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Terapija poslije ciklusa - PCT

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Ovo ce biti tema gdje cu ja a nadam se i vi postavljati textove i misljenja (naravno na engleskom...zao mi je bebac  :lol: ) na koje naletim vezano za PCT (Post cycle therapy) i srodne teme.
Ovu  temu nisam  otvorio zbog ubjedivanja da li treba ili ne treba raditi PCT nego da bi sve vezano za temu bilo na jednom mjestu!!!

Post Cycle Therapy


When you take AAS, your body stops making natural hormones (i.e., test). Once you stop taking steroids, you can be left with a gap until your body starts making its own again, which can take months. Here, you can be faced with low levels of androgens and normal levels of corticosteroids. Corticosteroids have a pronounced catabolic (muscle-depleting) state on our bodies, and without the androgens to balance the catabolic effects of corticosteroids, a good deal of your new muscle mass may be lost. To help your body maintain its size, you will want to restore endogenous (natural) testosterone production quickly. The methods for doing this seem to be different everywhere you look: "Take HCG, don't take HCG, use an aromatase inhibitor, just take Clomid, forget Clomid and just take Nolvadex." What option is reall best? Without an understanding of what is really happeningin your body, and why certain compounds help to correct the situation, choosing he correct PCT program can be quite confusing.

The HPTA Axis

The Hypothalamic-Pituitary-Testicular Axis (HPTA) is the thermostat for your body's natural production of testosterone. Too much testosterone, and the furnace will shut off. Not enough, and the heat is turned up (to put it very simply). For the purpose of our discussion, we can look at this regulating process as having three levels. At the top is the hypothalamic region of the brain, which releases the hormone GnRH (Gonadotropin-Releasing Hormone) when it senses a need for more testosterone. GnRH sends a signal to the second level of the axis, the pituitary, which releases Luteinizing Hormone in response. LH for short, this hormone stimulates the testes (level three) to secrete testosterone. The same sex steroids (testosterone, estrogen) that are produced serve to counterbalance things, by providing negative feedback signals (primarily to the hypothalamus and pituitary) to lower the secretion of testosterone. Synthetic steroids send the same negative feedback. This quick background of the testosterone-regulating axis is necessary to furthering our discussion, as we need to first look at the underlying mechanism involved before we can understand why natural recovery of the HPTA post-cycle is a slow process. Only then can we implement an ancillary drug program to effectively deal with it.

Testicular Desensitization

Although steroids suppress testosterone production primarily by lowering the level of gonadotropic hormones, the big roadblock to a restored HPTA after we come off steroids is surprisingly not LH. This problem was made clearly evident in a study published back in 1975. Here, blood parameters, including testosterone and LH levels, were monitored in male subjects who were given testosterone enanthate injections of 250mg weekly for 21 weeks, a low dose for even a beginner's cycle. Subjects remained under investigation for an additional 18 weeks after the drug was discontinued. At the start of the study, LH levels became suppressed in direct relation to the rise in testosterone, which was to be expected. Things looked very different, however, once the steroids had been withdrawn. LH levels went on the rise quickly (by the 3rd week), while testosterone barely budged for quite some time. In fact, on average, it was more than 10 weeks before any noticeable movement in testosterone production started at all! This lack of correlation makes clear that the problem in getting androgen levels restored is not necessarily the level of LH, but more so testicular atrophy and desensitization to LH. After a period of inactivation, the testes have lost mass (atrophied), making them unable to perform the required workload. The protracted post-cycle window can, likewise, no longer be looked at as one of low testosterone and low LH. Much of it actually involves low testosterone and normal (even high) LH.

The PoWeR PCT Program

The PCT program outlined below represents what I consider to be an ideal and effective PCT program. It was developed by the doctors at the Program for Wellness Restoration (PoWeR), who have a formidable history helping patients recover from abnormal 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/hypogonadotropic 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 subject 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 clinical 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 there is a disadvantage to such us; perhaps it is indeed the better option.

NOLVADEX: ran for 45 days from day 1
CLOMID: ran for 30 days from day 1
HCG: ran for 16 days from day 1
(Day after drug cessation)

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 doctors undoubtedly recognize that when HCG is taken for too long or at too high a dosage it can desensitize the LH receptor. This would only further exacerbate the post-cycle program, not help it. Anti-estrogens are used during and after HCG, with a dosage of 10mg of Nolvadex and 100mg of Clomid per day, rounding out this compliment of drugs. Clomid is used for a shorter period of time than Nolvadex, likely because of the desensitizing effect it too can have (on the pituitary gland) with continued use. Among other things, these two anti-estrogens will continue to foster LH release as testosterone levels start to go back up, as well as combat any potential estrogenic side effects that may be caused by HCG's up-regulation of testicular aromatase activity. Although the first couple of weeks the anti-estrogens probably do very little, they should be much more helpful toward the middle and end of the program. During this clinical investigation, normal hormonal function was restored in all subjects within 45 days of drug cessation. This is a definite success, far more favorable than the protracted recovery window noted in studies without PCT, such as the 250mg/week testosterone enanthate investigation. Such a detailed 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.

HPGA Normalization Protocol After Androgen Treatment
N Vergel, AL Hodge, MC Scally
Program for Wellness Restoration, PoWeR

Objective Results Discussion

To develop an approach to cycle androgens that would result in significant changes in body composition and accelerate the normalization of the hypothalamic pituitary gonadal axis (HPGA) after cessation of androgens.


An uncontrolled study of 19 HIV-negative eugonadal men, ages 23 – 57 years, administered testosterone cypionate and nandrolone decanoate for 12 weeks, and then were treated simultaneously with a combined regimen of human chorionic gonadotropin (hCG) (2500 IU/QODx16d), clomiphene citrate (50 mg PO BID x 30d) and tamoxifen (20 mg PO QD x 45d), to restore the HPGA.


Mean FFM by DEXA increased from 64.1 to 69.8 kg (p<.001); percent body fat decreased from 23.6 to 20.9 (p<.01); strength increased significantly from 357.4 lb to 406.4 lb (p=.02). No significant changes in serum chemistries and liver function tests were found. HDL-C decreased from a mean value of 44.3 to 38.0 (p=.02). Mean values for luteinizing hormone (LH) and total testosterone (T) were 4.5 and 460, respectively prior to androgen treatment. At the conclusion of the 12-week treatment with androgens the mean LH <0.7 (p<.001) and total testosterone was 1568 (p<.001). The mean values after treatment with the combined regimen were LH=6.2 and testosterone=458.


The use of androgens has been reported to improve lean body mass, strength, sexual function, and mood accompanied by side effects caused by continuous uninterrupted use of these compounds (polycythemia, testicular atrophy, hypertension, liver dysfunction [oral androgens] and alopecia.) Androgen-induced HPGA suppression causes a severe hypogonadal state in most patients that often require an extensive period of considerable duration for normalization. This prevents most if not all individuals from cycling off these medications due to the adverse impact of this state on their previously gained LBM and quality of life. The protocol of hCG-clomiphene-tamoxifen was successful in restoring the HPGA within 45 days after androgen cessation. Further controlled studies are needed to determine if these results can be duplicated in HIV positive subjects.


The esters used in the abstract were cypionate and deconate however the administration of the PCT medications were started the day after aas cessation. Essentially the aas esters were still active when PCT began. The first 16 days a large amount of HCG was used in order to increase the mass of the testes so that they could sustain output of testosterone sooner. The HCG was stopped about the time the esters cleared so that estrogenic activity from the HCG would be reduced. During those first 16 days 2 different SERM’s were also employed (Clomid and Nolvadex)  This is a 100% success rate! After the HCG was discontinued both SERM’s were continued. The following is the exact protocol in laymen’s terms.

Day 1-16 : 2500iu HCG every other day.
Day 1-30 : Nolva 20mg/day; Clomid 100mg/day (50mg was taken twice per day)
Day 31-45 : Nolva 20mg/day

Post Cycle Therapy
by Anthony Roberts, Author of Anabolic Steroids - The Ultimate Research Guide

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…

…and I’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 “Post Cycle Therapy” or “PCT” for short.

First, I’m going to tell you what anabolic hormones are typically low when a cycle ends, and which catabolic ones are high, then I’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’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’ll just try to find out what’s gotten into me?

I’m not re-inventing the wheel here, and you may have seen a piece of this information elsewhere (possibly in something I’ve written, possibly somewhere else on the internet or in a magazine), but I’m sure of two things:
You’ve never seen this PCT protocol anywhere
This is the most effective PCT you’ll ever see
First, I’ll give you a brief explanation on the body and how it works, and why there’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’t worry, I’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…). 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’s known as non-receptor mediated effects. When an androgen (your own natural testosterone or an anabolic steroid you’ve injected or ingested) binds to a receptor inside the cell, it activates the transcription of specific genes. What does this mean? Don’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’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’s known as a “negative feedback loop”. 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… 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…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.

So what I’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’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’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’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’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’s the “selective” 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’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’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’m suggesting…and in fact, avoided in general…it’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…and no, using it along with Nolvadex will provide no “synergy” that I’ve ever seen in any relevant study.

SO how much Nolvadex should you use during PCT? I favor using, 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’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’t use huge doses of any Anti-Estrogen, actually, and expect huge increases in our natural hormones, actually. Arimidex (an Aromatase Inhibitor –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 PCT, because Mega-Doses of one compound will not I think it’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’d steer very clear of listening to anyone who makes those types of recommendations…

All of this tells me that you can’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…hopefully decreasing our recovery time.

We’ll need something to go with Nolvadex, which acts in a different manner, and Human Chorionic Gonadatropin (HCG) is the clear choice here. Here’s where things get a bit controversial (no, really…I know you , because I’m pretty much the only person around (currently) who recommends HCG for Post-Cycle Therapy. Although I’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 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’s hormones (can anything really be said to control a pregnant woman’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!’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’t be very effective. Unfortunately, this lack of an increase in testosterone doesn’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’s important to me and I suspect most men as well. It would also appear that HCG works very well when it’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’ll be using it when LH/Gonadatropin levels are very low anyway …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 “priming” by circulating gonadotrophins. This is great news for us, because we are going to be using HCG during 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…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’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’t be inhibited by it at all! Right? 

Well…maybe…but there’s still the issue of estrogen caused by that HCG-stimulated surge in testosterone. Well…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’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 HCG, since it increases the responsiveness of plasma testosterone levels to 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’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….

Lets add in an Aromatase Inhibitor! Which one, though? Well, since we are already using Nolvadex, we can’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 AI, because it’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 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’t reduce exemestane’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 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’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…it simply prolongs the time you aren’t doing anything positive to regain your natural hormones. And how long do we run this for? Well…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’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…but weekly bloodwork isn’t really an option for most of us. Failing the option of monitoring recovery with blood-work, I’m going to give you my best thoughts on the time you should be running your PCT. It’s important to note I haven’t discussed nutrition or other compounds that may be beneficial…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:
  Week   Nolvadex   HCG   Aromasin   Vitamin E
1   20mgs/day   500iu/day   20mgs/day   1,000iu/day
2   20mgs/day   500iu/day   20mgs/day   1,000iu/day
3   20mgs/day   500iu/day   20mgs/day   1,000iu/day
4   20mgs/day       20mgs/day   
5   20mgs/day           
6   20mgs/day           

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Effect of vitamin E on function of pituitary-gonadal axis in male rats and human subjects. Umeda F, Kato K, Muta K, Ibayashi H.
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Inhibitory effect of combined treatment with the aromatase inhibitor exemestane and tamoxifen on DMBA-induced mammary tumors in rats.
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Hormonal changes in tamoxifen treated men with idiopathic oligozoospermia Exp Clin Endocrinol. 1988 Dec;92(2):211-6


--- Citat: Pedja Petrovic  Septembar 21, 2009, 09:40:23 pre podne ---

seleto nije sindorm vec cinjenica KOJU RADIM HVALA BOGU VEC EVO 10 GODINA!!!
tako da bb krugovi koje ti spomenuh itd,ja ne priznajem iz jednostavnog ralzoga sto ni ja a ni oni koji su mu govrili celu pricu oko ovog sporta NE RADE PCT osim u EXTREMNIM SLUCAJVIMA tj kada su povezivali celu godinu u takmicenjima
ja nemam maeru da bilo koga ovde nabedujem ili ubedjujem ali svi moji jarani ili drugari pocevis od igora milanovica,marka dimitrijiveca,marka petrovica,sase stankovica itd itd itd itd tj ljudi koji u u oom sportu NEKO I NESTO ili se bar tako kaze  :rolleyes01:,NE RADE NITI SU RADILI PCT z asve ove godine AKTIVNOG BAVLJENJA TAKMICARSKIM BB
a mogu pouzdano da ti kazem da i gustavo badel,denis wolf,marcos cahon,mustava mohamed,denis james itd it itd tid SU PCT RADILI U EXTREMNIM SITUACIJIMA tj kao sto sam gore naveo.

drage volje ti mogu dati SVE NALAZE da vidis  :clap: :clap: :clap:
i da...da ne mislis...14 weeks off  :yes: :yes:

--- Kraj citata ---

--- Citat: Pedja Petrovic  Septembar 21, 2009, 02:41:13 posle podne ---
ja sam radio jednom pct kada mi je palo na pamet da se igram sa velikim dozama tj velikim dozama za mene te sam isao 1250mg i to je za mene bilo razor sistema
oprovaljao sam se skoro 6 meseci od te ludosti sto sam uradio i hormonalne pretrage su tada pokazale DA TREBAM TERAPIJU za vrcanje hormona
samo to samo hteo da naglism da sam misljenja da neko na 500 mg testa kroz 10 nedelja tj mislljena sam da vecina ne treba pct
i naravno da ja ne protivrjecim medicini stari moj,ali pojam PCT je veoma sirok i velik a klinci ga pogresno shvataju tj ne razumiju i oni pct gledaju kao nesto sto ce da im sacuva kao misice koje nisu ni dobili i onda se vrtimo u krug em su se trovali sa aas i sada se razbijaju sa citostaticima
eto...valjda sad uspjedoh da objasnim
ma mozda sam naveo npr pogresne ljude tj za ove znam licno da je tako kako sam rekao,i da su oni stalno online i to je tacno,ali znam i npr periode gde je i denis bio off ali nije uzmao nista,hidetada npr dok je gulio zatvor skinuli su ga dirketno sa hemije i to posle ko zna nakog kolkog vremena i verj mi a rec da mu u zatvor nije mogao niko da donese lekove za pct itd
da sada ne nabrjam sve i svasta

eto npr,a ja sam ti gore nabrojao momke sa kjima sam stalno a i pored njih znam toliko momamka koji su aktivni takmicari a da ti ne nabrajam one koji se ne takmice i da niko ne radi pct...a nisam ih ja nagovarao majke mi  :lol: :lol: :lol: :lol:

--- Kraj citata ---

Pedja Petrovic:
ovo moje nije na engleskom tako da bebac moze da uziva  :blowkiss: :blowkiss:
a i posto nije na engl znaci da je relevantno  :evillaugh: :evillaugh:
bravo za textove u ideju u svakom slucaju,kako god da se tumaci

Anabolic Steroid Induced Hypogonadism (ASIH)
by Michael C. Scally, M.D.
Dr. Scally early on recognized the lack of research and treatment for individuals using anabolic-androgenic steroids (AAS). He has remained as the sole physician by reputation and publication to actively pursue and advocate the proper use of AAS to optimize health. Dr. Scally has personally cared for thousands of individuals using AAS. His protocol for Anabolic Steroid Induced Hypogonadism has been presented before the Endocrine Society, American Association of Clinical Endocrinologists, American College of Sports Medicine, & International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV.

Since the introduction of steroids into mainstream culture, the media, sports organizations, medical community and public have all expressed their values and judgment of their ethical use outside of medical necessity. Within the medical establishment there is a pervasive atmosphere of fear and intimidation towards physicians who treat AAS users or prescribe AAS. This has created a vacuum or void in the proper use of AAS; an abandonment of basic scientific principles; and an ever increasing population of men at risk for significant health problems. For the greater part of 10 years I have found that the medical treatment provided for the condition termed anabolic steroid induced hypogonadism (ASIH), is nonexistent or ignored by the great majority of medical professionals. As predicted since my entry into this field in 1995 more and more cases of ASIH would appear due to this negligence. Clear and convincing evidence of this is demonstrated by recent articles in peer-reviewed medical literature affirming concerns for the long term effects of untreated ASIH [[2]], rapidity and severity of symptoms in ASIH [[3]], and inappropriate treatment with AAS based upon a flawed clinical study design [[4]]. 

An unproven and unfounded assumption has been made in the medical establishment that the treatment for an individual suffering from ASIH is to do nothing which is coined ‘watchful waiting’ and in time HPTA functioning will return to normal. This premise can be traced back to Knuth et al. (1989) [[5]] studying semen parameters in AAS users. He concluded, “Results suggest that even after prolonged use of extremely high doses of anabolic steroids, sperm production may return to normal.” The ability to create spermatozoa does not equate with a normal functioning HPTA. Hypogonadal males are known to have the ability to produce spermatozoa. There are no studies that demonstrate that serum testosterone levels sufficient for spermatozoa production are positively associated with the clinical effects of testosterone elsewhere within the individual. At the very same time members of the medical community announce an alert to suicide risk after AAS cessation. Kirk J. Brower, M.D. from the University of Michigan stated, “… whereas depressive episodes and suicide attempts are most likely to occur within three months of stopping AAS use.”[[6]]  Shortly thereafter Texas HB 3563, “Use Of Anabolic Steroids By Public School Students,” was passed and signed into law June 18, 2005. Of particular importance is the bill analysis citing the problem of “clinical depression when steroid use is stopped.” [[7]]  The obvious question is who are these astute physicians that are able to know the individual to attempt suicide during the treatment plan of ‘watchful waiting’ or do nothing?


Testosterone and testosterone analogues, anabolic-androgenic steroids (AAS), have long been used in the athletic community for improving lean muscle tissue and strength. A positive correlation has been shown with testosterone to include: increased protein synthesis resulting in lean muscle tissue development [[8]], enhanced sexual desire (libido) [[9]], increased muscular strength [[10]], increased erythropoiesis [[11]], a possible positive effect on bone development [[12]], improved mental cognition and verbal fluency [[13]], and male masculinizing characteristics [[14]]. Recently, however, clinicians have recognized the potential benefits of their use in the treatment of various conditions and ailments. Numerous studies have discussed the use of AAS in the treatment of HIV-associated conditions [[15]], hypogonadism [[16]], impotence [[17]], burn victims [[18]], various anemia’s [[19]], deteriorated myocardium [[20]], glucose uptake [[21]], continuous ambulatory peritoneal dialysis (CAPD) [[22]], alcoholic hepatitis [[23]], hemochromatosis [[24]] and prevention of osteoporosis [[25]]. Since there has been such strong evidence for the medicinal use of AAS in the treatment of various conditions, these medications have become more prevalent in the medical community.

While the use of AAS by physicians has become more prevalent, this class of medicines is not without their inherent problems. AAS have been shown to induce hypogonadotropic hypogonadism [[26]]. This condition typically results from an abnormality in the normal functioning of the hypothalamic-pituitary-gonadal axis (HPTA), either from an over-or underproduction of one of the hormone secreting glands, causing a cascading unbalance in the rest of the axis. This condition may be the result of a physiological abnormality (i.e. mumps orchitis, Klinefelters syndrome, pituitary tumor) or as an acquired result of exogenous factors (i.e. androgen therapy, anabolic-androgenic steroid administration). Clerico et al found a dramatic suppression of serum gonadotropin levels in athletes given methandrostenolone, suggesting a direct action of AAS on the hypothalamus [[27]]. Similar results of suppressed gonadotropins have been found in patients supplementing solely testosterone [[28]]. Case report studies discussed a 36-year old male competitive bodybuilder and a 39-year old father, each using various AAS regimens over extended periods of time, who showed a blunted response to GnRH stimulation tests [[29]]. Bhasin et al showed a complete suppression of serum luteinizing hormone levels after administration of 600 mg testosterone enanthate over ten weeks [[30]]. A similar study administered 600 mg of nandrolone decanoate to 30 HIV-positive males over twelve weeks [[31]]. The results documented mild elevations in hemoglobin and alanine aminotransferase levels but no reference to LH or testosterone levels. The lack of gonadotropin response is puzzling as the data showed 12 of 30 subjects experienced testicular shrinkage, implying Leydig cell dysfunction and suppressed testosterone levels. A contraceptive investigation found that 6 of 9 men receiving 200mg of testosterone enanthate per week became azoospermic with suppressed gonadotropin levels after 16-20 weeks [[32]]. Other studies using AAS also showed no reference to LH or FSH levels but suppressed values are expected in each case [[33]].

Declining, or suppressed, circulating testosterone levels as a result of either pathophysiological or induced hypogonadal conditions can have many negative consequences in males. Declining levels of testosterone have been directly linked to a progressive decrease in muscle mass [[34]], loss of libido [[35]], decrease in muscular strength [[36]] impotence [[37]], oligospermia or azoospermia [[38]], increase in adiposity [[39]] and an increased risk of osteoporosis [[40]].


In 1982, more than two decades ago, it was shown that nandrolone decanoate caused a suppression of the HPTA in males. [[41]] A 1989 study demonstrated the period of hypogonadism after androgenic-anabolic steroid cessation in male hemodialysis patients.[[42]] The authors warned that the cessation of anabolic steroids caused hypogonadism stating: "Nandrolone decanoate are anabolic steroids prescribed for uremic anemia and those may possibly exacerbate uremic gonadal damage. This clinical study suggests that some anabolic steroids play a role in uremic hypogonadism.”

The sequence of changes in body composition induced by testosterone and reversal of changes after cessation was studied in 1992. Testosterone treatment produced a progressive increase in lean body mass and a progressive decrease in body fat. After the testosterone was stopped a period of hypogonadism ensued and the body composition reverted slowly back to normal. [[43]]

Each of the studies done prior to 1995 is designed correctly taking into consideration the characteristics of life. The characteristics of life are to physiology as Newton's Laws of Motion and Gravity are to physics. If one was to disregard or fail to consider the Law of Gravity in a physics experiment the conclusions drawn from such a study would be erroneous and wrong. The Characteristics of life are the following: All living things follow the tenets of cell theory; Living things acquire and use energy and produce wastes; Living things reproduce, grow, and develop; Living things evolve;. Living things respond to stimuli; Living things maintain a state of homeostasis; All living things are made up of some kind of atoms and molecules. The scientific method is a method of collecting evidence through observation, questioning, hypothesis formation, and hypothesis testing. Similarly, if one was to disregard or fail to consider the characteristics of life in a physiology experiment their conclusions would be erroneous and wrong.



In the paper by Pena et al. many of the adverse events associated with ASIH are displayed. But even more remarkable is that the ignorance and unfamiliarity with AAS is there for all to see in a Board certified endocrinologist and urologist.


The patient was an HIV+ married male discovered to be azoospermic when the couple was exploring artificial insemination as an option to have children. His medications included testosterone enanthate and oxandrolone. To restore spermatogenesis the urologist discontinued only the testosterone and allowed the patient to remain on oxandrolone. Within months of this action the patient's testosterone level was 30 nanograms per deciliter, with luteinizing hormone (LH) and follicle-stimulating hormone (FSH) both below normal range, and suffering from notable depression and irritability that necessitated antidepressant medication. A repeat semen analysis continued to demonstrate azoospermia.


At this point the patient was referred to a medical endocrinologist for the evaluation of central hypogonadism. Pituitary and thyroid disorders were ruled out by normal serum prolactin and thyroid hormone levels, respectively. Magnetic resonance imaging of the brain and pituitary were normal. Finally, a decision was made that the patient’s continued hypogonadism after testosterone cessation was due to the oxandrolone. After discontinuing both testosterone enanthate and oxandrolone for three months the patient’s serum testosterone rose to 134ng/dL which was sufficient for the production of spermatozoa. The patient was then encouraged to restart his androgen supplementation to improve both physical and emotional well-being.[[49]]


The evaluation and management of this patient was extraordinarily poor and inept. First, it is incredulous that these physicians are apparently unfamiliar with oxandrolone. Despite this they continued to treat him and order test which are costly and unnecessary. The MRI was without any medical indication, particularly in the face of the known medications testosterone and oxandrolone. It is fortuitous that the MRI was negative since ~10% of the general populations have asymptomatic pituitary adenomas.


This patient demonstrates the pervasive effect upon the health and welfare those AAS studies which failed to account for homeostasis. Clinicians across the USA and beyond are using these studies as a basis for the clinical care of patients. That neither of these physicians even knew the most rudimentary AAS knowledge and was unaware as to ASIH after AAS cessation is horrific and shocking. But what is particularly disheartening is no one displayed any sense on what to do regarding the patient’s HPTA. There are literally tens of thousands of patients in the United States who are receiving similar androgen treatment as the patient in Pena et al., each is potentially being left in the state of HPTA dysfunction.


Urhausen et al. (2003) studied serum parameters in 15 AAS users. The mean time after steroid cessation was 43 months with the minimum length of time 1 year and the maximum 10 years in the study. The average amount of medication used was a mean of 700 milligrams for 26 weeks, half a year, for 9 years. [[50]] The long-term side-effects of anabolic steroid use were demonstrated to be most pronounced on the HPTA. It was found A13/15 ex-AAS users were found in the lower 20 percent of the normal reference range for testosterone, 2/15 ex-AAS users were found below the normal range with values of 6.6 and 9.0 nanomoles per liter.

vanBreda et al. (2003) presents a case study in a 37y male who after AAS cessation had persistent HPTA dysfunction. [[51]] Restoration of HPTA dysfunction was achieved with the use of LH-RH.


In 2004, Schroeder et al. included an equivalent amount of time for follow-up after AAS cessation as AAS administration. The study found that the positive body composition changes produced by the androgen in the study had completely disappeared after cessation. This was due to the state of hypogonadism induced by the administration of androgens (ASIH). Anabolic improvements were lost 12 weeks after discontinuing the androgen.[[52]]




There are vast differences between the health of an individual with frank hypogonadism (primary hypogonadism or testicular failure; secondary hypogonadism – hemochromatosis, Kleinfelters, etc.) and the individual with Andropause or PADAM (Partial Androgen Deficiency in Aging Male). The morbidity observed with true hypogonadism have been documented. While there are clinical indicators that are improved with AAS administration in Andropause there are no studies to show that these are factors for increased morbidity or an overall decreased quality of life. Until these studies are done care should be taken regarding the continuous long term administration of AAS.

There are also clinical situations which would necessitate AAS cessation for health concerns. With increasing AAS use these clinical conditions are sure to become increasingly prevalent. Compliance in taking medication is not 100% for a number of reasons. This would lead to ASIH and potentially adverse events. A clinical situation would be elevation of LFTs (liver function tests) and impending liver dysfunction. Pens et. al. was a clear example of the adverse consequences with AAS cessation. AAS cessation was required in the treatment of polycythemia brought upon by continuous AAS administration.[]

A medical quandary for many physicians presented with hypogonadal patients, standard treatment to this point has been testosterone replacement therapy, human chorionic gonadotropin (hCG), or conservative therapy (i.e. nothing  :lol: ). The primary drawback of testosterone replacement is that this therapy is infinite in nature. Exogenous testosterone serves only to remedy the symptoms of suppressed testicular/gonadotropin production. While it may transiently combat the lean muscle atrophy, declining muscular strength, decreased libido, erection dysfunction, and depression associated with hypogonadism, it will not stimulate endogenous testosterone production. Administered testosterone will only suppress testicular function further.

It is important to understand that the use of a treatment for HPTA restoration at this time would only be effective in those individuals who had a normal HPTA functionality prior to AAS administration. This is not to say that there may be developed something in the future that will be effective for other causes of HPTA dysfunction. The regulation of the HPTA is an active area of investigation. There are other factors that interact with the HPTA which may show promise in their ability to restore HPTA health. The influences of other hormones within the endocrine system and the HPTA have only partially been explored.

The normal operation of both the testicular and hypothalamic-pituitary regions is crucial in returning HPTA function to normal. Returning one component of the axis to normal without concurrently returning the other would sabotage and inhibit the operation of the entire HPTA. The ability to produce a cure whereby there is no longer a need for medication is small. Discounting costs and focusing strictly on medicine reasons for this include inadequate stimulation for a critical part of the HPTA for full restoration, secondary inhibition of the HPTA, inadequate follow up and monitoring, and compliance due to the length of time the medicines are prescribed.


It is time for the medical community to act responsibly, intelligently, and forcefully and take control of the medical care for individuals. At the very minimum the

I. Uniform definition and diagnosis of ASIH.

II. Investigations on a more accurate estimate of ASIH prevalence.

III. A does-response study on AAS and HPTA normalization. Clinical investigations regarding AAS (type, dose, duration, etc) to development of ASIH (severity of signs & symptoms, duration, HPTA normalization).

IV. Clinical investigations on medical treatments (prevent, eliminate, or minimize) for ASIH.

V. Investigations on the development of protocols or programs to effect positive body composition changes without the attendant consequences of ASIH.

VI. Collaborative clinical investigations regarding dependence, abuse, and addiction of androgens in relation to ASIH.


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