(Forum for members to discuss the use of anabolic steroids)
- Rep Power
Test only 1st cycle
28 5"10 170 14%
Just started test 400/12 weeks. I only have 1 vial so i'm shorting myself every week. Turns out to be 333mg test/12 weeks.
Will post my results weekly.
I have Arimidex, Nolvadex, and Clomid on hand for PCT and possible sides during cycle. If sides occur what do you recommend for treatment?
moved to the appropriate forum.....
Stone Cold..............................Never Too Old
Disclaimer: Steroidology.com does not promote the use of anabolic steroids without a doctor's prescription. The information we share is for entertainment purposes only.
Just run the arimadex on cycle-save nolva clomid for pct.
I would actually just save nolva for gyno sides-keep it on hand and only use if needed-run the just clomid for your pct
This way you won't have to buy nolva on future cycles if you don't use it
What sides are u concerned about?
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i agree other then running just the clomid...
I'd run just the Nolva...no sides and its a superior serm.....
I have seen many articles and blog's on the clomid vs nolva thing. Some say novla is better-although a lot of people say clomid is actually better at restarting HPTA. This would lead me to believe clomid would be a better choice unless you body acts negatively to it.
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LOL most that I've read states Nolva is better...
WTF tho they both work...right?
Here is a good read...
The stuff about clomid and nolva are in red
Post Cycle Therapy (PCT)
By: Anthony Roberts
After a cycle, we have one goal: to hold onto the gains we made during the cycle. Unfortunately, this is easier said than done, because the levels of various hormones and other substances that were circulating around your body during the cycle (huge amounts of testosterone, insulin-like growth factor, growth hormone, and lower amounts of muscle-wasting glucocorticoids) are now changing. Sadly, they are making way for lower amounts of the hormones we want for building muscle, and higher amounts of the catabolic ones. What needs to be done, as quickly as possible, is to get your body to begin production of your own natural anabolic hormones, and produce less of the catabolic ones. Unfortunately, your body has other plans.
But then, so do I***8230;
***8230;and I***8217;m very confident that this protocol will allow you to recover your own natural hormonal levels quickly and lose far less of the gains you worked so hard for on the cycle. This protocol, which is typically implemented after a cycle is called ***8220;Post Cycle Therapy***8221; or ***8220;PCT***8221; for short.
First, I***8217;m going to tell you what anabolic hormones are typically low when a cycle ends, and which catabolic ones are high, then I***8217;ll tell you what drugs can change that condition as fast as possible. Is all of this necessary? No, not at all. You can skip to the end of the article and look for a little chart I made - the extent of my computer skill - which has all of the dosage recommendations and compounds involved to properly recover from your cycle. I think, however, that you***8217;ll see some very odd recommendations if you simply skip to the end, and will find yourself reading through the whole article to find out where they came from - or maybe you***8217;ll just try to find out what***8217;s gotten into me?
I***8217;m not re-inventing the wheel here, and you may have seen a piece of this information elsewhere (possibly in something I***8217;ve written, possibly somewhere else on the internet or in a magazine), but I***8217;m sure of two things:
* You***8217;ve never seen this PCT protocol anywhere
* This is the most effective PCT you***8217;ll ever see
First, I***8217;ll give you a brief explanation on the body and how it works, and why there***8217;s a lag-time after the cessation of Anabolic Steroids before the body returns to normal. Remember, during this lag-time you lose gains, so we really need to make it as short as possible. First, we need to understand a bit of what is going on in your body, what causes it to happen naturally, and what hormones are performing what function. Don***8217;t worry, I***8217;ll try to make it painless.
At the age of puberty, Gonadatropin Releasing Hormone (GnRH) is increasingly released from the Hypothalamus, in turn causing the secretion of Follicle Stimulating Hormone (FSH) and Luetenizing Hormone (LH) from the pituitary, and finally the male gonads (testes) are then stimulated by those pituitary hormones (LH and FSH). (1). FSH, although generally thought to only have a role in production of sperm, actually aids the in regulation of Leydig Cell function (2), while LH directly causes the Leydig Cells in the testes to secrete androgenic hormones such as testosterone (which is causes a surge in other anabolic hormones: Insulin Like Growth Factor, Growth Hormone, etc***8230;). Androgens do this by then targeting other tissues inside the body, either by attaching to the Androgen Receptors (AR), which are found primarily in the cytoplasm of specific cells, or by what***8217;s known as non-receptor mediated effects. When an androgen (your own natural testosterone or an anabolic steroid you***8217;ve injected or ingested) binds to a receptor inside the cell, it activates the transcription of specific genes. What does this mean? Don***8217;t worry, it just means that the steroid molecule gives the cell a message to do something. In the case of testosterone, for example, one of the messages it sends to the cell is to increase nitrogen retention in your body, thus allowing you to use more of the protein you take in, and build more muscle. In the case of testosterone (or anabolic steroids in general), this transcription causes a lot of different anabolic effects to take place: an increase in IGF, a decrease in cortisol, an increase in Red Blood Cell count, and the increased protein synthesis I already told you about. This is not to say that AR binding is the only thing that causes anabolic or androgenic effects, however. Oxymetholone and Methandrostenolone (Anadrol and Dianabol) both bind very weakly to the AR yet are both highly anabolic and androgenic. The diagram below is an example of an androgen***8217;s entry into a target cell, where it (in this case) stimulates protein synthesis, which is a major anabolic effect:
Under the control of this heightened state of androgens, you also go through androgenic development as well as anabolic development. This can be seen in puberty when males grow body hair experience voice changes, as experience genital development and growth.
Another characteristic of androgens in the body is that they are subject to what***8217;s known as a ***8220;negative feedback loop***8221;. Lets review one of the first things I mentioned, ok? Your Hypothalamus secretes GnRH, thus making the pituitary secrete LH & FSH, finally in turn causing the testes to stimulate the Leydig cells to produce testosterone (by conversion of cholesterol), remember? Ok, now, once testosterone is created however, it has the ability to in turn to undergo various metabolic processes that will inhibit GnRH, which in turn inhibits the secretion of LH and FSH, and that brings a halt to natural testosterone production. Once testosterone has stopped being produced, it no longer sends this negative signal, and GnRH eventually begins to do its job again. In this way, your body prevents excess hormones from being secreted and thus maintaining homeostasis (the status quo***8230; in this case a state where you are neither gaining nor losing muscle) (1). This negative feedback loop is partially why we use anabolic steroids***8230;we want more testosterone for anabolic purposes (or more Anavar or whatever) than our body will let us produce (not that our bodies produce Anavar, but you get the idea). When we use that injectable testosterone, it sends the message to our body to begin the negative feedback loop and discontinue producing/secreting the hormones that cause our natural testosterone production. The chart below clearly shows this process, displaying both the negative and positive feedback system(s):
So what I***8217;m saying is that anabolic steroids increase androgen levels in the blood, bringing a halt to GnRH, making the pituitary gland (eventually) responds by reducing the release of LH; this loss of LH has the effect of shutting down testosterone, of course, which you know is produced by the Leydig cells in the testes after they are stimulated by LH. Am I being repetitive? Yes. Do you need to understand all of this in order to understand the PCT protocol I***8217;m about to outline? Yes. Remember, the negative feedback loop is, of course, no problem while we are on a cycle. Want more testosterone (or androgens) in your body? Fill up a few more syringes!
But all good things come to an end, and most of us choose to end our cycles at some point. At this point, while there is still some androgens floating around in us, our natural production won***8217;t begin, and even once they are out, there may be some lag time before your body figures out that it needs to start producing its own androgens again. As I said before, this lag time is severely catabolic and it***8217;s where you lose a lot of your gains. SO what we need to do is coax the body into quickly producing its own androgens.
One of the first drugs we***8217;ll consider for this purpose is what is typically called a SERM. Nolvadex (Tamoxifen) is a SERM (Selective Estrogen Receptor Modulator, which means that it has the ability to act as an anti-estrogen with regard to certain genes, yet also acting as an estrogen with respect to others. That***8217;s the ***8220;selective***8221; part I guess. It does this by blocking gene transcription in some cases, and initiating gene transcription in others (3). Luckily for us, it has estrogenic effects on bones (meaning it increases their density), and blood lipids -meaning it lowers cholesterol-, (4)(5)as well as preventing gynocomastia by preventing estrogen gene transcription in breast tissue. However, it acts as an anti-estrogen in the pituitary, thus increasing LH and FSH, which results in an increase in testosterone. 20mgs of Nolvadex will raise your testosterone levels about 150% (6)...Nolvadex actually has quite a few applications for the steroid using athlete. First and foremost, it***8217;s most common use is for the prevention of gynocomastia. Nolvadex does this by actually competing for the receptor site in breast tissue, and binding to it. Thus, we can safely say that the effect of tamoxifen is through estrogen receptor blockade of breast tissue (7).
Estrogen is also important for a properly functioning immune system, and not only that, but your lipid profile (both HDL and LDL) should also show marked improvement with administration of tamoxifen (34).
Nolvadex also has some important features for the steroid using athlete. In hypogonadic and infertile men given nolvadex, increases in the serum levels of LH, FSH, and most importantly, testosterone were all observed (35)It can also block a bit of estrogen in the pituitary, which is a great benefit when used with HCG (more on that later) (36)(37). The increase in testosterone Nolvadex can give someone with a dysfunctional is basically that 20mgs of Nolvadex will raise your testosterone levels about 150% (6)...Why don***8217;t we use Clomid, another SERM? Well, basically because it takes much more to do the same thing. In comparison, it would require 150mgs of Clomid to accomplish that type of elevation in testosterone, but Nolvadex also has the added benefit of significantly increasing the LH (Leutenizing Hormone) response to LHRH (LH-releasing hormone) (6). This most likely indicates some kind of upregulation of the LH-receptors due to the anti-estrogenic effect Nolvadex has at the pituitary. Although both Nolvadex and Clomid are both SERMs, they are actually quite different. As you already know, Nolvadex is highly anti-estrogenic at the hypothalamus and pituitary, while Clomid exhibits weak estrogenic activity at the pituitary (7), which as you can guess, is less than ideal. It should be avoided for the PCT I***8217;m suggesting***8230;and in fact, avoided in general***8230;it***8217;s simply not as good as Nolvadex.
Need I even add that the 150mgs of Clomid you need to get the hormonal increase experienced with 20mgs of Nolvadex is much more expensive? So lets dump the Clomid***8230;and no, using it along with Nolvadex will provide no ***8220;synergy***8221; that I***8217;ve ever seen in any relevant study.
SO how much Nolvadex should you use during PCT? I favor using 20mgs.day, although to be totally honest, you can probably even get away with far less than that. Doses as low as 5mgs/day have proven to be as effective as 20mgs/day for certain areas of gonadal stimulation. (8) 20mgs/day, however, is a dose that myself and others have used with great success, and the research I***8217;ve done in this area typically uses this milligram amount. SO lets stick with 20mgs/day for now.
So that effectively suggests Nolvadex can not be used at Mega-doses to get a mega-increase in your natural hormones. We can***8217;t use huge doses of any Anti-Estrogen, actually, and expect huge increases in our natural hormones, actually. Arimidex (an Aromatase Inhibitor ***8211;which means it stops the conversion of testosterone into estrogen-another drug used to fight breast cancer like Nolvadex) exhibits basically the same effects when .5mgs or a full 1mg is used (9) and I have even read studies where up to 10mgs/day of Arimidex is studied with no clear benefit over 1mg/day. Letrozole (another Aromatase Inhibitor) is capable of inhibiting Aromatase maximally at a mere 100mcg/day (10.). So clearly we need to add in other compounds to our post cycle therapy (pct), because Mega-Doses of one compound will not I think it***8217;s absurdly funny to see people recommending upwards 40-80mgs/day of Nolvadex, or a full milligram (or two!) of Arimidex, in their post-cycle or on-cycle suggestions. I***8217;d steer very clear of listening to anyone who makes those types of recommendations***8230;
All of this tells me that you can***8217;t simply use mega-doses of Anti-Estrogens or SERMS to do anything more than reasonable doses. It must be, therefore, that your body can only respond with so much vigor to any one drug in those families. So lets add in another drug or two, ok? This way we can use reasonable doses of a few drugs and produce some synergy***8230;hopefully decreasing our recovery time.
We***8217;ll need something to go with Nolvadex, which acts in a different manner, and Human Chorionic Gonadatropin (HCG) is the clear choice here. Here***8217;s where things get a bit controversial (no, really***8230;I know you , because I***8217;m pretty much the only person around (currently) who recommends HCG for Post-Cycle Therapy. Although I***8217;m seen as Old School in this respect, really, this is a totally new paradigm for HCG use, made possible only by the inclusion of the other compounds I am introducing to you for post cycle therapy (pct). HCG is the natural choice, as it has been used successfully to cure AAS induced (11), and this alone warrants its inclusion to our cycle.
HCG is a peptide hormone manufactured by the embryo in the early stages of pregnancy and later by the placenta to help control a pregnant woman***8217;s hormones (can anything really be said to control a pregnant woman***8217;s hormones except ice-cream and chocolate?). Obviously, as you can guess from the name, it is a substance that stimulates the gonads (hence: gonadotropin). It does this by initiating gene transcription that is identical to that of Luetenizing Hormone, thereby causing the Leydig Cells to produce testosterone. Sounds great right? We can stimulate LH and FSH production with our Nolvadex, and then directly stimulate the Leydig Cells as well, to produce tons of testosterone by different routes! Well...it***8217;s not all that simple.
Unfortunately, while HCG increases Testosterone, it increases estrogen as well(12). As you probably know, estrogen acts directly on the Leydig cells to effect changes in the activities of enzymes important for testosterone synthesis (13) and may actually be considered an important part of that negative feedback loop I mentioned earlier. In addition, an increase in circulating levels of LH have been shown to induce down-regulation of LH-receptors in both rodent studies (14), as well as in human studies (15); since HCG mimics LH, you can expect it to do the same. This LH downregulation can cause an increase in steroidogenic cholesterol (the cholesterol earmarked by your body for conversion into testosterone). (16). Thus, after the initial HCG induced surge in testosterone is over, if you have used enough to downregulate your LH-receptors and increase estrogen too much, then more steroidogenic cholesterol is available. This is telling me that less is being converted to testosterone. In fact, rodent models suggest that if you take a dose large enough to cause a sharp increase of plasma testosterone, you will actually desensitize your Leydig cells to your next shot, and will possibly not experience any rise in testosterone from the second dose at all, or may only experience a very slight one at best (17.). Since this is due to LH-Receptor downregulation, and that occurs in human models too, it is pretty fair to assume that if your first dose of HCG is too large, your second won***8217;t be very effective. Unfortunately, this lack of an increase in testosterone doesn***8217;t necessarily mean that the HCG may be unable to increase circulating levels of Estrogen (18) And remember that increase in Estrogen will (most likely) cause your body ultimately to produce less testosterone. Low LH post-cycle is not the primary cause of slow recovery, because LH generally rises to levels above baseline after a cycle much sooner than testosterone production does. This is probably because the pituitary is working very hard to get your atrophied Leydig cells to start producing testosterone again. HCG should also bring back testicular volume; I feel the need to mention this because it***8217;s important to me and I suspect most men as well. It would also appear that HCG works very well when it***8217;s used on men who have low levels of LH to begin with (as you would be after a cycle), as many studies on pre-pubertal boys and Hypogonadotropic Hypogonadal men would suggest (19)
This suggests that a pre-exposure to normal LH levels or gonadatropins in general is necessary for HCG-induced Leydig Cell desensitization. This, of course is not a problem for us, as we***8217;ll be using it when LH/Gonadatropin levels are very low anyway ***8230;we just need to stop using it before we regain normal function, or it will work against us eventually. (19) (20). Luckily, the temporary Anabolic steroid induced hypogonadism that is experienced after a cycle basically allows us to respond to HCG like anyone with low LH levels (21), and thus, as I told you, a lot of the possible inhibitory effect of HCG is not going to be relevant because there was no prior ***8220;priming***8221; by circulating gonadotrophins. This is great news for us, because we are going to be using HCG during post cycle therapy (pct), when we need to get back some HPTA function, and not when we have levels of gonadatropins high enough to cause HCG-induced desensitization.
But are we still risking some inhibition and possibly delaying our recovery by using HCG? Probably not***8230;you see, some studies in humans have shown that HCG does not actually have a direct effect on inhibiting LH release in men (22)(23), but rather (probably) works to inhibit LH secretion indirectly, simply by stimulating the production of testosterone (thus activating the negative feedback loop). Another factor involved is the induction of testicular aromatase, which raises estrogen levels, again causing inhibition. Unfortunately, yet another process, the downregulation of the Leydig Cell LH receptor itself, seems to also play a role in high dose HCG testicular desensitization. This is also done by HCG actually blocking the conversion of 17 alpha-hydroxyprogesterone (17 OHP) to testosterone (24). Nolvadex actually stops this blocking-action of HCG from taking place (25). Most likely, because of Nolvadex***8217;s direct antiestrogenic effect and LH-upregulating effect on the Pituitary, suppression of gonadotropins via HCG is (25) almost totally stopped with concurrent administration of Nolvadex! So if we Use Nolvadex and we are only using HCG when we are low in gonadatropins, we won***8217;t be inhibited by it at all! Right?
Well***8230;maybe***8230;but there***8217;s still the issue of estrogen caused by that HCG-stimulated surge in testosterone. Well***8230;we can use low doses (300iu or so) to avoid some of that major spike in estrogen, and thus cause far less inhibition from the HCG (26). Of course, I***8217;d want to use a bit more HCG per injection (500iu), if I could, to get my body functioning fully more quickly, and lose less of my gains. Maybe we can get away with taking some Vitamin E with our Human Chorionic Gonadotropin (HCG), since it increases the responsiveness of plasma testosterone levels to Human Chorionic Gonadotropin (HCG), making them significantly higher during vitamin E administration than without it (27). So we can get a better response with our HCG by taking Vitamin E (I recommend 1,000iu/day), but that doesn***8217;t get rid of the problem that we have, which is the estrogen increase the HCG will cause.
Lets solve that pesky estrogen problem now***8230;. Lets add in an Aromatase Inhibitor! Which one, though? Well, since we are already using Nolvadex, we can***8217;t use Letrozole or Arimidex, as the Nolvadex will actually greatly decrease the blood plasma levels of them (28)!
So we have to use Aromasin (exemestane) as our Aromatase inhibitor (AI), because it***8217;s an aromatase inactivator, meaning it makes estrogen receptors useless, and instead of just inhibiting production (as an anti-aromatase would do) it cuts off production totally. Aromasin can also cause androgenic sides (29)(30)(31), which may help to elevate your mood while you are on post cycle therapy (pct). This final drug in my recommended PCT can effectively remove up to about 85%+ of estrogen from your body (32). Most importantly, using Aromasin together with Nolvadex doesn***8217;t reduce exemestane***8217;s effectiveness (33). So now, I think the problem of ANY inhibition possible with HCG is solved, and we can use that 500iu/day dose that I wanted to use previously.
With this post cycle therapy (pct), there will be a rapid increase in LH, FSH, and testosterone, as well as almost a complete block on all the factors that could be causing your natural hormones to be delayed in returning to baseline. For this reason, I feel that the second your cycle is over is when you should start this PCT (a week after your last shot, or the day after your last pill is fine). Remember, waiting for some of the extra androgens you***8217;ve been taking to leave your body is nonsensical, as we want to start recovery as soon as possible to retain maximum gains. There is no evidence to suggest waiting any length of time after your cycle is over will increase PCT effectiveness***8230;it simply prolongs the time you aren***8217;t doing anything positive to regain your natural hormones. And how long do we run this for? Well***8230;we need to stop the HCG relatively soon for reasons discussed earlier. But the Nolvadex, and Aromasin can be used for awhile longer. Ideally, we***8217;d be getting weekly blood work, but we could also get it done monthly, and just running this PCT until we see our natural hormones restored***8230;but weekly bloodwork isn***8217;t really an option for most of us. Failing the option of monitoring recovery with blood-work, I***8217;m going to give you my best thoughts on the time you should be running your post cycle therapy (pct). It***8217;s important to note I haven***8217;t discussed nutrition or other compounds that may be beneficial***8230;this is because in this article, I am primarily concerned with the restoration of hormonal function, nothing else. And with no further delays, here are my recommendations for PCT:
(The suggested PCT ouldnt cut/paste correctly....)
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 - leutenizing hormone - 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 - leutenizing hormone - 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 - leutenizing hormone - 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 - leutenizing hormone - 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 - leutenizing hormone - 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 [sex hormone binding globulin ] 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," Öa 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 - leutenizing hormone - 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 - leutenizing hormone - response. Furthermore it mildly blocked the effects of estrogen when both were incubated in the same culture.
To summarize the above research succinctly, Nolvadex is the more purely anti-estrogenic of the two drugs, at least where the hpta - hypothalamic-pituitary-testicular axis - (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 - hypothalamic-pituitary-testicular axis - , 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 - leutenizing hormone - 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 sex hormone binding globulin 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 gynecomastia 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.
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
Have any scientific articles supporting clomid as the superior serm?
Doesnt matter if Nolva is superior or not, I prefer Clomid, thats me..
I do but i dont have time to post them tonight-I will tom
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Cool, I'm interesting in reading them...
Originally Posted by newbie23
They both work... If you prefer one over the other that is cool.
Originally Posted by Biggin
With the peeps that say that clomid is superior... I'd like to see some scientific research supporting their arguments. Every legitimate article I've read supports Nolva...
I'd like to read anything comparing the two that claims clomid is better...
Awesome info dude..thanks. I ll be starting soon and researching...Thanks..
Wow! Got to tell you, this is the place for info. Ythrashin great post. Very informative. Insightful.
Originally Posted by ythrashin
I agree with your insight, and Iím an olítimer. I read and use whatís best, as most should do on here. When I started taking AAS, sites like time wasnít available. We, those of us in the gym exchanged info we Fucked up at times. We didnít have a large database that informed us of whatís best.
Ok Ythrashin I am home from the lake. When I first started thinking I was going to do a cycle I did a lot of research on PCT because thats what I was told was the most important part of your cycle. I came up with all the same studies you did regarding Nolva post cycle therapy (pct). So I originally ordered Nolva with my cycle for post cycle therapy (pct), turns out my supplier was out of Nolva. I knew there were only small differences between Nolva Clomid so I ask them to send me clomid instead so I could start my cycle right away.
Then I started noticing some very reputable guys on this sit ( stonecold and ozzy) say that clomid was actually better at restarting the HPTA. So when I started to dig deeper I realized they were right of course.
I cant remember if it is in this article or another I read that nolva also acts negatively towards Aromasin and I am a fan of Aromasin. The is overwhelming suggestions that it is a better Aromatase inhibitor (AI) than Adex because of the results vs sides ratio.
I have to paste this whole article here cause I am on an Apple and do not know how to put the link here. This is from Ozzy,s thread he posted it a couple months back.
More good Info on PCT/HCG/Recovery/Gyno....... by "Visions"
This is a very long read with helpful info....covering many area's. Enjoy
HCG & PCT
Post Cycle Therapy actually starts from the beginning of the cycle... To ensure recovery during post cycle therapy (pct), HCG is used to keep the leydig cells of the testes functioning throughout the cycle so that shutdown doesn't happen... Each shot of HCG triggers a peak output in 72hrs... taking shots sooner then 72hrs can run the risk of overstimulation which can impede their output... Clinical studies do take shots every 48hrs but for our use I would prefer to err on the side of caution... anyway for our needs taking the shots e3d or 2 X a week works great... but I must say that e3d is optimal... HCG needs to be started from the beginning of the cycle, contrary to what most guys believe, shutdown starts when they take their first steroid shot and the body quickly notices an androgen and starts to shutdown its production of Test... Waiting longer to start runs the risk that partial shutdown happens and not all the leydig cells will respond...
What I have recommended in the past is either 500iu's e3d or 500iu 2 X a week from the beginning of the cycle until 4 days before PCT starts... what I would like to see changed is to take 1500iu's for each of the last 2 shots... this will ensure full functioning for when PCT starts... My PCT recommendation will stay the same except now I'll recommend that as little as 25mg of Clomid a day is highly effective at stimulating normal test production... Week 1-3 of PCT = 25-100mg Clomid ed,,,You choose your dose of Clomid as anything in that range works great. Week 1-6 of PCT = 25mg Aromasin ed... I would like to add that its been shown in clinical studies that as little as 25mg ed of Clomid is effective to stimulate normal test production and at this dose no negative sides were noted so if you used clomid in the past and didn't like the negative sides then it may have been dose related... Gustavo77 found this study and this info is sure to help out alot of guys that would normally get negative sides from clomid and at this 25mg dose they can now bipass the negative sides yet be very effective... Here is the link to the study... This study will show test levels 600+ which is good... Other studies that I havn't given a link to yet show test levels 800+ when 100mg is taken... so its your choice to how much Clomid you want to take as both doses are effective...
Wiley InterScience :: Session Cookies
Deca and Tren can shut guys down hard and the last 2 shots of HCG being 1500iu's will greatly help ensure full funtioning before PCT starts...
Anytime you use Deca or Tren , Cabaser(Cabergoline, Dostinex) needs to be used from the beginning and through PCT... I find that taking a smaller dose ed works best and it keeps the libido up and running much better... .25mg ed works great for me... less or more can be taken to find what works for you...
As with any drug you should be aware of any potential side affects and Clomid does have the potential for a certain side affect that is rare and I've never known anyone to get it at all yet I believe you should be aware of it so you can make an imformed judgement before using it for the first time...
Here is the study:
Visual disturbance secondary to clomiphene citrate. [Arch Ophthalmol. 1995] - PubMed Result
Visual disturbance secondary to clomiphene citrate.
Midwest Eye Institute, Methodist Hospital of Indiana, Indianapolis, USA.
OBJECTIVE: To identify a distinctive constellation of persistent visual abnormalities secondary to treatment with clomiphene citrate. DESIGN: Description of the clinical findings in three patients with visual disturbance secondary to clomiphene treatment. SETTING: A neuro-ophthalmology referral center. PATIENTS: Three women aged 32 to 36 years treated for infertility with clomiphene for 4 to 15 months. RESULTS: All three patients experienced prolonged afterimages (palinopsia), shimmering of the peripheral field, and photophobia while undergoing treatment with clomiphene. The results of the neuro-ophthalmologic examination and electrophysiologic studies were normal in all three patients. Unlike previously reported cases, visual symptoms did not resolve on cessation of treatment. Patients remain symptomatic from 2 to 7 years after discontinuing treatment with the medication. CONCLUSIONS: Treatment with clomiphene can cause prolonged visual disturbance. Patients who develop such symptoms should be advised that continued administration may cause irreversible changes. Women with characteristic visual symptoms should be questioned about past use of clomiphene.
PMID: 7710399 [PubMed - indexed for MEDLINE]
Recommendations without Clomid
For those that havn't used Clomid before and are afraid to use it here are my recommendations:
500iu HCG 2 X a week throughout the cycle,,, the last 2 shots before PCT use 1500ius each shot,,, this will be a boost to get all leydig cells to respond... PCT= 500iu's HCG e3d for 5 shots along with 25mg Aromasin ed for 6 weeks... The HCG during PCT is getting your leydig cells up to full production but HCG as I mentioned before mimics LH and FSH so during this time LH and FSH is suppressed... LH and FSH production will kick in when the HCG is stopped and estrogen levels drop below normal which with the Aromasin will ensure that it does and LH will kick in on high as it normally would do after any cycle the difference is now the leydig cells are ready to respond and they will at full production...
I want to explain this further so you completely understand... Lets say you did a cycle with no HCG throughout the cycle and did a Nolva PCT,,,Clomid Aromasin PCT or the use of HCG Aromasin PCT... During the cycle the leydig cells of the testes would completely shut down... After shutting down the leydig cell have a hard time responding to the body's natural production of LH... Even after this cycle the body's LH production will go into high gear... the problem is the leydig cells don't respond well now because of being shut down... Now you do your Nolva pct... Nolva isn't shown in any studies that I can find to increase Test production so what it would do for PCT I don't know(if a study is found I will take that into consideration but there is overwhelming evidence how AI's work so even if 1 study is found there is much more evidence showing how AI's work fantastly)... Even a clomid/Aromasin PCT without HCG throughout the cycle makes recovery hard because it will take time for the leydig cells to respond to the LH production that Clomid is telling your body to produce... infact you may not completely recover 100% after any cycle if the leydig cells are allowed to shut down during the cycle... Even the use of HCG PCT after allowing the leydig cells to shut down makes it hard for the leydig cells to respond and their response is progressive as the shots progress...
I receive many PM's about PCT and have given this simular advice with great success... mostly to guys that did other PCT's using Nola and didn't recover... also alot of them were on very long cycles without the use of HCG... The key is using the HCG throughout the cycle and starting it from the beginning because if you skip this part its harder for the testes to respond to anything...
Gyno, Estrogen, AI's, Nolva and HCG
Misconceptions during PCT
Pound4Pound: Could I get your thoughts on this, someone else was telling me not to use an Aromatase inhibitor (AI) in PCT because it will drive estrogen TOO low and cause an estrogen rebound. This is what he said,
His Friend: "Arimidex should not be used post cycle because the risk of driving estrogen too low, and therefore further damaging an already compromised Lipid Profile, is too great (this also drives libido back into the ground, and we don't want that, do we?).
If you overlap the Arimidex with the Nolvadex, then your estrogen levels will be kept in check. On cycle, there is more test to be converted into estrogen, so Arimidex would be more of a necessity if you're sensitive to estrogen. However, post-cycle, during post cycle therapy (pct), you natural testosterone levels are being restored which range from 2-11mg per day. The estrogen conversion will be significantly lower with your natural testosterone range, therefore Nolvadex (and Clomid if you include this in the mix) will be sufficient at combating estrogen while increasing LH production. In addition, there is no estrogen rebound when discontinuing the Nolvadex. There is estrogen rebound when discontinuing Arimidex. By switching over to Nolvadex you will be fighting estrogen from the rebound. If you decided to use Arimidex during PCT along with hCG, then you will have nothing to fight the rebound of estrogen."
Visions: Glad you brought this up... Unfortunately your friends logic is completely wrong and I'll prove it to you... I'll Pick it apart one by one... Your friend talks about Arimidex but I'm going to talk about Aromasin too because thats what I recommend for good reasons... There are alot of statements so try to follow everything I say by first reading over his statement... I'll break it apart and make comments... Some sentences I'll have to break apart because of the complex answer to each statement... to be able to follow you may need to reread the full sentence again because my answers are long... at the end I'll sum it up and then explain what happens when you follow my protocol...
His Friend: "Arimidex should not be used post cycle because the risk of driving estrogen too low,
Visions:Since your friend didn't talk about the use of HCG during a cycle he's probably used to the old way of thinking so I'll pick apart this first statement as if HCG wasn't used since he didn't mention it... but even if he did my answer would be the same but would point out the need for the Aromatase inhibitor (AI) even more... Most PCT's start 2 weeks after their last shot of Test E or Cyp... The 1/2 life of these is roughly 7 days... this means that in 7 days 1/2 of the steroid is out of your system... another 7 days half of that is out etc so in reality its not out of your system for 3 weeks but after 2 we don't really feel it but its there... this is why when Dr's give you a shot of Sust they say its good for 4 weeks yet we as body builds say its only good for 3 weeks yet in reality its still in our system for 4 buy by the 4th week its not an amount we thing does much so we start our PCT in 3 weeks... Now you have to take into consideration that the amounts we use are usually 5 X or more then what the Dr would give you... Example: 500mg of Test E a week... within 7 days 250mg is out of our system... 7 more days and now we are at 125mg ... that means starting week 3 we have 125mg in us and thats an amount for a testosterone replacement therapy (TRT) dose from the DR so in week 3 we have normal or above normal levels of Testosterone and estrogen... Yet your friend states that estrogen is already too low to use an Aromatase inhibitor (AI) when in fact its in the perfect level to start to trigger test production...
Roid Calculator - half lifes steroids ester half-life
His Friend: and therefore further damaging an already compromised Lipid Profile,
Visions:#1 Arimidex isn't good for the lipid profile and its why I recommend Aromasin which doesn't affect the lipid Profile... 2 weeks after your last shot you can see you still need an AI... yes the Aromatase inhibitor (AI) will drop estrogen below normal but this is what stimulates test production by putting LH in high gear... Now you have to consider the biggest players in the bad lipid profile---The high androgens from the cycle plus the diet with huge amounts unsaturated fats from all the proteins... The lipid profile isn't something you will be able to control during the cycle unless you use a statin... The short period for PCT isn't the culprit and keeping estrogen low at this point isn't going to change the damage during the cycle but what it will do is stimulate test production which in return will increase estrogen levels to just below normal as production gets to full production...
His Friend: the risk of driving estrogen too low is too great (this also drives libido back into the ground, and we don't want that, do we?).
Visions: Low estrogen doesn't kill the libido... high estrogen can and does... If you don't believe me give yourself a shot of estrogen... high estrogens bind to androgen receptors making them useless... high estrogens raise shbg which binds to free test... free test is what makes you horny... guys that follow the nolva protocol end up with too much estrogen at the beginning of PCT because of the rebound they get from stopping the Aromatase inhibitor (AI) before estrogen is in the normal range and Nolva has a hard time controling the estrogen at the receptor... Also I would like to see the study that says estrogen makes you horny... Low estrogens killing the libido is a huge misconception and is a funny statement to me... go to your Dr and ask him for a shot of estrogen to make you horny and see how he laughs...
His Friend: If you overlap the Arimidex with the Nolvadex, then your estrogen levels will be kept in check.
Visions: This is completely wrong and is the reason for estrogen rebound after a cycle... I hear about it all the time,,, guys are fine during the cycle using an Aromatase inhibitor (AI) , then 2 weeks after their last shot they switch to Nolva for PCT and then they wonder why they get gyno and blame it on estrogen rebound... The reason is they still have too much test in them when they start PCT because the Aromatase inhibitor (AI) is keeping Test levels high by not aromatising,,,then they stop the Aromatase inhibitor (AI) and the Test aromatises and they start on Nolva which only binds to the estrogen receptors and doesn't do anything to control estrogen... now they have high estrogen levels because they stopped the Aromatase inhibitor (AI) which allowed the high Test level to aromatise and Nolva can't protect them enough from getting gyno so they blame the Aromatase inhibitor (AI) when in fact its their own fault for not continuing the Aromatase inhibitor (AI) at least another1-2 more weeks... Also the high estrogens will keep you shut down until they drop below normal...
His Friend: On cycle, there is more test to be converted into estrogen, so Arimidex would be more of a necessity if you're sensitive to estrogen.
Visions: ( Correct)
His Friend: However, post-cycle, during post cycle therapy (pct), you natural testosterone levels are being restored which range from 2-11mg per day. The estrogen conversion will be significantly lower with your natural testosterone range, therefore Nolvadex (and Clomid if you include this in the mix) will be sufficient at combating estrogen while increasing LH production.
Visions: As I have shown estrogen and test levels are still high when PCT starts so an Aromatase inhibitor (AI) is needed and in fact your friend proved it when he talked about getting estrogen rebound during PCT... Next is the use of the Aromatase inhibitor (AI) lowering estrogen stimulates test production into high gear and up to 60% higher then normal and this is starting with normal levels of estrogen which I have shown is what we start with even without using HCG during the cycle (big point to remember)... Nolva as I have stated before does nothing to raise Test production and I have yet to find one study saying that it does yet I have found many that say Test levels don't change with its use...what Nolva can do is increase seamen production and it is sometimes used for that if the guy has a problem getting his wife pregnant but at the same time in those studies they said test production didn't increase...
His Friend: In addition, there is no estrogen rebound when discontinuing the Nolvadex.
Visions: He is right to a point... there is no rebound when a normal person takes nolva and in saying this he makes my point one more time that nolva doesn't increase test because if it did you would read in the studies that it could have a rebound because of the higher output of test now being made above normal that is being converted to estrogen... but when on cycle and your Test levels are above normal you will have above normal conversion to estrogen and when you take Nolva it blocks the estrogen from binding but as soon as you stop the use of the nolva that already converted estrogen will now bind to the estrogen receptor and cause the gyno... when people read the studies on drugs like this they have to keep in mind that they are used in normal people with normal levels yet as body builders our levels are well above normal...
His Friend: There is estrogen rebound when discontinuing Arimidex.
Visions: This is true since by stopping Test from converting into estrogen you have more test and this is why the Aromatase inhibitor (AI) should be continued until at least the Test levels are in the normal range which happens about 3 weeks after your last shot as I showed above... There is less rebound from the use of Aromasin since it permanently binds to the armatase enzyme which destroys it leaving less aromatase to convert the Test.... called an irreversible,
steroidal aromatase inactivator.
His Friend: By switching over to Nolvadex you will be fighting estrogen from the rebound.
Visions: I covered this already
His Friend: If you decided to use Arimidex during PCT along with hCG, then you will have nothing to fight the rebound of estrogen."
Visions: The use of the Aromatase inhibitor (AI) until test is in the normal range = no rebound
The old school way of thinking lets the testes shutdown during the cycle while also not controling estrogen properly with an AI... Most used to use Nolva and it only blocked the estrogen receptors leaving the high estrogens to fill the androgen receptors and if you have been in the game for a long time and used to do it this way you may have run into the problem of your libido dropping mid cycle and definately during PCT... Also a huge misconception I haven't mentioned yet is guys thought they needed the high estrogens to build more muscle and they would think that blocking or stopping the estrogen hindered gains which is further from the truth since estrogen doesn't build muscle and even though as estrogens rise gh rises, IGF drops which is what builds the muscle...Gyno and bloating were always a concern... recovery can take a long time and you could drop alot of weight and this is another reason why guys would just bridge instead of PCT cause during PCT they would drop too much muscle...
I don't recommend Nolva because there isn't enough evidence pointing to its benifits for PCT for me... maybe there is some info but I can't find it... but there is a ton of info for the use of AI's for not only controling estrogen but also increasing test production safely...
Here are the benifits of using my protocol... first you never get shutdown which is the key benifit,,, not getting shutdown means the leydig cells never stop working as normal,,,(500iu is shown in studies while using 200mg of test a week to make you make 26% more of your own test even while on TRT)... this allows the leydig cells to respond to your normal LH when the cycle ends... Even without the use of Clomid the body's production of LH goes into high gear... clomid just ensures that it happens and at a higher rate... the use of the Aromatase inhibitor (AI) throughout the cycle keeps estrogen in the normal range which has many benifits because high estrogens can bind to androgen receptors not only making the androgen receptor useless but in doing so can kill the libido,, high estrogens can upregulate an androgen receptor and turn it into an estrogen receptor... as estrogen rises so does shbg,,, as estrogen rises so does gh but at the same time IGF lowers... high estrogens can cause fatigue and memory problems etc... The use of the Aromatase inhibitor (AI) into PCT prevent any estrogen rebound... The use of HCG up until 4 days prior to PCT not only keeps your testes working, it keeps your Test level in the normal range or above when PCT starts and at the same time estrogen will be just below normal which will soon trigger Test production as soon as your Test level drops below normal... HCG mimics LH which keeps your natural LH production shutdown and this is why we switch to Clomid because Clomid triggers natural LH and FSH production into high gear... Clomid triggers higher then normal estrogen levels and the Aromatase inhibitor (AI) helps control this while at the same time the Aromatase inhibitor (AI) is triggering more Test production by up to 60% by keeping estrogens low... Even though the Aromatase inhibitor (AI) lowers estrogens this eventually evens out more as the higher test level causes more aromatising and estrogen ends up being in the low normal range...
So when you start PCT your estrogens are about in the normal range because of the use of HCG during the cycle and may be a bit higher because of starting the cycle 2 weeks after your last shot of test which I have shown that you'll still have test in you when PCT starts... Yes during PCT estrogen will be greatly lowered but this is what triggers test production and is safely used in many studies to stimulate test production in men
Info on HCG
I recently received this PM and think its important and I'll add more studies when I have time:
Originally Posted by 4thAD
can you point me in the right direction to find the studies of HCG use @ 500iu 2xew. I know Ive seen them before, but cant seem to locate them on pubmed. Any ideas. I have a friend that is worried about desensitization to LH, and I want to show him that 500iu is safe..
What you will find is studies on boys where they give them HCG for 2yrs and they give it to them eod... also studies on the optimal dose being 500iu... I have these studies posted here on the site... where... hahah... i forget... let me find the links
1) This study will show that taking shots everyday doesn't stimulate the leydig cells to respond any better then taking one shot every 72hrs... and from reading other studies I know it can desensitize them...
2) This study shows that even while on 200mg of Test a week HCG can get the testes to work and produce Test... you will see they gave different amounts of HCG and 500iu's gave a 26% higher response then baseline... meaning they are making 26% more test then normal even with the Testosterone shot... the abstract sums it up but you have to read carefully to understand everything... the shots were given eod but as you already know from the other study shots can be given every 72 hrs with the same results... this is why you will see in my HCG and PCT protocal that for optimal results shots should be given e3d instead of 2 X a week,,, still for our needs we just need the testes to keep working so they dont shut down...
3)This study shows that if you are shut down during a cycle the response to HCG or LH is progressive... I have another study that shows this even more ... if I can find it... I have hundreds of studies to sort through... I try to sort them as I go but alot of them I havn't and I havn't had time to do it...
4)Here is a study that shows a small amount of desensitation after 23 months of using 1500iu's eod... Thats what I would call over stimulation anyway... too much was used and the shots were taken too often... other studies will show no desensitation because they used 500ius... anyway... we will never use that much HCG and never for that long... desensitation isn't going to happen because I have erred on the safe side of everything taking into account all aspects of HCG use in many many studies...
I have more studies... I would have to find them like I said before... this should get you started and you'll see I'm not making things up and that there is logic and studies to back up what I recommend...
PS... If in any way you have messed up your cycle and not done it properly then start a thread and I'll help you get back on track...
Ozzy's post was much better than this one-if you go to his name and find his posted threads it will have all the links to the studies that are reffered to.
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Very interesting newbie.... I found ozzy27's post with the link....
I'm confused....should I be using aromasin/nolvadex for post cycle therapy (pct) - XtraXXL Message Board
I'm going to further investigate this subject...
There is some conflicting info...need to dig through it all.
Your absolutely right Ythrashin-it is highly debatable topic
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After reading up on the toxic effects of both clomid and nolva. I've come to the conclusion that nolva is more carcinogenic then clomid.
Its been linked to liver cancer, liver disease and uterene cancer
"Tamoxifen is toxic to the liver, and there have been reports of acute hepatitis in patients treated with tamoxifen. Liver damage has occurred in every animal given tamoxifen. According to Gary Williams, medical director of the American Heart Foundation, tamoxifen has been shown in animal studies to be a "rip-roaring" liver carcinogen, inducing highly aggressive cancers in about 12 per cent of rats. (7)
The latest human studies show a six-fold increase in liver cancer among women taking tamoxifen for more than two years." Liver failure and tamoxifen-induced hepatitis, although rare, have been reported. Even Zeneca admits that tamoxifen is a liver carcinogen ó while nevertheless aggressively promoting its use. "
Although all studies conducted with both for the purpose of HPTA restoration Nolva won every time.
So perhaps its better to take clomid to prevent any liver damage that could be caused by nolva....
Better to have temporary sides then a dead liver...
I think peoples biggest mistake when using Nolva and clomid is using to much. 40mg Nolva ED is to much IMO... 20mg is sufficiant to stimulate your HPTA anything more is a waste. With clomid anything over 100mg ed is to much...
Your HPTA can only be stimulated so much and adding more nolva or Clomid into the mix is just a waste... Mega doses or throwing another serm into the mix wont make things start back up any faster. All you succeed in doing if you mega dose or mix serms is put extra strain on your liver and body....
- Rep Power
Hey What sup I'm new here looking to post more
Love the forum already!
- Rep Power
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why fuck around with it, for the money Ill just run both nolva and clomid together for pct.
- Rep Power
Originally Posted by jim parsons
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