worst thing during PCT becasue it lowers your natural GH and IGF-1 levels. Do you not think that is important while trying to recover from an AAS cycle?

    As for natural test recovey, I would still use clomid over nolva. Always.

    My issue is.... a few people are coming to the same conclusion as you are, based upon that article. But, that article says nothing about the affects of Clomid on IGF; it *only* mentions Nolva. So people start rallying against Nolva (and therefore in support of Clomid), but not knowing the effects of Clomid.

    It's like... Obama is proven to be bad for the economy, so therefore, Republicans are GOOD. The argument just doesn't make complete sense...

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    Quote Originally Posted by Du View Post
    My issue is.... a few people are coming to the same conclusion as you are, based upon that article. But, that article says nothing about the affects of Clomid on IGF; it *only* mentions Nolva. So people start rallying against Nolva (and therefore in support of Clomid), but not knowing the effects of Clomid.

    It's like... Obama is proven to be bad for the economy, so therefore, Republicans are GOOD. The argument just doesn't make complete sense...

    That is not the only article in which I am basing my opinion on. There are several others. I will find them and post them up for you. Give me a little time as I'm not sure exactly where they are at the moment.

    My first response to this entire thing was nolva causes igf-1 and gh supression, nothing more. You are turning this into a nolva vs. clomid thing, which is never what I stated. I said that I would use clomid over nolva. Nothing more.

    As far as politics go......they're all crooked so that's that.

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    Special thanks to Heavyiron for this one:

    Effect of tamoxifen on GH and IGF-1 serum level in stage I-II breast cancer patients.

    Mandal* M, Moro C, Ferretti G, Calabro MG, Nolè F, Rocca A, Munzone E, Castro A, Curigliano G.

    Division of Medical Oncology, European Institute of Oncology, Via Ripamonti 435, 20141-Milan, Italy. mario.mandala@ieo.it

    OBJECTIVE: Tamoxifen suppresses insulin-like growth factor-1 (IGF-1) plasma levels in early and advanced breast cancer patients. Relationships between tamoxifen (GH) and IGF-1 are complex and not completely described yet. The present investigation was performed to evaluate the effect of acute and chronic tamoxifen administration on GH response to growth hormone-releasing hormone (GHRH), as well as on IGF-1 serum levels. MATERIALS AND METHODS: Evaluation of GH after administration of GHRH was performed (a) at baseline, (b) 3 hours after 20 mg oral administration of tamoxifen and (c) after 12 weeks of 20 mg a day oral tamoxifen treatment, in fifteen postmenopausal stage I-II breast cancer patients. IGF-I was measured at baseline and after chronic tamoxifen administration. RESULTS: The GH response to GHRH was significantly reduced after 12 weeks of tamoxifen 10 mg administered twice a day orally (mean peak 3.2 +/- 0.2 micrograms/l, mean AUC 261.3 +/- 18.2 micrograms/minute p < 0.01 versus basal AUC). A concomitant significant reduction of IGF-1 was observed after 3 months of tamoxifen treatment. Basal pretreatment levels of 113.2 +/- 15.5 micrograms/l were suppressed to 70 +/- 7.9 micrograms/l (p < 0.01). CONCLUSION: Our study confirm the inhibitory effect of tamoxifen on IGF-I and suggested, as shown in previous in vitro data, that its suppression could be directly related to GH reduction in response to GHRH stimulation

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    nolva works great 4 me.I switch it up sometimes use nova sometimes clomid.I swear the nova jumpstart me quicker.USE WHAT WORKS 4U



    -All of my posts are for entertainment purposes only, & not to be taken seriously
    -All content posted is nothing more than a comical skit, & a joke

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    Quote Originally Posted by CT View Post
    That is not the only article in which I am basing my opinion on. There are several others. I will find them and post them up for you. Give me a little time as I'm not sure exactly where they are at the moment.
    Yea that'd be huge; Id love to see. That might change my mind...

    Quote Originally Posted by CT View Post
    My first response to this entire thing was nolva causes igf-1 and gh supression, nothing more. You are turning this into a nolva vs. clomid thing, which is never what I stated. I said that I would use clomid over nolva. Nothing more.
    Your first response was:

    Quote:
    Why are you using nolva? It decreases your natural GH and IGF-1. That is the WORST thing you can do to yourself during PCT. Drop it NOW.

    You need clomid and aromasin. NOTHING ELSE.
    :UnQuote

    You told him to drop nolva "NOW" and use Clomid and Asin, "NOTHING ELSE". So to be fair... (I think, too, that I've already replied to this last time you said I'm making the issue up...) In any case, moot point.



    Quote Originally Posted by CT View Post
    As far as politics go......they're all crooked so that's that.
    It was a comparison to your position on the article.

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    Anyways CT, not looking to head toward a pissing match at all; hope you don't get that impression by my posts.

    I'd love to see the articles that you mention... but I am thinking perhaps starting a new thread with those would be the best route, as it would certainly be great to get the idea out to everyone, with supporting info.

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    Quote Originally Posted by Du View Post
    Anyways CT, not looking to head toward a pissing match at all; hope you don't get that impression by my posts.

    I'd love to see the articles that you mention... but I am thinking perhaps starting a new thread with those would be the best route, as it would certainly be great to get the idea out to everyone, with supporting info.

    Pissing matches on an internet forum is the saddest thing. Nobody wins and nobody learns. The only impression I ever got from your posts are that we are both passionate about our beliefs and we can agree to disagree. Nothing more than that.

    I could only find the one from Heavyiron. Honestly, we could both throw different studies up that contradict one another. Bottom line is if it works for you, why change it?

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    yea, i read many many articles on the subject of clomid not being as effective, that the companies were simply trying to get rid of it, by toting it as "just as effective". The vision sides are not worth it either, and can be long term..........look it up, i am not datbtrue lol...i am to lazy to pull articles up, i read em', extensively, then i read more, then more and more, I love the peptide world, myostatin and aas amazing future and it excites me!!!

    In clomids defense, i have noticed that a lower level fsh/lh prompt, is better than a larger pulse like Nolva would offer. I say this in terms of specific with ghrp-6 and cjc-1295...needs estrogen, yet estrogen was not effective on its own...SO I AM HAVING AMAZING POST CYCLE RESPONSE WITH THE USE OF PEPTIDES COMBINED WITH CLOMID, 100MG ED (DID 150 @2 DAYS)

    They all have there place, there is no monster, inferior, superior....and I am sure that tamox would serve well in another capacity....check it out

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    I do know for a fact that Dr's prescribe clomid for hypogonadotrophic hypogonadism, to try to jumpstart natural testosterone production.

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    What Bill states in Anabolics 9th Edition

    The methods for doing this seem to be different everywhere you 100k:/Take HCG, don't take HCG, use an aromatase inhibitor,just take Clomid, forget Clomid and just take Nolvadex." What option is really best? Without an understanding of exactly what is going on in your body, and why certain compounds help to correct the situation, choosing the right Post-Cycle Therapy (PCT) program can be quite confusing. In this section, the roles of anti-estrogens and HCG during this delicate window of time are discussed, while detailing an effective strategy for their use.
    ----------------------

    The PCT program outlined below represents what I consider to be an ideal and effective post-cycle program. It was developed by the doctors at the Program for Wellness Restoration (PoWeR), who have a formidable history helping patients recover normal hormonal functioning following steroid therapy. One of the key
    doctors on this program, Dr. Michael Scally, claims to have successfully treated more than 100 cases of hypogonadism/hypogonadotrophic hypogonadism, and is very well known in the field of androgen replacement therapy. PoWeR published this program as part of a recent clinical study, which involved 19 healthy male subjects who were taking supraphysiological (highly suppressive) doses of testosterone cypionate and nandrolone decanoate for 12 weeks. Their HPGA Normalization Protocol focuses on the combined use of HCG, Nolvadex' and Clomid, and is perhaps the only clinically documented post-cycle therapy program to be found in the medical literature (it is amazing how little attention has been paid< to hormone normalization in clinical medicine). The most notable variation from a classic PCT stack, such that I have (been a longtime supporter of, is the combined use of two anti-estrogens. In this case I cannot say that there is disadvantage to such use; perhaps it is indeed the better option.
    Examining the program closely, we note that the testes are hit hard with HCG at the onset of therapy. Its intake however, is limited to only 16 days. The doctor, undoubtedly recognize that when HCG is taken for too long or at too high a dosage, it can desensitize the L~ receptor.349 this would only further exacerbate the post cycle problem, not help it. Anti-estrogens are used during~ and after HCG, with a dosage of 10 mg of Nolvadex and 100 mg of Clomid per day rounding out this compliment of drugs. Clomid is used for a shorter period of time the Nolvadex, likely because of the desensitizing effect it to' can have (on the pituitary gland) with continued Use
    l
    Among other things, these two anti-estrogens will continue to foster LH release as testosterone levels start ~ go back up, as well as combat any potential estrogenic side effects that may be caused by HCG's up-regulation <I testicular aromatase activity.350 Although in the first couple of weeks the anti-estrogens probably do very Little they should be much more helpful towards the middle and end of the program. During this clinical investigation: normal hormonal function was restored in all subjects, I within 45 days of drug cessation. This is a definite success~ far more favorable than the protracted recovery wind9 noted in studies without post-cycle therapy, such as t~! 250 mg/week testosterone enanthate investigated, highlighted in Figure I. For me, I believe such a detail~ recovery program should follow any serious steroid cycle~ It is the best way to maintain your gains at their maximum and that is, after all, what we are after.



    Protocols: Human chorionic gonadotropin (hCG) is taken at 2500lU every other day for 16 days. Clomiphene citrate 50 mg is taken twice per
    day for 30 days.Tamoxifen citrate is taken 20 mg per day for 45 days.


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    Quote Originally Posted by jbryand101b View Post
    The methods for doing this seem to be different everywhere you 100k:/Take HCG, don't take HCG, use an aromatase inhibitor,just take Clomid, forget Clomid and just take Nolvadex." What option is really best? Without an understanding of exactly what is going on in your body, and why certain compounds help to correct the situation, choosing the right Post-Cycle Therapy (PCT) program can be quite confusing. In this section, the roles of anti-estrogens and HCG during this delicate window of time are discussed, while detailing an effective strategy for their use.
    ----------------------

    The PCT program outlined below represents what I consider to be an ideal and effective post-cycle program. It was developed by the doctors at the Program for Wellness Restoration (PoWeR), who have a formidable history helping patients recover normal hormonal functioning following steroid therapy. One of the key
    doctors on this program, Dr. Michael Scally, claims to have successfully treated more than 100 cases of hypogonadism/hypogonadotrophic hypogonadism, and is very well known in the field of androgen replacement therapy. PoWeR published this program as part of a recent clinical study, which involved 19 healthy male subjects who were taking supraphysiological (highly suppressive) doses of testosterone cypionate and nandrolone decanoate for 12 weeks. Their HPGA Normalization Protocol focuses on the combined use of HCG, Nolvadex' and Clomid, and is perhaps the only clinically documented post-cycle therapy program to be found in the medical literature (it is amazing how little attention has been paid< to hormone normalization in clinical medicine). The most notable variation from a classic PCT stack, such that I have (been a longtime supporter of, is the combined use of two anti-estrogens. In this case I cannot say that there is disadvantage to such use; perhaps it is indeed the better option.
    Examining the program closely, we note that the testes are hit hard with HCG at the onset of therapy. Its intake however, is limited to only 16 days. The doctor, undoubtedly recognize that when HCG is taken for too long or at too high a dosage, it can desensitize the L~ receptor.349 this would only further exacerbate the post cycle problem, not help it. Anti-estrogens are used during~ and after HCG, with a dosage of 10 mg of Nolvadex and 100 mg of Clomid per day rounding out this compliment of drugs. Clomid is used for a shorter period of time the Nolvadex, likely because of the desensitizing effect it to' can have (on the pituitary gland) with continued Use
    l
    Among other things, these two anti-estrogens will continue to foster LH release as testosterone levels start ~ go back up, as well as combat any potential estrogenic side effects that may be caused by HCG's up-regulation <I testicular aromatase activity.350 Although in the first couple of weeks the anti-estrogens probably do very Little they should be much more helpful towards the middle and end of the program. During this clinical investigation: normal hormonal function was restored in all subjects, I within 45 days of drug cessation. This is a definite success~ far more favorable than the protracted recovery wind9 noted in studies without post-cycle therapy, such as t~! 250 mg/week testosterone enanthate investigated, highlighted in Figure I. For me, I believe such a detail~ recovery program should follow any serious steroid cycle~ It is the best way to maintain your gains at their maximum and that is, after all, what we are after.



    Protocols: Human chorionic gonadotropin (hCG) is taken at 2500lU every other day for 16 days. Clomiphene citrate 50 mg is taken twice per
    day for 30 days.Tamoxifen citrate is taken 20 mg per day for 45 days.


    AGAIN, NOT TO BE RUDE, BUT THIS IS ALL JUST WHAT WORKS FOR YOUR CHEMISTRY, YOUR PREF, YOUR OPINION......BASED ON ARTICLES AND RESEARCH YOU HAVE BEEN EXPOSED TO. THE ONLY PEOPLE I WOULD TRUST TO GIVE ADVICE, TBH, ARE PROFESSIONAL BODYBUILDERS AND IF NOT MORE SO, SCIENTISTS THAT ARE IN THIS PARTICULAR FEILD OF RESEARCH, AND HAVE SOME YEARS BEHIND THEM.

    WITH THAT...I AGREE WITH HCG, THE AMOUNTS I DO NOT. I HAVE READ MANY PAPERS BASED ON THE FACT THAT REGULAR LARGE DOSES ARE MORE BENEFICIAL (IE ABOVE 1500MG)....BUT EVERY TWO DAYS, NOT LIKELY, NOR AFFORDABLE, AND THE FIRST I HAVE HEARD OF IT. UNDERSTAND THAT PEOPLE HERE READ 10 OR MORE ARTICLES ON A SUBJECT, SCIENTIFIC, AND IF YOU FALTER OFF THE PATH TO FAR, DEDUCTIVELY WHAT YOU ARE SAYING IS JUST A COPY OF A FEW ARTICLES AND YOU OPINION, LIKE I SAID JUST ANOTHER OPINION.
    PH BALANCE, TRAINING INTENSITY, PAST CHRONIC ISSUES, AGE, BODYFAT TO LEAN MASS, TRAINING HISTORY, TIME ON AAS OR OTHER AND SO MUCH MORE.....THESE ARE AT THE ROOT OF WHICH PCT WORKS BEST, AAS AND SLIN ARE THE SAME.
    I SAY, READ ALL YOU CAN FROM ACTUAL SCIENTIFIC RESEARCH, LOOK UP THE COMPANY THAT MAKES IT AND GET TRIAL RESEARCH...THEN USE YOUR BEST JUDGEMENT AS TO WHICH WORKS BEST...THERE IS NO MAGIC ONE, NEVER WILL BE, HOWEVER THERE IS A BEST ONE, AND ITS FOR YOU TO FIGURE OUT, NOT EXPECT OTHERS TO DO YOUR WORK FOR YOU.

    B-

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