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Ishrana, suplementi, stimulativna sredstva => ::Androgeno-anabolicki steroidi:: => Topic started by: sele137 on September 23, 2009, 12:14:03 PM

Title: Terapija poslije ciklusa - PCT
Post by: sele137 on September 23, 2009, 12:14:03 PM
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




BACKGROUND

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.

Methods

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.


(http://img62.imageshack.us/img62/7906/22221321321.jpg) (http://img62.imageshack.us/i/22221321321.jpg/)

Results

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.


(http://img233.imageshack.us/img233/6100/erwer55554.jpg) (http://img233.imageshack.us/i/erwer55554.jpg/)


Discussion

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.


(http://img8.imageshack.us/img8/9504/sdfrt55676.jpg) (http://img8.imageshack.us/i/sdfrt55676.jpg/)

PRACTICAL APPLICATION

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
Title: Odg: Terapija poslije ciklusa-PCT
Post by: sele137 on September 23, 2009, 12:15:24 PM
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 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’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! Well...it’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 lower versus higher doses of tamoxifen on pituitary-gonadal function and sperm indices in oligozoospermic men.m Dony JM, Smals AG, Rolland R, Fauser BC, Thomas CM
J Clin Endocrinol Metab 2000 Jul;85(7):2370-7, "Estrogen Suppression in Males"
J Clin Endocrinol Metab. 1995 Sep;80(9):2658-60
Hypogonadism Postgrad Med J. 1998 Jan;74(867):45-6
J Steroid Biochem. 1984 Jan;20(1):161-73.
J Clin Endocrinol Metab. 1978 Dec;47(6):1368-73
J Steroid Biochem. 1989;34(1-6):205-17
Endocrinology. 1981 Feb;108(2):632-8
Endocrinology. 1985 May;116(5):1745-54a
Mol Cell Endocr inol. 1984 Jan;34(1):31-8
Proc Natl Acad Sci U S A. 1979 Sep;76(9):4460-3
Kinetics of the steroidogenic response of the testis to stimulation by hCG. V. Blockade of 17-20 lyase induced by hCG is an age-dependent phenomenon inducible by pre-treatment with hCG. Forest MG, Roulier R
J Clin Endocrinol Metab 1982 Jul;55(1):76-80
J Steroid Biochem 1986 Jul;25(1):109-12
Postgrad Med J. 1998 Jan;74(867):45-6.
J Clin Endocrinol Metab. 1989 Jul;69(1):170-6.
Eur J Endocrinol. 1997 Apr;136(4):438-43.
Andrologia 1991 Mar-Apr;23(2):109-14
J Clin Endocrinol Metab. 1984 Feb;58(2):327-31
Effect of vitamin E on function of pituitary-gonadal axis in male rats and human subjects. Umeda F, Kato K, Muta K, Ibayashi H.
J Steroid Biochem Mol Biol. 2001 Dec;79(1-5):85-91.
Clin Cancer Res. 2003 Jan;9(1 Pt 2):468S-72S.
J Clin Endocrinol Metab 2000 Jul;85(7):2370-7
J Steroid Biochem Mol Biol 1997 Nov-Dec;63(4-6):261-7
Eur. J. Cancer. 2000, May;36(8):976-82
Inhibitory effect of combined treatment with the aromatase inhibitor exemestane and tamoxifen on DMBA-induced mammary tumors in rats.
Bruning PF, Bronfer JMG, Hart AAM, Jong-Bakker M, tamoxifen, serum lipoproteins and cardiovascular risk, Br. J. Cancer 1988 Oct, 58 (4) 497-9
Stimulation of calcitonin secretory capacity by increased serum levels of testosterone in men treated with tamoxifen. Int J Androl. 1987 Dec;10(6):747-51.
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
Hormonal changes in tamoxifen treated men with idiopathic oligozoospermia Exp Clin Endocrinol. 1988 Dec;92(2):211-6
Title: Odg: Terapija poslije ciklusa-PCT
Post by: sele137 on September 23, 2009, 12:21:56 PM


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.

nema potrebe za ovim jer bas sam u petak RADIO KOMPLETAN HORMONALNI PANEL,KRVNU SLIKU I ULTRAZVUK UNUTRASNJIH ORGANA
drage volje ti mogu dati SVE NALAZE da vidis  :clap: :clap: :clap:
i da...da ne mislis...14 weeks off  :yes: :yes:
I SVAKE GODINE RADIM OVO NA KRAJU GODINE I JESTE DA MA SVE KOSTA 200 eu,ali SVAKE GODINE HVALA BOGU IMAM ISTE NALAZE koji mi daju za pravo ono sto govrim i sto radim vec DECENIJU!!!!!!
haleluja




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:
Title: Odg: Terapija poslije ciklusa-PCT
Post by: Pedja Petrovic on September 23, 2009, 12:35:24 PM
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
Title: Odg: Terapija poslije ciklusa-PCT
Post by: sele137 on September 23, 2009, 12:53:47 PM
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?



ANDROGENIC ANABOLIC STEROIDS (AAS)

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]].


CHRONOLOGY

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.


(http://img32.imageshack.us/img32/6285/homeostasis.jpg) (http://img32.imageshack.us/i/homeostasis.jpg/)


THE FAILURE TO ACCOUNT FOR HOMEOSTASIS WOULD BE THE EQUIVALENT OF STATING GRAVITY DOES NOT EXIST.

ADVERSE EVENTS

 

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.

LONG-TERM EFFECTS

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.

DURABILITY

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]]




HPTA NORMALIZATION & RESTORATION

TREATMENT


(http://img32.imageshack.us/img32/8786/image006ow.jpg) (http://img32.imageshack.us/i/image006ow.jpg/)


Autonomy.

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.

FUTURE DIRECTIONS

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.
Title: Odg: Terapija poslije ciklusa-PCT
Post by: Pedja Petrovic on September 23, 2009, 12:59:26 PM
Quote
conservative therapy (i.e. nothing

 ;) ;) ;) ;)
ooo yeahhhhhh
and its working  ;) ;) ;)
Title: Odg: Terapija poslije ciklusa-PCT
Post by: sele137 on September 23, 2009, 01:03:24 PM
PCT and HPTA Normalization   
by Michael C. Scally, M.D.


Q: I just recently finished a 7 day treatment of Clomid at 100 mg a day. prescribed by my endocrinologist. What is the best case scenario of this protocol?

Can you tell me more about Clomid and how it works?

If the Clomid did raise my testosterone levels, then what is the doctor going to do next? I assume if it didn't raise my levels then he is going to put me on testosterone replacement therapy (TRT).


A: Clomiphene is classified as a selective-estrogen receptor-modulator (SERM).

Tamoxifen is classified as an estrogen receptor blocker.

Arimidex, Aromasin, Femara are aromatiziation enzyme inhibitors.

Clomiphene is classified as a selective-estrogen receptor-modulator (SERM) due to its ability to compete with estradiol for estrogen receptors at the level of the hypothalamus. Clomiphene blocks the normal negative feedback of circulating estradiol on the hypothalamus, preventing estrogen from lowering the output of gonadotropin releasing hormone (GnRH). During clomiphene therapy, the frequency and amplitude of GnRH pulses increase and stimulate the pituitary gland to release more FSH and LH.

In turn, FSH and LH stimulate the testicles to produce more testosterone. LH and FSH then apparently stimulate the testicles to produce testosterone and sperm. Sperm volume and density are increased; however, clomiphene may not increase sperm maturation or motility. Testosterone is converted to estradiol as well as dihydrotestosterone (DHT). The estrogenic effects of clomiphene are secondary to the primary effects on HPTA function. Clomiphene exhibits no androgenic, anti-androgenic, or progestational effects, nor does it affect pituitary-thyroid or pituitary-adrenal function. In some clinical situations clomiphene citrate will produce negative feedback inhibition on The HPTA. This can usually be determined by clinical signs and laboratory profile.

Secondary hypogonadism is more common than primary gonadal failure and is seen in chronic and acute illnesses. Although testosterone has a role in erections, its importance in erectile dysfunction (ED) has been controversial. Hypogonadism produced by functional suppression of pituitary gonadotropins has been shown to correct with clomiphene citrate in a % of patients, but with a modest effect on sexual function.

It does appear that many men may have functional suppression of the central component of their hypothalamic–pituitary–testicular axis resulting from a variety of acute and chronic medical conditions and multiple drug use. The same is true for various types of anxiety.


Endurance Athlete:

Patients with an intact hypothalamic-pituitary-gonadal axis are most likely to respond to clomiphene citrate. To assess the efficacy of estrogen antagonist therapy on the function of the hypothalamic-pituitary-testicular axis in a young male runner with significant morbidity attributable to idiopathic hypogonadotropic hypogonadism. Clomiphene citrate (CC) at doses up to 50 mg two times per day over a 5-month period. Barely detectable levels of LH and FSH associated with hypogonadal levels of T were restored to the normal range with CC therapy. The patient experienced improved erectile function, increased testicular size and sexual hair growth, and an improved sense of well being. Exercise-induced hypogonadotropic hypogonadism exists as a clinical entity among male endurance athletes, and CC may provide a safe and effective treatment option for males with .tating hypogonadism related to endurance exercise.

Long Term AAS Use:

Tan, R.S. and D. Vasudevan, Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse. Fertil Steril, 2003. 79(1): p. 203-5.

OBJECTIVE: To report a case of symptomatic hypogonadism induced by the abuse of multiple steroid preparations that was subsequently reversed by clomiphene.

DESIGN: Case report.

SETTING: University-affiliated andrology practice within family practice clinic.

PATIENT(S): A 30-year-old male.

INTERVENTION(S): Clomiphene citrate, 100-mg challenge for 5 days, followed by treatment at same dose for 2 months.

MAIN OUTCOME MEASURE(S): Clinical symptoms, androgen decline in aging male questionnaire, total T, FSH, LH.

RESULT(S): Reversal of symptoms, normalization of T levels with LH surge, restoration of pituitary-gonadal axis.

CONCLUSION(S): Clomiphene citrate is used typically in helping to restore fertility in females. The axis was previously shut off with multiple anabolic steroid abuse.

Multiple Causes:

A total of 178 men with secondary hypogonadism and ED received clomiphene citrate for 4 months. Sexual function improved in 75%, with no change in 25%, while significant increases in luteinizing hormone and free testosterone occurred in all patients.

It was found clinically that if the primary cause of the problem is corrected, clomiphene can occasionally be tapered and stopped, and the testosterone level will remain normal . In some patients the total treatment needs to be extended beyond 6 months. Quite frequently in men with ED and hypogonadism, correcting that the sexual problem may require additional methods of treatment. Nevertheless, correcting the testosterone deficit may have other beneficial effects. These may include increasing energy and well-being, as well as prevention of anemia or bone loss, depending on the severity of the hypogonadism. If patients cannot maintain their testosterone levels in the normal range after clomiphene is discontinued, permanent testosterone replacement with intramuscular injection, transdermal patches, or gels should be considered.

A minority, 39%, of the men will clinically respond to this treatment totally and this group will not have to consider artificial means of correcting their sexual dysfunction, or treatment of their comorbid medical or psychological factors. Decreased responses also occurred in men with diabetes, hypertension, coronary artery disease, and multiple medication use. Since these conditions are more prevalent with aging, chronic disease may be a more important determinant of sexual dysfunction. Men with anxiety-related disorders responded better to normalization of testosterone. Assessment of androgen status should be accomplished in all men with ED. For those with lower than normal age-matched levels of testosterone treatment directed at normalizing testosterone with clomiphene citrate is a viable alternative to giving androgen supplements.

Clomiphene citrate is generally well tolerated. Adverse reactions usually have been mild and transient and most have disappeared promptly after treatment has been discontinued. Visual Symptoms - Blurred vision, lights, floaters, waves, unspecified visual complaints, photophobia, diplopia, scotomata, phosphenes and headaches are those most common I have encountered. Reducing the dosage or discontinuing the medication resolves these side effects.

Clomiphene is administered orally and is well absorbed from the GI tract. Clomiphene is a combination of racemic isomers, enclomiphene and zuclomiphene, which may have different pharmacokinetic and pharmacodynamic parameters that have not been completely elucidated. Zuclomiphene is thought to be the more estrogenic isomer. The metabolic fate of clomiphene has not been completely established, but the drug appears to undergo hepatic metabolism. Both unchanged drug and its metabolites are excreted in the feces via the bile. Stereo-specific enterohepatic recycling or sequestering seems to occur also, with the zuclomiphene isomer accumulating over several cycles of treatment. However, even with continued cycles of use, combined maximum plasma levels of enclomiphene and zuclomiphene do not appear to exceed 100 mmol/L. The half-life of clomiphene is reported to be 5 days, but studies with radiolabeled doses have demonstrated that the drug may be found in the feces for up to 6 weeks.


Title: Odg: Terapija poslije ciklusa-PCT
Post by: sele137 on September 23, 2009, 01:08:09 PM
HCG timing and dosing for shut down recovery....logic behind it all by Michael C. Scally, M.D.

Q: What's the logic behind all the different timing and dosing of HCG ?? We hear taking it every day, every other day, every 3rd, 4th, or 5th day. What's the logic or science behind all the different timings? Shouldn't HCG timing mimic the bodies natural pulsing of LH? What is that exactly? Where do all you guys get the timing from? Articles, studies, colleagues?

What about the dosing ? I hear to take it easy to prevent desensitizing the testes. With this you hear anywhere from 100 units to 250 units to play it safe. Others say anywhere from 500 to 2500 units at a time...Isn't that a bit much ?

What about the length of time? I hear two clinics suggest 10 days; others say 3-5 weeks. Where does all this come from and who's right? Help me! Does anyone have any hard info here ?

A: Almost everything you hear or read will be anecdotal and therefore subject to no verification. Experiences with hCG while on TRT are posted. The use of hCG for PCT is only partly related to its use on TRT.

hCG while on TRT is used for two reasons. One reason is cosmetic. While on TRT it is not unusual and more often expected to have testicular atrophy. This is variable from individual to individual. The other reason is to act as a stimulus so the testicles do not shut down and therefore will be easier to initiate independent function after AAS cessation.

Desensitization is a potential problem with hCG. I do not think you will experience it with doses of 500IU or less 3X/week. Studies have used this dose for considerably long periods. In my patients when hCG was used while on AAS the dose was 1000IU every 3 days with one month on hCG followed by one month off hCG.

hCG for PCT involves additional concepts. This is the timing of hCG in relation to other medications for return of HPTA functionality. Under normal conditions the HPTA is a tightly coupled dynamic feedback loop. It is this coupling that has to be achieved after AAS cessation to return to normal. The analogy I use is the starting of a car by pushing it from behind. Alone the care will not start but with pushing the clutch can be popped and the car started.

After AAS cessation the secretion of LH is nil. It will not be able to initiate T production until a certain stimulus LH level is reached. Studies have shown that the time for this to occur can be lengthy. Thus the idea is to ‘push’ the testicles with hCG and get them started. Once T production is initiated the dependent variable is LH. If the hCG is withdrawn without adequate LH to couple with the testicles return of HPTA functionality will fail.

The increased production of LH is achieved by a dual action of clomiphene citrate and tamoxifen. Clomiphene is a mixed agonist/antagonist (SERM) at the estradiol receptor. Clomiphene will increase the secretion of LH by action at the hypothalamo-pituitary area. Clomiphene will cause an increase in LH and secondarily increases in T and estradiol. Estradiol has a negative feedback influence on the HPTA. Estradiol is 200X the inhibitory effect of T per molar basis. Normal serum levels are the following:

Testosterone: 3-10 ng/ml (10-35 nM/L)
Estradiol: 15-65 pg/ml (55-240 pmol/L)

Tamoxifen will counteract the effect of the estradiol. Once the hCG is withdrawn the LH, initiated by clomiphene and tamoxifen, will couple with the testicles and take over production of T by the testicles. The levels of LH to maintain and couple with the testicles are maintained by clomiphene and tamoxifen. Clomiphene is continued for 15 days while Tamoxifen is continued for 30 days.

In healthy adult men, circulating levels of testosterone have a distinct pattern, with increasing levels during sleep toward a maximum around the time of awakening and a decrease during the day. In PCT hCG is administered every other day. I suggest the same time each injection in an attempt to simulate this rhythm. This is purely empirical but I recommend hCG at bedtime (2200). Clomiphene is taken in divided doses of 50mg 2X/day.
Title: Odg: Terapija poslije ciklusa-PCT
Post by: sele137 on September 23, 2009, 01:13:31 PM
Why Use Both Clomid and Nolvadex Together by Michael C. Scally, M.D.

Q: I have read that Clomid and Novadex are very similar products. Is this true? If so why would you need to take both?

A: The administration of antiestrogens is a common treatment because anti estrogens interfere with the normal negative feedback of sex steroids at hypothalamic and pituitary levels in order to increase endogenous gonadotropin-releasing hormone secretion from the hypothalamus and FSH and LH secretion directly from the pituitary. In turn, FSH and LH stimulate Leydig cells in the testes, and this  lead to increased local testosterone production, thereby boosting spermatogenesis with a possible improvement in fertility. There may also be a direct effect of antiestrogens on testicular spermatogenesis or steroidogenesis.

Clomiphene is a synthetic derivative an estrogen. Clomid is a mixed agonist/antagonist for the estradiol receptor. Tamoxifen is a pure estradiol receptor antagonist. Clomid acts as an estrogen, rather than an antiestrogen, by sensitizing pituitary cells to the action of GnRH. Although tamoxifen is almost as effective as Clomid in binding to pituitary estrogen receptors, tamoxifen has little or no estrogenic activity in terms of its ability to enhance the GnRH-stimulated release of LH. The estrogenic action of Clomid at the pituitary represents a unique feature of this compound and that tamoxifen may be devoid of estrogenic activity at the pituitary level.

Perusal of the literature thus indicates that clomiphene acts in several ways in the human male; (a) due to its similarity of structure to stilbesterol it binds with receptor sites in the hypothalamus and pituitary, (b) It stimulates gonadotrophin secretion by acting on the hypothalamo-hypophyseal system, (c) the inhibitory effects of high levels of circulating estrogens (produced under the influence of clomiphene) on hypothalamo-hypophyseal axis are possibly prevented by its potent antiestrogenic behaviour. The result of these varied effects of clomiphene is an overall increase in gonadotrophin and estrogen secretion and accounts for their increase under clinical conditions.

In one study the administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels.

Cochran database summary showed ten studies involving 738 men were included. Five of the trials did not specify method of randomization. Antiestrogens had a positive effect on endocrinal outcomes, such as serum testosterone levels. Antiestrogens appear to have a beneficial effect on endocrinal outcomes, but there is not enough evidence to evaluate the use of antiestrogens for increasing the fertility of males with idiopathic oligo-asthenospermia.

In the over one-thousand patients I have treated for HPTA normalization after AAS cessation i have used the combination of clomiphene citrate and tamoxifen. I have used clomiphene citrate alone in many cases. I added tamoxifen to the protocol to see if I could get a better clinical response. This seemed to be the case although I have not had the opportunity to evaluate the data. When both compounds are used the clomiphene citrate is discontinued first and the tamoxifen is continued for 2 more weeks. as I stated in the post on hCG injections it is imperative to be tested while on the medications. thus one would be tested ~3-5 days before the tamoxifen expires. In the 1st stage described in the hCG post one tests for testosterone only. the serum T level determines whether or not the hCG is halted. In the typical situation the hCG is stopped and the CC & tamoxifen continued. the lab tests at the end of the oral meds is LH & T.
Title: Odg: Terapija poslije ciklusa-PCT
Post by: zzz on September 23, 2009, 01:25:26 PM
google translate extra prevodi ove textove :)  :clap:

http://translate.google.com/translate_t (http://translate.google.com/translate_t)
Title: Odg: Terapija poslije ciklusa-PCT
Post by: sele137 on September 23, 2009, 10:01:54 PM
AAS: Post Cycle Therapy

Bodybuilders are athletes interested in building up musculature while minimizing body fat. Bodybuilding is a constant evolution through various stages of building and refining, overindulgence and restraint, intensity and moderation. The cessation of mass-building cycles using anabolic-androgenic steroids presents a vulnerable transition for a bodybuilder. Most importantly, his system’s natural androgen production must be quickly and efficiently resumed since administering AAS inhibits signals to produce anabolic hormones within the body. The changing of the guard, from exogenous back to endogenous androgens, can make or break the permanent nature of the acquired muscle mass. Proper post-cycle therapy is crucial.



Some preliminary attention must be paid before a steroid cycle begins. Six to 12 weeks before embarking on a drug-assisted cycle, metabolic issues associated with overeating should be cleared up. It’s best to address insulin insensitivity before muscle building even begins. Taking time to optimize metabolism and body composition beforehand helps ensure proper calorie partitioning during the cycle. Total body fat should present a reasonable fat-to-muscle ratio. Throughout periods of overfeeding, a lean body will be predisposed to build more muscle than fat. It’s also important to not be afraid to overeat during a mass-building cycle – the anabolic environment must be properly fueled for growth to be maximized. This is even more significant when administering AAS. Testosterone and its derivatives, administered to deliver supra physiological amounts of androgens, increases caloric requirements due to improved protein synthesis. Without the bricks and mortar, it doesn’t matter how many contractors you employ to build your house.

To effectively terminate a cycle, it’s necessary to look at the transition in its entirety. A holistic approach can ensure a pleasant return back to training natural. Post-cycle psychology, endocrinology, nutrition and training need to be properly adjusted to ensure a quick and successful recovery.

Post-cycle psychology

The psychological impact of coming off a profitable AAS-assisted muscle building phase is considerable. It’s helpful to build up a desire to come off. If the trainee actually spent several weeks – peddle to the medal – he should be ready to transition into a less intense period. The training and nutritional requirements to make impressive muscle gains using progressive overloads should make anyone look forward to a break in the routine. After accumulating some additional fat and water weight, leaning up a little should be a welcomed event. Frequent injections required to maintain even blood-androgen levels can get tiresome as well. Each phase of training – such as muscle building, fat burning, maintenance and detraining – should be viewed as a requirement to transition to another, in order to build a bodybuilder’s physique. Program variation in itself plays a crucial role in preventing overreaching in resistance training.

Post-cycle endocrinology

A week or two before an AAS cycle ends, the diet should begin restricting high-carbohydrate, high-sugar food choices. Taking the time to increase insulin insensitivity, developed from the previous period of over-eating, will make post-cycle therapy more effective. Insulin insensitivity and low testosterone levels predispose the body to accumulate adipose tissue – to get fat.

The most vulnerable period is after the final steroid fully metabolizes in the body. From that time on, the athlete is once again solely dependent on the hypothalamus signals for androgen secretion. High levels of AAS shut down the hypothalamus’s signals to produce gonadotropin-releasing hormone. Luteinizing hormone normally travels from the pituitary to the testes where it triggers the production of testosterone; without GnRH, the pituitary gland stops releasing LH. Without LH, the testes shut down their production of testosterone. Since administering AAS inhibits natural testosterone production, impairment of the hypothalamic-pituitary-testicular axis must be quickly addressed – to quickly shift the anabolism-to-catabolism ratio back into the athlete’s favor.

Everything must be geared toward stimulating maximum endogenous testosterone production from the testes, as well as suppressing supra physiological levels of female sex steroids in the blood. Estrogen can build up to significantly high amounts depending on the particular steroid cycle; more specifically, how it interacts with the aromatase enzyme. Excessive estrogen will further delay recovery of the HPTA. A lot of bodybuilder’s do not realize that high levels of post cycle estrogen will keep them suppressed.

Ancillary drugs have long been used to support the post-cycle transition back to a natural environment; such as, Clomiphene (Clomid), Tamoxifen (Nolvadex), Anastrozole (Arimidex), and Human Chorionic Gonadotropin (HCG). The exact post-cycle prescription is based on the steroid compounds used, the total hormone burden, and the how long the system was exposed to supra physiological plasma levels – drugs, dose and duration. The old method of tapering the steroid dose down only delays HPTA recovery and extends the cycle’s duration.

Clomid is a common anti-estrogen drug used after a steroid cycle. It is an effective estrogen antagonist in the hypothalamus. In a clinical setting, it is primarily used to help women ovulate (produce eggs for procreation) but has also been used to treat male infertility. Studies have demonstrated that insulin sensitivity increases Clomid’s effectiveness as a female fertility drug. Men coming off an anabolic steroid cycle should address issues with insulin resistance prior to beginning post-cycle therapy drugs.

Sexual abstinence is linked to increasing testosterone levels. The body perceives ejaculation – through intercourse or masturbation – as a major triumph! The act is vital for promoting the continued success of the species through procreation. Prolonged periods of no sexual interaction are easily rebutted by an increase in testosterone, to promote sexual aggressiveness. In 2003, researchers in China examined the relationship between ejaculation and serum testosterone levels in 28 men. On the seventh day of abstinence, serum testosterone levels peaked, reaching 145.7% above baseline. No further elevation was noticed after this climax, no pun intended.

In addition to the testes, the adrenal glands also pump a small amount of testosterone. Stimulating adrenalin rushes may also serve some post-cycle benefits – such as running brief sprints or drinking caffeinated beverages.

Post-cycle nutrition

It’s necessary to calculate the change in daily caloric requirements after gaining a greater amount of lean body mass. Insufficient food intake can promote low androgen production. If a trainee eats in a deficit, the body will strip metabolically expensive muscle mass. Human metabolism does not see accumulating massive amounts of muscle as a safe condition, from an evolutionary stand point. If the body notices a caloric deficit for too long – or inadequate rest for that matter – it will become more efficient by lowering metabolism. A great way to become more economical in energy consumption is by decreasing endogenous androgen production (leading to conditions like depression and decreased sexual interest). This sets the stage for several events that inevitably lead to muscle wasting.

Many dietary supplements can be invigorating and foster proper disposition. Omega-3 and omega-6 fatty acids play a crucial role in the function of brain chemicals, particularly serotonin and dopamine. Some studies suggest 5-HTP, a by-product of tryptophan, may be as effective as antidepressants. Inositol is a naturally occurring substance involved in the production of certain brain chemicals. Tyrosine, a nonessential amino acid synthesized in the body from phenylalanine, is a building block for several important brain chemicals. Tyrosine is needed to make epinephrine, norepinephrine, serotonin, and dopamine, all of which work to regulate mood. Central nervous system stimulants can be helpful. Some reports indicate that the mineral selenium significantly affects mood.

Dietary fat intake is linked to influencing androgen secretion. To avoid fat gain, a high-fat diet should be kept reasonable while testosterone levels are quite low; such as the period immediately after an AAS cycle has ended. Also, a high-fat diet in combination with insulin resistance and currently low testosterone can counteract any potential benefits. Research indicates that monounsaturated and saturated fat raises testosterone levels, but polyunsaturated fat does not. Moreover, foods high in healthy omega-3 fatty acids are good fat-raising options. The best sources of omega-3s are fatty fish like mackerel, herrings, sardines, tuna, sturgeon and salmon. Various plant foods also provide these fatty acids; such as walnuts, pumpkin seeds, flax seeds, flax seed oil, and canola oil. Oily fish is a much richer source than plant-based alternatives.

Post-cycle training

Providing time to detrain allows the body to rest and fully recover from a preceding cycle of intense exercise – especially when flirting with signs of overtraining syndrome. Muscular characteristics of detraining in humans, published in the official Journal of the American College of Sports Medicine, cultivates over 50 studies and over 30 years of research into detraining. When 12 weight lifters stopped training for 14 days, they experienced a modest 6.4 percent decrease in fast-twitch muscle fiber cross-sectional area. Interestingly, increases were observed in plasma concentrations of growth hormone (58.3 percent), testosterone (19.2 percent) and the testosterone-to-cortisol ratio (67.6 percent); cortisol levels decreased by 21.5 percent. The hormone changes would benefit any athlete trying to recover after an AAS cycle.

There seems to be a direct relationship with the type of training used prior to an inactive period. Performance of slow eccentric muscle contractions are essential in promoting greater and more long-lived neural adaptations to training; also known as, muscle memory.

An entire two-week break from training is often too much post cycle. Depending on signs of overtraining syndrome, a three- to seven-day lay off would sufficiently help kick start the gonads. After detraining, an abbreviated training routine, with adequate rest days, should be used from one to four weeks, depending on the AAS cycle – drugs, dose and duration.

The post-cycle maintenance routine should focus on compound free-weight exercises and center on enjoying what has been built thus far – not showing impressive new numbers in a training log. This will help stimulate natural testosterone levels, as well as solidify muscle gains. A 2006 study at the Research and Sport Medicine Center in Spain, compared 11 weeks of failure versus non-failure resistance training on hormonal responses, strength and muscle power gains. Strength gains were strikingly similar, but most importantly for this context: non-failure resistance training resulted in reduced resting cortisol concentrations and an elevation in resting serum total testosterone concentration. Researchers even noted that non-failure training demonstrated a beneficial stimulus for improving strength and power, “especially during the subsequent peaking training period, whereas performing sets to failure resulted in greater gains in local muscular endurance.” Maintenance routines should avoid advanced failure principles; keep it abbreviated and simple. Sets using high repetitions (15 or more) should be avoided since they task the cardiovascular system and are less productive for supporting functional and forceful strength levels. Low repetitions (five or less) should also be discouraged since they heavily task the nervous system. It’s important to enjoy working out during this period – to take pleasure in the gains and simply fight to maintain. It is not feasible to try and grow forever, but rather in spurts.

If done correctly, you can solidify gains post cycle and even continue to make small improvements. The workout journal should document any loss of limit strength. In advanced trainees, strength and muscular power is directly proportional to muscle mass. These little books are so important in gauging progress or digress; to train or go through post-cycle therapy without one is ridiculous. Great battles are not won without a map. Bodybuilding also needs a well-written, thought-out plan.

Effective AAS cycling is not determined by any one phase. Proper attention must be paid pre, during and post cycle. These powerful little hormones play big roles in the human body – influencing growth, metabolism and reproduction. Responsible integration, combined with a well thought out plan, will lead to greater achievements in muscular growth at minimal risk. Long-term sustainment requires persistent and sufficient training and nutritional support over the long haul. Bodybuilding is not a sprint – it’s not even a marathon – it’s supportive education and innovative strategies, combined with regimented application.
Title: Odg: Terapija poslije ciklusa-PCT
Post by: sele137 on September 23, 2009, 10:29:17 PM
How to KEEP GAINS from steroids



This info I have gleaned from self research, trial and error, from my endochrinologist, from SWALE and from training hundreds of clients over the years.



First of all I would like to stress that I and my endochrinologist do not believe one can keep gains above ones natural max, or that level of muscular developement that can be held to without steroids. In other words, I think one will always shrink down to the size that can be held to with ones own T production.

In reality what usually happens is that many(not all) steroid users fall BELOW their natural max within months of discontinuing steroids for one or all of the following reasons......poor HPTA recovery and or lack of knowledge in regard to what makes up proper steroid free training.

If HPTA recovery is not fairly rapid and complete then obviously one risks dropping BELOW ones natural max in time. If one does not know how to train effectively without steroids then one will rapidly overtrain and drop below natural max in time, not to mention the strong possibilty of injury which also will hinder gainskeeping.

You can, however, makes gains well above your natural max while on steroids and then with prudent use of ancillaries, and proper natural training, hold to your natural max well into ones 50's and perhaps early 60's.

As an estimate of natural max.......the average guy of average height( 5"9 or 10" and with average bone structure and genetically typical recuperative abilities (vast majority of men) can usually get to a lean 190-195 with a bench of 275-300, full squat of 375-400 and a deadlift of about 500 pounds without steroids.


ANCILLARIES....HCG


Dare I say that HCG use is more important than SERMS(nolva or clomid) for good hpta recovery after a LONG cycle( 12 weeks or longer)
Personally I would use hcg during any cycle 8 weeks or longer...and if you are really paranoid and want the absolute most rapid hpta recovery then use it during any cycle for next to zero testicular shrinkage.

Now you will recover hpta without hcg, and fairly quickly if you truly have not suffered from much testicular atrophy, but not as rapidly as you could and that will cost you at least some gains.

HCG, human chorionic gonadotropin, is a hormone taken from placentas during pregnancy. It limics the action of LH from the pituitary and stimualtes testosterone production in the testes.

It is important to the male bodybuilder in that proper use of this hormone PREVENTS testicular atrophy caused by HPTA shut down from steroid use.

If the testes are shut down they will shrink, it's as simple as that. The degree of shrinkage depends upon the length of time "on" androgens. Some guys literally see their testes atrophy down to raisen size..NO ****. Others see modest shrinkage and a few say they see NO shrinkage. In the latter this is BS and has to due with poor pre-cycle assessmant of testicular size....after all how many of us sit down before a cycle and really feel the true size of our balls.  :lol:


NOTE: all steroids will shut you down 100% and at a very low dose, and that includes Primo and anavar for you sceptics. As little as 100mg a weekof testosterone administered exogenously in the form of injections will shut you down in as little as a few weeks.




HOW TO USE HCG

It is best to prevent testicular atrophy in the first place rather than trying to bringing the boys back to size after they have already atrophied.
With this in mind prudent use of hcg is DURING a cycle.

HCG can be taken either IM or sub Q in the fat and yes you can mix it with your oils.

Take it at 500iu's every 3rd or 4th day while on cycle.


Some use it post cycle at higher doses after their testes have already shrunk. This method works but I do not believe that it is the best way to use HCG. In this method one injects a high dose of hcg right near the end ofa cycle but before clomid. The opening dose is often 3000iu's followed sometimes by another 3000 4 days latter and then 1500iu's every 4th or 5th day and then the last shot is usually only 1000iu's....total time three weeks.
No use taking clomid or nolav with the HCG since HCG will supress the hpta all by itself via the testosterone production it stimulates.

WARNING.....if you use hcg at a high dose for too long you might desensitize the testes to LH so don't get carried away with it.




SERMS clomid and nolva

After any cycle a SERM should be used, either clomid or nolva.

SERMS help to "kickstart" a sleepy hpyothalmic GnRH response.

GnRH is pretty quick to recover but SERMS help the hypothalamus to "turn the key" on the GnRH impulse generating engine.

SERMS block the affect of estrogen at the hypothalamus and since estrogen is highly inhibitory this blocking affect allows for greater LH production. This "greater LH production" strongly stimulates the testes to produce testosterone.
If you use only gear that does NOT aromatize to estrogen then you don't have to worry about the inhibitory affect of estrogen post cycle(from the steroid)...but SERMs should still be used to counter the inhibitory affect of the estrogen seen form the T production(from the hcg use).....and also from the estrogen production from the aromatization of the T production form your testes after the hcg is stopped.

*Even if you never used HCG you should still use a SERM after a cycle with non aromatizing gear to counter the inhibitory effect of normal estrogen production(from the aromatization of T from your improving T production)

You have to wait until exogenous androgen levels drop to a similar level of what a normal T production would be, in order for this LH stimulating affect from SERMS to work, since androgens are also highly inhibitory on the hypothalamus.

So you must have to have a good grasp on the half lifes of the various gear you use. You also have to be aware of the how the dose taken factors into the equation. ie: test cyp has a half life of around 6 days so with this in mind 500mg of test cyp will reduce to 250 mg in a week and about 125 in another week. That 125mg is about 100mg of pure testosterone(minus ester weight) and you can now begin SERM therapy because that level is near what a normal T output would be(slightly higher though)

NOTE: There is no penalty for starting a SERM too early but there is one for starting too late.



On opening "SERM day", post cycle, you want to do a "loading dose" of about 200-300mg of clomid in divided doses in order to get blood levels up pronto. Then take 50-100mg/day for a week and then 50mg/day for 3 more weeks MINIMUM... and longer after deca use.
Alternatively you can use nolva at 80mg on day one in divided dose and then 40mg /day for a week and then 20mg/day for at least 3 more weeks.



PROPER STEROID FREE TRAINING POST CYCLE.....for the genetically typical(most men)...not easy gainers.

Thanx to all the glossy magazines out there very very few bro's really know how to train for gains without steroids. Dare I say that not a few of you turned to gear simply because you could not make very good gains as a natural.

Thanx JOE WEIDER, and others, for NOT telling the whole story in the glossy mags. THE ROUTINES IN THE MAGS WILL NOT WORK FOR 90% OF ALL MEN UNLESS THEY ARE, #1 ON GEAR AND #2, AT LEAST SOMEWHAT GENETICALLY GIFTED. Guys these pro's are so out of touch with what works for the typical man training naturally that it isn't funny.
These guys are genetic freaks on a ton of gear...like 2-4 grams of test a week, other steroids, growth and slin! Not only that but they don't have jobs outside the gym to drain them either!

Steroids not only help muscle building but more importantly they GREATLY improve recuperative powers.

Most guys continue to train in a very similar fashion while off gear as they did while on gear, especially in regard the number of days in the gym each week, and this is a HUGE ERROR.
Many many guys simply overtrain after they stop the gear and loose huge amounts of muscle and many actually end up below their natural max potential in time. Others do not even bother training at all without juice!

I went to a Dorian Yates seminar a few years ago and he mentioned all this. Dorians recommendations in regards to training without gear where almost identicle to mine. Dorian said that most trainees should train no more frequently than three days a week on a three way split while "off" steroids and that all should use a low volume of sets and work primarily on the big basic compound movements with very hard work. FINIALLY A PRO THAT KNOWS AND TELLS THE TRUTH!



Most men simply cannot recuperate from frequent trips to the gym and even moderately high volume without the assistance of steroids. Most men are genetically typical in the recuperation department....and thats at least 90% of you bro's.

I have good genetics for bodybuilding and I could train in almost any manner while on gear and gain well but even while on gear I choose to train infrequently, every other day on a three way split while "on" and Mon-Wed and FRI on a three way split while "off", and with low volume and very hard work...WHY?...for three reasons....#1. I have other things to do in my busy life and #2. I make even better gains and get even bigger with this style of training...#3. I like it

****SO>>>>>How much more is it important for the typical trainee to train in a similar way without steroids in his system.

GUYS...you don't have to be in the gym 5 and 6 days a week and train with high volume in order to see excellent gains while"on" steroids and in fact most of you would do better training fewer days and with lower volume but with more effort on those sets.
For those that are in the gym 6 days a week and like 10-20 sets per body part and are making good gains then more power to ya...but you just might do better training less frequently and with less volume.
**** I am genetically gifted and I have seen my best gains on gear training every other day on a three way split with low volume and big efforts.
Remember you easy gainers...the pro's are very genetically gifted, on more gear than most of you and don't have jobs or go to school.


Title: Odg: Terapija poslije ciklusa-PCT
Post by: sele137 on September 23, 2009, 10:44:01 PM
Understanding PCT

PCT, what does it mean?
Post Cycle Therapy.

What does it do?
It returns your Hypothalamus, Pituitary, Testicular, Axis (HPTA) back to producing its own endogenous testosterone production.

How long does it last?
Good question but in my opinion the normal 21 to 30 days protocol is too short unless suppression of the HPTA is minor.

Ok, you produce about 7 mg of testosterone a day or around 49 mg a week on average, some more, some less (usually older guys).
So, you go on a cycle of lets say 500mg of testosterone a week or about 10 times your natural production. The body sees this as too much testosterone and will lower production of testosterone to try to maintain homeostasis (balance). The body loves homeostasis.
Testosterone in a man gets converted into two other hormones; one of those hormones is DHT (dihydrotestosterone) this is done by an enzyme called 5-alpha-reductace. DHT is actually about 3-5 times more androgenic than testosterone.
The other hormone it gets converted to is estradiol (E2), this is a strong estrogen but from now on we will just refer to it as estrogen, even though there are 3 different kinds of estrogen. Testosterone gets converted into estrogen by another enzyme called aromatase. The conversion is called aromatization.

Ok, the body will convert more testosterone into estrogen probably to try and maintain homeostasis, so the more test, the more estrogen. For most this estrogen is not a problem. But for some it will be a problem and this extra estrogen can give side effects like gynecomastia (gyno) or water retention, but one big problem is estrogens suppressive effects on Luteinizing Hormone or (LH) LH is what the pituitary gland sends as a chemical hormone to the Leydig cells in the testicles where the testicles will product testosterone. Estrogen is probably 100-200 times as suppressive as testosterone.
So when LH production stops (exogenous testosterone will do this too) the testicles will stop producing and like anything not being used will atrophy.
What does this mean?
You will get some small balls, no kidding mine have been the size of almonds without the shell.

OK, so you come off a cycle, the exogenous testosterone is tapering down and after about a couple of weeks (this is the clearance time for testosterone cypionate and enanthate) you end up with low levels of testosterone as your endogenous production has long been stopped. Now here where the problem starts. You potentially have the testosterone of a woman, and high estrogen from all that aromatization.
This can be a recipe for disaster, why? Because men need test to feel normal and not only that hard earned muscle will be eaten up by being in a catabolic environment, not to mention there is still going to be some suppression because of elevated estrogen.
I have seen big strong men carry on like crying women in this state; it is very bad, sex drive is zero, no energy, emotional, insecure, the list is long.

So, what can you do?
First of all in my opinion bringing the nuts back online is very important, the most important. This is done with the use of Human Chorionic Gonadotropin (HCG)
It basically is pregnant woman’s urine. HCG mimics LH and as we learned above that LH is the chemical hormone that stimulates the Leydig cells to produce testosterone. HCG is very strong and many times stronger than the amount of LH that the pituitary puts out.
The typical dose is anywhere around 350iu to as much as 2500iu and even in some cases more but I don’t recommend this. Best advice is to use as little as possible to achieve success at bringing the nuts back to life from their nice little vacation.
The half life of HCG is around 3 days or so, so Subcutaneous (Sub-Q) shots or Intramuscular Shots (IM) are done about Every Other Day (EOD or Every 3 Days (E3D).
If you use too much for too long desentization of the Leydig cells can happen and this is not good.
One other thing is HCG aromatizes pretty heavily. So an anti estrogen is always recommended if you shoot more than 500iu and even that if you are gyno prone would be a good idea to add an anti E.
HCG comes in tow bottles or vials and one is powder and the other is a solvent or bacteriostatic water, the water gets added to the powder and this is called reconstitution. Once HCG is mixed it must be refrigerated. In bacteriostatic water it will last around a month.

Now next we want to block the hypothalamus and pituitary gland from that excess estrogen as that in itself is suppressive.
How is this done? With a drug called Clomiphene citrate (clomid). This is really a drug to help women ovulate but it acts as a Selective Estrogen Receptor Modulator (SERM).
It occupy’s the estrogen receptors in the hypothalamus and pituitary and blocks estrogens exertion on those glands. It’s like putting a key in a lock but not turning the key. It is just occupying that space without really doing anything.
Clomid in my opinion works better than another SERM that many people use called Nolvadex. Both pretty much do the same thing but together I have found to be far superior than using any of them by themselves.
Clomid is used to test the pituitary for secondary hypogonadism, clomid @ 100mg a day after 5 to 7 days will double LH responce and increase FSH by 20% to 50%, that is huge.
Both clomid and nolva are in pill form as well as liquid form.
What these do is block estrogen. The body sees this as it is low in testosterone and estrogens suppressive effects are not there as the receptors are blocked. So it see’s this as low testosterone and low estrogen so the body turns on the hypothalamus to produce Gonadotropin Releasing Hormone (GnRH) which in turn tells the pituitary gland to produce LH and FSH (follicle stimulating hormone). FSH is another hormone that stimulates the Sertoli cells in the testicles to produce sperm.

Ok, so lets put this all together.
There are a couple of ways you can do this.
First you can take HCG in small amounts during the cycle to maintain testicular function or you can take it after the cycle is finished to start your PCT.
Either way is fine but if the cycle is very long then long use of HCG can be a problem due to the possibility of desentization of the Leydig cells.
That’s pretty much the last thing you want to do as you want your own LH production to keep the testicles producing test.

So, what you can do is wait about 2 weeks for the testosterone to clear your system or be around base levels of normal producing test and start your HCG, clomid and nolvadex all at the same time.
You don’t have to worry about the aromatization issue because both clomid and nolvadex are anti-estrogens or act as anti-estrogens in the body.
By the way nolvadex is used in estrogen sensitive cancer tissues like in treating breast cancer.

I take clomid at 50mg twice a day (12hrs apart) for 30 days.
I take nolvadex at 20 mg a day for 45 days.
I take anywhere from 1000iu EOD to 2500 EOD for 8 shots (16 days).

So the HCG is taking care of the nuts and taking them off vacation and putting them back to work and the nolvadex and clomid will help the hypothalamus produce GnRH which will tell the pituitary to produce LH and FSH.
Once the testicles are producing test on their own you stop the administration of HCG and let the body take over, kind of like handing a baton when doing a relay race.

Depending on the type of gear, length of time on, amount of gear, all play in this factor of recovery, not to mention the genetic factors involved in shutdown.
I shutdown very hard and I notice atrophy in as little as 3 weeks.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: CRonaldo on September 23, 2009, 10:53:56 PM
Tooooo Sele, svaka cast za tekstove  :clap:  :clap: Sad idu na printanje, lisio si me smaranja u skoli sutra  :lol:
Title: Odg: Terapija poslije ciklusa - PCT
Post by: sele137 on September 23, 2009, 11:48:15 PM
Mora da ti je u skoli pravo dosadno kad ces citati ovo  :lol:
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Pedja Petrovic on September 24, 2009, 07:09:06 AM
Mora da ti je u skoli pravo dosadno kad ces citati ovo  :lol:

 :lol: :lol: :lol: :lol: :lol:
uce deca
trebat ce im kako da sacuvaju misice  :yes: :yes:
jebes sve ono sto si pisao o tome KAKO DA IH DOBIJU tj dzaba truda u u pm-jos malo pa ce PCT da se koristi nakon kure sa whey proteins i creatin,a ako na to se nabaci jos glm i bcaa ihaaaaaa...PCT for 8 wekks  :lol: :lol:
uffff :wallbash1: :wallbash1: :wallbash1:

and

Quote
Good question but in my opinion the normal 21 to 30 days protocol is too short unless suppression of the HPTA is minor.
:clap: :clap: :clap: :clap: :clap:
Title: Odg: Terapija poslije ciklusa - PCT
Post by: CRonaldo on September 24, 2009, 04:53:04 PM
brateee ja jedva cekam da mi bude gotovo stampanje knjige one Anabolics 2009 :D znaci kad god budem isao negde nosim to sa sobom :D na fax obavezno :D :lol: :lol:

pa taj fazon ;D e koliko ce te izaci to stampanje? ja isto planiram da odstampam tu i jos par knjiga

@milan:  hahahahaha  :lol:

@Lokk:    bash jbt  :) a inace danas pitam profesoricu jel mogu da radim maturski na temu ishrana sportista kaze bilo prosle godine, reko moze onda doping sportista kaze bilo prosle godine, reko moze anatomija misici tako nesto kaze bilo je i to, reko jel moze nesto o hormonima npr o testosteronu kaze bilo je i to, reko jel moze o suplementaciji sportista kaze bilo i to pa hebem ti zivot  :wallbash1: :wallbash1:

uce deca
trebat ce im kako da sacuvaju misice  :yes: :yes:
jebes sve ono sto si pisao o tome KAKO DA IH DOBIJU tj dzaba truda u u pm-jos malo pa ce PCT da se koristi nakon kure sa whey proteins i creatin,a ako na to se nabaci jos glm i bcaa ihaaaaaa...PCT for 8 wekks  :lol: :lol:
uffff :wallbash1: :wallbash1: :wallbash1:

znam da nisi mislio na mene s ovim, ali ja to citam zato sto mi je ta materija jako zanimljiva, kako nase telo funkcionise, da nisam matematicar i informaticar studirao bih medicinu  :lol: hebiga neko cita romane, neko cita o automobilima, neko ovo... i upijam sve sto procitam bas iz tog razloga sto tu materiju obozavam, o nutricionizmu sam bas puno procitao i malo me smorilo pa sam presao na ovaj napredni level :) smatram za obavezu svakog coveka da zna bar osnove kako mu telo funkcionise, jbt ljudi znaju da upravljaju tamo nekim ekstremnim masinama a ne znaju ni ono najosnovnije o svojoj telesnoj masineriji
Title: Odg: Terapija poslije ciklusa - PCT
Post by: sele137 on September 24, 2009, 08:27:41 PM
PCT and Cycle Recomendations: Estrogen, Progesterone and Cortisol control


SERM's (Selective Estrogen Receptor Modulator) : These block certain estrogen receptors, ***ending on the drug, and dont actually lower estrogen in the blood. Estrogen is left to circulate with nowhere to go. Because of this, SERMS have a positive effect on cholesterol levels. They have a negative effect on IGF-1, so if bulking, only take them if totally necessary. They are good at blocking gyno. Commonly used during PCT, and less often used while cycling. A SERM like nolvadex is widely used in PCT to help kickstart the HPTA back to normal function, in conjunction with other beneficial drugs. To learn how this works, please refer to Anthony Roberts PCT in the PCT section.

Nolvadex (Tamoxifen Citrate) : Nolvadex is a SERM. It selectively binds to certain estrogen receptors, effectively blocking the estrogen and stopping unwanted sides such as gyno. It DOES NOT lower estro levels in the blood, it only blocks it from binding to certain receptors. It also helps your blood fat levels. It does not suppress LH, blocks desired estro receptors and helps stop HCG from desensitizing your testicles to natural LH. Nolva should be used during HCG therapy, at 20 mg a day, for the reason i just mentioned. Can be used during cycle if you see signs of gyno. Its mainly used to block the estrogen spike when you come off cycle, and should be used right through to the end until natural test levels are back. One drawback to consider about Nolva is that it may cause progesterone receptors to become more sensitive. This means that while using progestins such as Deca or Tren, you may become more sensetive to progestin related gyno.

Faslodex (Fulvestrant) : Approved for use in 2002 for breast cancer research, this drug is unlike most we have seen. It is classified as an estrogen receptor downregulator. It prevents estrogen from exerting its influence on the estrogen receptor. Similar to Nolvadex, but is not selective. It hits all estrogen receptors. It also does this to progesterone receptors to a lesser degree. It is injectable, at 250mg a month. No information on how it affects blood lipids. It is also very expensive.

Clomid (Clomiphene Citrate) : This drug is also a SERM, almost identicle to Nolva. It is said to be a weaker blocker mg for mg than Nolva. Its common use is in PCT, usually for about a month, used after HCG and all AAS esters have run out of your body. Even though it is weaker than Nolva at blocking, it is believed to be quicker at bringing HPTA back to balance. Both are commonly used during PCT. It binds to different receptors than Nolva. There is a lot of debate on this, but until there is solid proof, it may be prudent to include this in your PCT. Commonly taken at about 100mg a day.

Fareston (Toremifene Citrate) : This is a second generation SERM. Approved for use in 1997. Chemically very similar to Nolva and Clomid, it is less powerful mg for mg. Fareston may have a stronger posotive effect on your cholesterol levels. For those who find this an important issue, this is a drug of choice. Used every day at around 60mg.

Evista (raloxifene)
: A newer SERM, Evista is shown to be a blocker in breast tissue, but acts as a receptor agonist in bone tissue (unlike Nolvadex). This action promotes bone density. Taken at about 60mg a day. Evista may prove to be very beneficial, as it also helps cholesterol levels (like Nolvadex). Evista is supposed to have a more powerful gyno blocking effect than Nolvadex.

Cyclofenil : Much like Nolvadex, this is also a SERM. Used at about 600mg a day, it is weaker mg for mg. A good alternative if Nolva is not available, which is usually not the case.


AI's (Aromatase Inhibitors) : There are 2 types of AI's. Type I (suicide inhibitor) attaches to the aromatase enzyme and permanently disables it. Type II compete for the enzyme, but dont destroy it. Both are effective at lowering estrogen substantially. Both are commonly used during both cycling and PCT. Used mainly when low estrogen levels are desired, like contest preparation/cutting. Beware that lowering estrogen with strong AI's can have a negative effect on cholesterol levels and low estrogen levels can lead to sore joints, cause your losing estrogens anti-inflammitory effect. Can also have a negative impact on your libido. Estrogen has an important role in mass building and joint health, as noted below where "estrogen" is explained.

Teslac (Testolactone) : This is a first generation steroidal aromatase inhibitor. Like a suicide, it permanently attaches to the aromatase enzyme. Taked at a maximum of 250mg a day. It is not as strong as the newer AI's, but some people still like to use it. It can lower estrogen about 50%. Streroidal in structure, it has no anabolic effect.

Aromasin (Exemestane) : This drug is classified as a Type I Suicide AI. It binds to the aromatase enzyme and kills it. It is effective at lowering estrogen up to 85%. Once again, you have to watch out for your cholesterol levels. Used mainly for cutting when low estrogen levels are desired. Aromasin is shown to help bone density. Clinical doses are about 25mg a day, but it has been shown that as little as 2.5mg a day can be as effective.

Lentaron (Formestane) : A Type I Suicide AI. Lentaron is not classified as a drug, and can be sold over the counter as a suppliment. Not as strong as the third generation AIs (arimidex, femera). Can lower estrogen by about 60%. Used as an injectable, it is dosed at about 250mg every 2 weeks. Due to poor bioavailability, daily doses of oral Lentaron are about 250mg.

Arimidex (Anastrozole) : This is a widely used type II AI. It competes with estrogen for the aromatase enzyme. This effectively lowers estrogen up to 80% in the blood. Approved for use in 1995 to fight breast cancer. At doses up to 1mg a day, it has been shown to be very effective at controlling estrogen while on cycle or in PCT. It is usefull for curbing the effects that come with aromatizing AAS's while in cycle, and can be used in PCT. Nolvadex is shown to decrease the effectiveness of Arimidex when used together. In this case a suicide inhibitor may be more well suited, like in PCT. It is also called L-dex, in its liquid form.

Femera (Letrozole)
: Letro is a competative Type II AI also. Also farely new compared to other compounds, it is shown to be effective at lowering estrogen by blocking the aromatase enzyme. Doses up to 2.5mg a day are used, but usually as low as .5mg a day can be just as effective. Clinical studies show Femera to lower estrogen by 75-78%, sometimes up to 95%. Once again, watch out for your blood lipids (cholesterol) to get out of whack. There may a noted rebound effect of estrogen levels that goes along with Letro use.


RI's (Reductase Inhibitors) : These drugs stop the conversion of testosterone into DHT wherever 5-alpha reductase enzymes are present. RI's work by blocking the action of the 5-alpha. There are 2 5a's. Type I 5a and Type II 5a. Different RI's block one or both of these 5a's. The main reason someone uses RI's is to stop hairloss. They are common anti hairloss drugs. The problem is, when you block the dht conversion, there are less androgens available and may reduce your gains. Sometimes people report less strength, aggression and drive to train.

Proscar (Finasteride) : This is primarily a Type II 5-alpha blocker. This means that when you are taking a high dose of testosterone, the resulting conversion of test to DHT in certain parts of the body become to high for ones own comfort, mainly hairloss and prostate enlargement. This is where the type II 5a enzymes are mainly found. This will not work against AAS that are already highly androgenic by design, without conversion. AAS like Tren will still exhibit high androgenic properties. Used at doses up to 5mg a day.

Avodart (Dutasteride) : Like Proscar but newer and more effective at blocking the effects of DHT in not only the scalp and prostate (which are Proscar's main strengths) but also in the skin, effectively reducing acne. This is because Avodart will block both Type I and Type II 5-alpha enzymes, covering more of the problem areas due to DHT. Available in .5mg softgels, this is an effective dose. Approved for use in 2002.


Estrogen : The first hormone we need to keep an eye on. Many AAS convert to estrogen via the aromatization process. Some AAS are worse than others. Also, estrogen spikes after a cycle. High levels of estrogen leads to gyno, water retention, fat storage etc. Estrogen plays a key role in progesterone related gyno. We either block its receptors with SERMS or reduce its production with AIs. We watch estrogen levels during a cycle and in PCT. Lowering estrogen too much will mess up your blood lipids. Letting it get out of control will cause sides like gyno, water retention etc. Estrogen plays a role in IGF-1 levels, may lower IGF-1 when blocked with a SERM. Estrogen is also beneficial hormone when bulking, promoting higher androgen receptor concentrations (!). It also is beneficial in another way - its supposed to act as an anti-inflammatory - this means blocking or reducing it too much during a heavy bulking cycle can result in injury to joints. Obviously different estrogen levels are desired for different goals, and it is not always good to block its action or its production. Usually, while bulking, estrogen is allowed to rise unless gyno or water retention (leading to high blood pressure) becomes a problem. When cutting and shedding water and lifting a little lighter (contest prep for example) estrogen is usually dropped with an AI. Proper diet and training can help the bad side effects high estrogen can have.

Progesterone : Its not so much progesterone that we watch, which is actually a healthy hormone, but progestins which may act upon its receptors. Progestins, like Tren or Deca (nor-9's), may act on its receptor or lower progesterone in the blood. Gyno and lactating are more common side effects. Some people use progesterone receptor blockers to combat this, or a prolactin production inhibitor.

Progesterone Control

Lilopristone, Onapristone: These are progesterone blockers also, said to be safer and possibly more effective than RU-486 when it comes to progesterone blocking. They were developed after RU-486 in an attempt to make more effective, less harsh drugs to block progesterone.

Dostinex (Cabergoline), Bromo (Bromocriptine), B-6 : These are used for Deca/Tren gyno sides. This type of gyno is related to progesterone and its receptors. Tren/Deca may act on the progesterone receptor, as they are progestins, and may increase prolactin in the blood (causing lactating). These drugs stop production of prolactin at the pituitary gland. Controlling estrogen levels with an AI also helps here, as progestins themsleves haven't been proven to cause gyno.

RU-486 (Mifepristone - abortion pill) : This drug has the ability to block estrogen, progesterone AND cortisol. It may or may not be very well tolerated, but I would like to find out more about it, as it is used in the bodybuilding world. In PCT it is used to block cortisol and progesterone. A powerful drug that may turn out to be a good choice, but i need more evidence and feedback from experience useing RU-486.




Cortisol
: The third hormone, the stress hormone. When elevated to long, it will store fat. Eat muscle. Cause lethargy. Moodiness. You may crave carbs by the boat load. Cortisol spikes after a cycle because AAS blocks it while on cycle, upping cortisol production and receptor sites. IMO not enough attention is payed to this. It has special functions in the body that are absolutely necessary, like its anti-inflamitory ability. However, when elevated for long periods, it turns into a muscle eating beast. The most important time to watch cortisol is after a cycle, when it spikes. There are a couple ways to help control this, explained below.

Cortisol Control

Cytadren (aminoglutethimide) : This drug has the ability to reduce cortisol at higher doses (1000mg a day), and act as an AI at lower doses (250mg a day). The cortisol effect is shortlived if taken for a number of consecutive days. Can lower estrogen a lot, anbout 90%. The higher dose has a long list of sides. More effective as an AI.

Mirtazapine :This is used to lower cortisol. Even though it may be effective in cortisol control, Johan has pointed out that it may cause some phycological side effects, like making you feel like a zombie. Here is a pubmed abstract for is effects on cortisol levels, among other things.http://www.ncbi.nlm.nih.gov/entrez/...1&dopt=Abstract

Cytodyne (Phosphatidylserine) : This is also used to lower cortisol, but is only effective in lowering about 30%. There are other ingredients in Cytodyne than Phosphatidylserine. Phosphatidylserine is the only real proven ingredient to lower cortisol, or so ive gathered so far. Effective at 800mg a day of PS as an ingredient.

Relacore : This over the counter cocktail of herbs and vitamins and minerals is supposed to reduce the amount of cortisol in your blood. I find it chills me out a little, however i read some places that it may raise estrogen. I used it for a bit, however I dont bother any more.

Vitamin C
: At doses of about 1.5 grams a day, can have a lowering effect on elevated cortisol, not to mention its other healthy effects.


LH Repalacement Therapy - Testosterone Stimulating Drugs

HCG (Human Chorionic Gonadotropin) : HCG is a replacement for your natural LH (luteinizing hormone). LH is what your body produces to tell your testicles to produce natural testosterone. LH levels drop when using AAS (HPTA suppression). Using HCG while on cycle prevents testicular shrinkage, speeding PCT when the time comes. Using Nolva while using HCG helps stop HCG from de-sensitizing your testicles to natural LH. In my opinion, any decent cycle/PCT should include HCG. It has been suggested to me that HCG can be used throughout a cycle at 500iu E4D, but im unsure of this from practical experience. The most favorable way is to use it in the last couple weeks of your cycle at a higher dose, like 500iu ED. The trick is to end the use of HCG just as the last AAS is running out of your system. So, 3 weeks before the the last ester leaves your blood, you would start the HCG/nolva combo. HCG at about 500iu ED and Nolva 20mg ED. This is done before Nolva/aromasin (for example) PCT starts, and runs about a few weeks longer than the end of the HCG. Always include Nolva with your HCG, they work together well. Be careful not to overdose on HCG and permanently desenstize your testicles to LH. HCG has an active life of about 3 days. Vitamin E is a booster, read the next one :

Vitamin E : As Anthony Roberts pointed out to me, vitamin E increases the response to HCG. This may be useful in making the low doses of HCG we use more effective at growing back shrunken testicles. Doses can be generally 1000iu a day while using HCG.

Fat Burning, Anti-Catabolic

Clen (Clenbuterol) : Clenbuterol is a bronchodilator. Everyone knows clen is used to burn fat. Why am I listing it here in a PCT thread? Well, for its anti-catabolic properties. Clen may lower the effect of AAS while on cycle, so I personally dont use it while cycling. It does, however, have an effect on cortisol levels. While on cycle, cortisol is not to much of a problem if you eat right. AAS use increases cortisol production, and increases receptor sites. This means that when you finish a cycle, cortisol spikes along with estrogen. This is a part of the "crash" that is often overlooked. People have reported that blocking cortisol in PCT speeds along fat loss. Clen is supposed to have a blocking effect on cortisol. So, along side of its ability to burn fat, it is anti catabolic in it ability to block cortisol until desired hormone levels are achieved in PCT. For me, it makes sense to use clen in PCT until desired hormone levels are achieved, as it also burns away fat in the process.


Title: Odg: Terapija poslije ciklusa - PCT
Post by: Pedja Petrovic on September 25, 2009, 07:14:44 AM
Quote
smatram za obavezu svakog coveka da zna bar osnove kako mu telo funkcionise, jbt ljudi znaju da upravljaju tamo nekim ekstremnim masinama a ne znaju ni ono najosnovnije o svojoj telesnoj masineriji

KAMO SRECE DA SVI RAZMISLJJU OVAKO KAO I TI!!!
BRAVO
Title: Odg: Terapija poslije ciklusa - PCT
Post by: MuscleFilip on September 25, 2009, 11:41:07 AM
o nutricionizmu sam bas puno procitao i malo me smorilo pa sam presao na ovaj napredni level :) smatram za obavezu svakog coveka da zna bar osnove kako mu telo funkcionise, jbt ljudi znaju da upravljaju tamo nekim ekstremnim masinama a ne znaju ni ono najosnovnije o svojoj telesnoj masineriji

evo ti endokrinologija, ima koju hiljadu stranica: http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=endocrin
evo ti i malo o mastima, samo 1100 stranica: Handbook of obesity: etiology and pathophysiology  (http://books.google.com/books?id=YBT4fPaitjkC&dq=human+leptin&ei=3428SrSfCJG-ywSX0sHRDw&hl=sr)
Title: Odg: Terapija poslije ciklusa - PCT
Post by: sele137 on September 26, 2009, 08:21:20 PM
'Nitrom'
Isprazni sanduce ako zelis da ti posaljem PP  :rolleyes01:
Title: Odg: Terapija poslije ciklusa - PCT
Post by: sele137 on September 26, 2009, 11:17:46 PM
Anastrozole (1 mg ED for 10 weeks):

http://jcem.endojournals.org/cgi/content/full/85/7/2370

..eight males (aged 15–22 yr; four adults and four late pubertal) had isotopic infusions of [13C]leucine and 42Ca/44Ca, indirect calorimetry, dual energy x-ray absorptiometry, isokinetic dynamometry, and growth factors measurements performed before and after 10 weeks of daily doses of Arimidex (1 mg ED)
...Anastrozole treatment was well tolerated by all subjects. Glucose and insulin concentrations remained unchanged during these studies, as did plasma lipid concentrations, blood chemistries, and cell blood counts...


-----------------------------------------


2.5 mg of letrozole ED + 1 mg/kg of test once every 4 weeks for 12 MONTHS


http://jcem.endojournals.org/cgi/con...ull/86/10/4887

The boys in the T-treated group (12 boys) received T enanthate (1 mg/kg, im, every 4 wk, six times). The T- plus-letrozole-treated group (13 boys) received T enanthate (as above) and, in addition, an aromatase inhibitor, letrozole 2.5 mg, orally, once a day for 12 months

Safety

The concentrations of total cholesterol, low and high density lipoprotein cholesterol, triglycerides, transaminases, the leukocyte count, and the bone density were determined during the follow-up. In these safety parameters, no changes sufficient to indicate discontinuation of the treatment were observed in any of the boys. Letrozole was well tolerated; no side-effects were observed.


-----------------------------------------


http://jcem.endojournals.org/cgi/content/full/86/6/2869

Fifteen eugonadal men over 65 yr were treated for 9 weeks with 2.0 mg/day of anastrozole, an aromatase inhibitor
... After 9 weeks of aromatase inhibition, total cholesterol decreased significantly by 7 ± 10% (P = 0.016), and HDL cholesterol decreased by 7 ± 9% (P = 0.013). Calculated LDL showed a small decrease that was not statistically significant ...


----------------------------------------


Effects of tamoxifen on lipid profile and coagulation parameters in male patients with pubertal gynecomastia.

Novoa FJ, Boronat M, Carrillo A, Tapia M, Diaz-Cremades J, Chirino R.

Department of Endocrinology, Hospital Universitario Insular, Las Palmas de Gran Canaria, Spain. jnovoa@cicei.ulpgc.es

BACKGROUND/AIM: The estrogenic actions of tamoxifen on lipid profiles and hemostasis have been extensively demonstrated in women. Due to limited experience with this drug in males, it is uncertain whether these effects are also present in men. The aim of our study was to assess the response of blood lipids, lipoproteins, and coagulation parameters in a group of men taking tamoxifen. METHODS: We studied 15 healthy boys with pubertal gynecomastia who were given 10 mg tamoxifen per day. Total testosterone, sex-hormone-binding globulin, estradiol, serum lipids, apolipoprotein B, apolipoprotein A-I, lipoprotein(a), fibrinogen, antithrombin III, von Willebrand factor, and markers of activated coagulation and fibrinolysis were determined at baseline and 1 and 3 months after beginning of the tamoxifen treatment. RESULTS: Total cholesterol and lipoprotein(a) showed moderate but significant decreases from baseline. Low-density lipoprotein and high-density lipoprotein cholesterol concentrations as well as triglyceride and apolipoprotein B levels became lower, but these changes were not statistically significant. Among clotting parameters, antithrombin III was reduced, and von Willebrand factor increased significantly. Markers of activated coagulation and fibrinolysis remained unchanged throughout the period of therapy. CONCLUSIONS: The effects of tamoxifen on blood lipids and hemostasis we found in this group of healthy young men were qualitatively similar, but lesser than those previously described in women. Copyright 2002 S. Karger AG, Basel


------------------------------------------


from:
http://circ.ahajournals.org/cgi/con...ull/103/11/1497

..The decreases in LDL-C in the treated TVD and NCA groups did not reach significance compared with the untreated TVD group, whereas decreases in HDL-C were significant (P=0.05 and P=0.015, respectively; Figure 3A). Overall, there was no significant effect of tamoxifen on LDL:HDL ratio. Triglyceride levels showed substantial decreases in response to tamoxifen, reaching significance in the NCA group....



---------------------------------------


Metabolism 1993 Apr;42(4):446-50 Related Articles, Links


The effect of testosterone aromatization on high-density lipoprotein cholesterol level and postheparin lipolytic activity.

Zmuda JM, Fahrenbach MC, Younkin BT, Bausserman LL, Terry RB, Catlin DH, Thompson PD.

Department of Medicine, Miriam Hospital, Providence, RI.

Stanozolol, an oral 17 alpha-alkylated androgen, increases hepatic triglyceride lipase activity (HTGLA) and decreases high-density lipoprotein cholesterol (HDL-C) levels, whereas intramuscular testosterone has comparatively little effect. In the present study, we tested the hypothesis that aromatization of androgen to estrogen blunts the lipid and lipase effects of exogenous testosterone. Fourteen male weightlifters received testosterone enanthate (200 mg/wk intramuscularly), the aromatase inhibitor testolactone (250 mg four times per day), or both drugs together in a randomized cross-over design. Serum testosterone level increased during all three drug treatments, whereas estradiol level increased only with testosterone alone (+47%, P < .05), demonstrating that testolactone effectively inhibited testosterone aromatization. Testosterone decreased HDL-C(-16%, P < .05), HDL2-C(-23%, NS), and apoprotein (apo) A-I (-12%, P < .05) levels, effects that were consistently but not significantly greater with simultaneous testosterone and testolactone administration (HDL-C, -20%; HDL2-C, -30%; apo A-I, -15%; P < .05 for all). In contrast, both testosterone regimens decreased HDL3-C levels by 13% (P < .05 for both). HTGLA increased 21% during testosterone treatment and 38% during combined testosterone and testolactone treatment (P < .01 for both). Lipoprotein lipase activity (LPLA) increased only during combined testosterone and testolactone treatment (+31%, P < .01), suggesting that estrogen production may counteract the effects of testosterone on LPLA. Testolactone alone had little effect on any lipid, lipoprotein, apoprotein, or lipase concentration.(ABSTRACT TRUNCATED AT 250 WORDS)


----------------------------------------


Contrasting effects of testosterone and stanozolol on serum lipoprotein levels.

Thompson PD, Cullinane EM, Sady SP, Chenevert C, Saritelli AL, Sady MA, Herbert PN.

Department of Medicine, Miriam Hospital, Providence, RI 02906.

Oral anabolic steroids produce striking reductions in serum concentrations of high-density lipoprotein (HDL) cholesterol. We hypothesized that this effect related to their route of administration and was unrelated to their androgenic potency. We administered oral stanozolol (6 mg/d) or supraphysiological doses of intramuscular testosterone enanthate (200 mg/wk) to 11 male weight lifters for six weeks in a crossover design. Stanozolol reduced HDL-cholesterol and the HDL2 subfraction by 33% and 71%, respectively. In contrast, testosterone decreased HDL-cholesterol concentration by only 9% and the decrease was in the HDL3 subfraction. Apolipoprotein A-I level decreased 40% during stanozolol but only 8% during testosterone treatment. The low-density lipoprotein cholesterol concentration increased 29% with stanozolol and decreased 16% with testosterone treatment. Stanozolol, moreover, increased postheparin hepatic triglyceride lipase activity by 123%, whereas the maximum change during testosterone therapy (+25%) was not significant. Weight gain was similar with both drugs, but testosterone was more effective in suppressing gonadotropic hormones. We conclude that the undesirable lipoprotein effects of 17-alpha-alkylated steroids given orally are different from those of parenteral testosterone and that the latter may be preferable in many clinical situations.


-----------------------------------------------


Metabolism 1997 Sep;46(9):992-6 Related Articles, Links


Effects of short-term stanozolol administration on serum lipoproteins in hepatic lipase deficiency.

Bausserman LL, Saritelli AL, Herbert PN.

Lipid Research Laboratory, Miriam Hospital, Brown University Medical School, Providence, RI, USA.

We have identified a kindred in Providence, RI, deficient in hepatic triglyceride lipase (HL). The two affected brothers have coronary heart disease and elevated levels of triglycerides, total cholesterol, high-density lipoprotein (HDL) cholesterol, and apolipoprotein [apo] A-I. The lipoprotein lipase (LPL) activity is normal. We and others have postulated that the effects of oral anabolic steroids on HDL metabolism are mediated by HL. To test this hypothesis, we treated these two men and two controls with the oral androgen stanozolol (6 mg/d) for 2 weeks. Consistent with other reports, HL activity increased a mean of 277% in controls with a concomitant decrease in HDL cholesterol (49%), HDL2 cholesterol (90%), HDL3 cholesterol (16%), and apo A-I (41%) and no change in apo A-II. Although stanozolol failed to induce HL activity in the HL-deficient man, HDL cholesterol, HDL2 cholesterol, and apo A-I were reduced a mean of 20%, 48%, and 32%, respectively. In contrast to controls, HDL3 cholesterol (46%) and apo A-II (14%) increased in HL-deficient subjects. Stanozolol treatment also increased LPL activity (124% +/- 86%, n = 4) and decreased lipoprotein(a) ([Lp(a)] 66% +/- 3%, n = 3) in the three men with detectable levels. The data indicate that in addition to stimulation of HL activity, stanozolol treatment changes HDL cholesterol concentration and subfraction distribution by other mechanisms.


Title: Odg: Terapija poslije ciklusa - PCT
Post by: sele137 on September 26, 2009, 11:54:12 PM
New Theory on PCT!
Opioid Modulation & Potential for Preventing anabolic androgenic steroids Induced hpta Suppression
:
By: Eric M. Potratz
________________________________________


Post Cycle Therapy (PCT - post cycle therapy) is a key component in a steroid cycle, as suppression of the Hypothalamus, Pituitary, Testicular Axis (HPTA) is seemingly unavoidable to a steroid user. What I will be presenting in this article is a new idea to the world of anabolic androgenic steroids users. This exciting new concept addresses the possibility of limiting and possibly preventing suppression of the (HPTA) during cycle. More specifically, we will learn how we can actively modulate the hypothalamus & pituitary pulse generator during cycle and how this can prime our endocrine system for a quicker, smarter, and healthier recovery from anabolic androgenic steroids (anabolic androgenic steroids).

For a moment, let’s forget the concept of "post cycle therapy", and embrace the idea of "constant cycle therapy" – active therapy throughout a steroid cycle. The HPTA involves a constant biological interplay of responses and feedback loops that can ultimately become shutdown and degraded during exogenous hormone administration. However, research suggests suppression of the hypothalamus and pituitary may be preventable during steroid use. Before we delve into the details, lets first take a quick recap on the HTPA and how it responses to anabolic androgenic steroids.

HPTA – The basics
When the hypothalamus senses low hormone levels, it secretes gonandotropin releasing hormone (GnRH). This GnRH then travels a short distance to the nearby pituitary gland to stimulate gonadotrope receptors. These, in turn, secrete the gonadotrophins, luteinizing hormone (lh) and follicle stimulating hormone (FSH). These gonadotrophins travel all the way down to the testis, to activate their respective leydig and seritoli cells. LH initiates testosterone production via the leydig cell receptor (steroidogenesis), while FSH initiates sperm production via the sertoli cell receptor (spermatogenesis).

anabolic androgenic steroids’s inhibit hormone production just as endogenous hormones do. Testosterone interacts with the androgen receptor (AR) and estrogen interacts with the estrogen receptor (ER). When these hormones are in high concentration, they cause the hypothalamus to decrease its release of GnRH, which decreases LH and FSH production from the pituitary.1 This cuts off the signal to the testis and halts all hormone production. This process is a daily event for the rhythmic endocrine system. Spikes in LH & FSH are followed by spikes in testosterone, and spikes in testosterone result in a reduction of LH & FSH release until testosterone levels decline and LH & FSH is released again. The caveat with most steroids, is that hormone levels remain chronically high (24/7) and do not allow release of LH or FSH, thus leaving the pituitary and testis in a dormant state for as long as the steroids are administered.

While low-dose on-cycle HCG is a good protocol to mimic LH and keep the testis from atrophy, (to be covered in a future article) it does nothing to prevent pituitary atrophy. We forget that the pituitary is susceptible to the same degradation and atrophy as the testis. That is, when the GnRH secretion from the hypothalamus stops (during a steroid cycle), the pituitary reduces its number of GnRH receptors and becomes less and less responsive to GnRH stimulation as weeks pass.11 This is analogous to atrophy of the testis, during absence of an LH or FSH signal. On the same accord, both the pituitary and testis will decrease receptor concentration during over stimulation as well, as its been found from too much hCG use or too much GnRH stimulation.12,13 The point here, is that only minor stimulus is required for preservation of function and sensitivity. Perhaps a completely neglected and suppressed pituitary may explain the lack of full and prompt recovery for many steroid users, despite adherence to a "tried and true" hCG, Clomid + Nolvadex regimen. So the question is – How can we prevent suppression of the pituitary, and better yet, how can we prevent suppression of the hypothalamus?

A closer look –
In should be mentioned that another mechanism in which AAS inhibit LH and FSH release from the pituitary is by direct suppression upon the pituitary GnRH receptors and consequent quenching of LH & FSH secretion.35,38 However its appears that AAS which bind strictly to the AR, do not exert a direct negative effect on pituitary function or sensitivity.34,37,39 This agrees with the theory that non-aromatizing steroids such as Primobolan, Proviron or Masteron are not nearly as suppressive as an aromatizing AAS’s such as testosterone or Dianabol. Evidence suggests that estradiol is about 200x more suppressive than testosterone on a molar basis37, and that administration of Arimidex can greatly reduce testosterones suppression on GnRH and LH release.42 So, we know anti-estrogens can limit suppression of AAS, but this only solves half the problem.

When it comes to suppression of the hypothalamus, and what seems to be basic endocrinology, we find it is not so simple upon closer examination. There is more than a simple on-off switch for the hypothalamus control center, a lot more. Evidence suggests that there isn’t even a direct AR or ER action upon GnRH release.2-6 That is, steroid hormones do not directly influence GnRH release from the GnRH neurons.7

It was well summarized here by A.J Tilbrook et al,
"It follows, that the actions of testicular steroids on GnRH neurons must be mediated via neuronal systems that are responsive to steroids and influence the activity of GnRH neurons."

And again here by FJ Hayes et al
"It was thus postulated that estrogen-receptive neurons were acting as intermediaries in the non-genomic regulation of GnRH by estrogen"

There is a network of neurogenic intermediaries in the hypothalamus for GnRH release that communicate the inhibitory effects of steroid hormones. More specifically, it is the combined efforts of neuro-active peptides and catecholamines which send the message of "suppression" to the GnRH neurons once activated by steroid hormones.16 These primary messengers are known as a group of neuro-active peptides called endogenous opioid peptides (EOP’s).7,16 The EOP’s consist of the three main peptides -- b-endorphin, dynorphin, and enkephalins, which act upon their respective u-opioid, k-opioid, and s-opioid receptors. It appears that the most influential EOP in GnRH modulation is b-endorphin, acting upon the u-opioid receptor. 8-10 For this reason, b-endorphin will be the main focus of the article, although there are other intermediates involved.

When steroid hormones reach the hypophysial portal, they activate the EOP’s, which suppress GnRH. We know that steroid hormones must communicate with these opioid receptors in order for them to inhibit the release of GnRH from the GnRH neurons, since the GnRH neurons do not have AR or ER receptors. What’s most interesting here is that the suppression on GnRH neurons can actually be intercepted by a u-opioid receptor antagonist – such as naloxone, and the orally active congers naltrexone, and nalmefene.
This is accomplished by blocking the u-opioid receptor and preventing the inhibitory effects of b-endorphin upon the GnRH releasing neuron. It should be noted that this "antagonism" of suppression is not due to antagonism of the AR or ER itself, since u-opioid antagonists to not bind to these hormone receptors.15,32


Essentially, a u-opioid antagonist such as naloxone takes the brakes off of GnRH release and allows pulses of GnRH to occur as if no steroid hormones are present.17 Naloxone, and related u-opioid antagonists have consistently proven to block the suppressive effects of testosterone, dihydrotestosterone, and estrogen administration in both animals and humans.18-25 It also appears that these drugs have the ability to increase pituitary sensitivity to GnRH.26,27

U-opioid antagonists have long been used for treatment of opioid dependence; not only to control cravings of narcotics, but to restore a suppressed endocrine system.28,29 It’s well known that strong opioid based drugs such as methadone, blow, heroin and alcohol can suppress GnRH and therefore suppress LH & FSH. It seems that this decease of GnRH is due to the same EOP mechanisms seen with AAS induced suppression.33 In alcoholics, blow and heroin users, naltrexone and naloxone have been used to restore LH and testosterone levels.28,29 Naltrexone has even been proposed as a treatment for male impotence and erectile dysfunction.30,31

Naloxone, naltrexone and nalmefene seem progressively more powerful in their potency to dis-inhibit LH release, respectively14,18 Naloxone lacks oral bioavailability therefore injection is required. An injectable preparation could easily be made with BA water due to the water solubility of the compound. A 40mg subcutaneous injection would be a typical dose of naloxone. Naltrexone is orally active, with a safe and effective oral dose being about 100mg for a 220lb male.18 While a lower dose of about 25-50mg of nalmefene would seemingly have the same benefit.20,24 Increasing the dose with either of these drugs will surely increase the likelihood of side-effects without notably increasing the benefit. An every 3rd day protocol would seem appropriate with these drugs, as only to increase GnRH and LH release enough to prevent pituitary and testicular shrinkage – Just enough to keep them in the "ball game". Also, a twice a week dosing protocol would most likely limit the increased opioid sensitivity induced by the long-term use of the drugs.

A word of caution: The opioids antagonists mentioned in this article are recognized as safe and non-toxic at the given dosages, however they can cause severe withdrawal symptoms in opiate users (methadone, morphine, blow, and heroin addicts.) Caution is also advised when using opioid antagonists prior to sedation or surgery as they can reduce effectiveness of anesthetics. Temporary nausea, headache or fatigue, are occasional side-effects associated with the use of these drugs. Naltrexone has been reported to heighten liver enzymes, while naloxone and nalmefene do not appear to have this issue. At any rate, a twice a week protocol for 4-16 weeks is unlikely to cause any liver issues that may be associated with naltrexone.

A few point to consider -
For those who choose to embark on a every 3rd day protocol of an opioid antagonist several things should be considered. First, total prevention of HPTA suppression is unlikely in a cycle of 1gm or more per week of AAS. However, by following smart cycling guidelines, suppression will at least be minimized to the point where normal HPTA function could be regained within days of AAS clearance, rather than months. The protocol suggested in this article would at least allow steroid users to limit the usage of classic selective estrogen receptor modulator’s for PCT. Several things shall be considered when planning an AAS protocol designed to limit suppression.

It appears that progestin based AAS such as trenbolone and nandrolone which bind not only to the AR, but also to the progesterone receptor  also have a directly suppressive effect on pituitary sensitivity36 (similar to estrogens). It also appears that no opioid receptor antagonist or anti-aromatase can prevent suppression via the PR. Therefore, a multiple gram stack of testosterones and nandrolones is no doubtingly going to completely suppress HTPA function by causing suppression via the ER, AR and PR.40,41 If one hopes for a prompt and full recovery post cycle, perhaps nandrolones are better avoided, or at least not stacked with heavily aromatizing AAS without the concurrent use of a strong aromatase inhibitor.

As it was pointed out earlier in this article, estrogen has a markedly stronger effect on suppression of LH release compared to androgens since estrogens suppresses the hypothalamus and pituitary. Usage of an aromatase inhibitor such as anastrozole, letrozole, or exemestane (Aromasin) can reduce estrogen and greatly reduce suppression on GnRH, LH and FSH release by preventing excessive ER activation in the hypothalamus and desensitization of the pituitary gonadotropes. 35,37,38 Anastrozole has ~50% maximal total estrogen suppression at 1mg/day. Exemestane has ~50% maximal total estrogen suppression at 25mg/day. While letrozole has ~60% at 1mg/day. These are averages based on compiled data from several studies. Similar estrogen suppression can also been seen from only twice a week administration of these aromatase inhibitor’s.43-47



References
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2. Absence of androgen receptors in LHRH immunoreactive neurons. Huang X, Harlan RE. Brain Res 1993; 624:309–311
3. Augmented hypothalamic proopiomelanocortin gene expression with pubertal development in the male rat: evidence for an androgen receptor-independent action. Kerrigan JR, Martha PM, Krieg RJ, Queen TA, Monahan PE, Rogol AD. Endocrinology.128:1029-1035. (1991)
4. Distribution of estrogen receptorimmunoreactive cells in the preoptic area of the ewe: co-localisation with glutamic acid decarboxylase but not luteinizing hormone-releasing hormone. Herbison AE, Robinson JE, Skinner DC. Neuroendocrinology 1993; 57:751–759.
5. Unmasking the neural progesterone receptor in the preoptic area and hypothalamus of the ewe: no colocalization with gonadotropin-releasing neurons. Skinner DC, Caraty A, Allingham R. Endocrinology 2001; 142:573–579.
6. Multimodal influences of estrogen upon gonadotropin releasing hormone neurons. Herbison AE. Endocrine Reviews 1998; 19:302–330.
7. Negative Feedback Regulation of the Secretion and Actions of Gonadotropin-Releasing Hormone in Males. A.J. Tilbrook and I.J. Clarke. Biol Reprod, Mar 2001; 64: 735
8. Steroid Control of Gonadotropin-Releasing Hormone Secretion: Associated Changes in Pro-Opiomelanocortin and Preproenkephalin Messenger RNA Expression in the Ovine Hypothalamus
James A. Taylor, Marie-Laure Goubillon, Kevin D. Broad, and Jane E. Robinson. Biol Reprod, Mar 2007; 76: 524
9. Do gonadotropin-releasing hormone, tyrosine hydroxylase-, and ß-endorphin-immunoreactive neurons contain oestrogen receptors? A double-label immunocytochemical study in the Suffolk ewe. Lehman MN, Karsch FJ. Endocrinology 1993; 133:887–895
10. -Endorphin blocks luteinizing hormone-releasing hormone release by inhibiting the nitricoxidergic pathway controlling its release. Alicia G. Faletti, Claudio A. Mastronardi, Alejandro Lomniczi, Adriana Seilicovich, Martha Gimeno, Samuel M. McCann, and Valeria Rettori. PNAS, Feb 1999; 96: 1722.
11. The frequency of gonadotropin-releasing hormone stimulation determines the number of pituitary gonadotropin-releasing hormone receptors. Katt JA, Duncan JA, Herbon L, Barkan A, Marshall JC. Endocrinology. 116:2113–2115. (1985)
12. Exogenous gonadotrophin-releasing hormone (GnRH) stimulates LH secretion in male monkeys (Macaca fascicularis) treated chronically with high doses of a GnRH-antagonist. Weinbauer GF, Hankel P, Nieschlag E. J Endocrinol. 133:439–445. (1992)
13. Chronic administration of the luteinizing hormone-releasing hormone (LHRH) antagonist cetrorelix decreases gonadotrope responsiveness and pituitary LHRH receptor messenger ribonucleic acid levels in rats. Pinski J, Lamharzi N, Halmos G, et al. 1996. Endocrinology. 137:3430–3436.
14. Acute effects of testosterone infusion and naloxone on luteinizing hormone secretion in normal men.
GB Kletter, CM Foster, IZ Beitins, JC Marshall, and RP Kelch. J. Clin. Endocrinol. Metab., Nov 1992; 75: 1215 - 1219.
15. Naloxone-induced increases in serum luteinizing hormone in the male: mechanisms of action
TJ Cicero, CE Wilcox, RD Bell, and ER Meyer. J. Pharmacol. Exp. Ther., Mar 1980; 212: 573.
16. Endogenous opioids participate in the regulation of the hypothalamic-pituitary-luteinizing hormone axis and testosterone’s negative feedback control of luteinizing hormone. CICERO, T. J., SCHAINKER, B. A. AND MEYER, E. R. Endocrinology 104: 1286-1291, (1979)
17. Opiatergic control of LH secretion is eliminated by gonadectomy. BHANOT, R. AND WILKINSON, M.: Endocrinology 112: 399-401, (1983)
18. Role of endogenous opiates in the expression of negative feedback actions of androgens and estrogen on pulsatile properties of luteinizing-hormone secretion in man. Veldhuis JD, Rogol AD, Samojlik E, Ertel MH. J Clin Invest. 74:47–55 (1984)
19. Counteraction of gonadal steroid inhibition of luteinizing hormone release by naloxone. VAN VUGT, D. A., SYLVESTER, P. W., AYLSWOWRH, D. F. AND MNRRAS J. J. Chro- naloxone. Endocrinology 34: 274-278, 1982
20. Unexpected effects of nalmefene, a new opiate antagonist, on the hypothalamic-pituitary-gonadal axis in the male rat. P Limonta, CW Bardin, EF Hahn, and RB Thau. Steroids, Dec 1985; 46(6): 955-65.
21. In vivo evidence for a direct effect of naloxone on testicular steroidogenesis in the male rat. TJ Cicero, ML Adams, LH O'Connor, and B Nock. Endocrinology, Aug 1989; 125: 957
22. Endogenous opioids participate in the regulation of the hypothalamus- pituitary-luteinizing hormone axis and testosterone's negative feedback control of luteinizing hormone. TJ Cicero, BA Schainker, and ER Meyer. Endocrinology, May 1979; 104: 1286
23. Effect of naloxone on the plasma levels of LH, FSH, prolactin and testosterone in Beetal bucks.
Singh B, Dixit VD, Singh P, Georgie GC, Dixit VP. Department of Animal Production Physiology, CCS Haryana Agricultural University, 125004, Hisar, India
24. Endocrinology: The effect of nalmefene on pulsatile secretion of luteinizing hormone and prolactin in men. G.R. Graves, T.G. Kennedy, R.F. Weick, and R.F. Casper. Hum. Reprod., Oct 1993; 8: 1598 - 1603.
25. Effects of the novel opiate antagonist, SDZ 210-096, on luteinizing hormone secretion in the rat
RA Siegel and L Revesz. J. Pharmacol. Exp. Ther., Apr 1989; 249: 264.
26. Effect of antagonists of dopamine and opiates on the basal and GnRH-induced secretion of luteinizing hormone, follicle stimulating hormone and prolactin during lactational amenorrhoea in breastfeeding women. C.C.K. Tay, A.F. Glasier, and A.S. McNeilly. Hum. Reprod., Apr 1993; 8: 532 - 539.
27. Naltrexone administration modulates the neuroendocrine control of luteinizing hormone secretion in hypothalamic amenorrhoea. Alessandro D. Genazzani, Mario Gastaldi, Felice Petraglia, Cesare Battaglia, Nicola Surico, Annibale Volpe, and Andrea R. Genazzani. Hum. Reprod., Nov 1995; 10: 2868 - 2871.
Revives LH and testosterone in heroin users
28. Heroin and naltrexone effects on pituitary-gonadal hormones in man: interaction of steroid feedback effects, tolerance and supersensitivity. JH Mendelson, J Ellingboe, JC Kuehnle, and NK Mello. J. Pharmacol. Exp. Ther., Sep 1980; 214: 503.
29. Alcohol effects on luteinizing hormone and testosterone in male macaque monkeys. NK Mello, JH Mendelson, MP Bree, J Ellingboe, and AS Skupny. J. Pharmacol. Exp. Ther., Jun 1985; 233: 588.
Opioid antagonist enhances erectile function
30. Erectile function and naltrexone. Goldstein JA. Ann Intern Med 105:799 (1986)
31. Opiate antagonists in erectile dysfunction: a possible new treatment option? Results of a pilot study with naltrexone. van Ahlen H, Piechota HJ, Kias HJ, Brennemann W, Klingmuller D. Eur Urol 28:246–250 (1995)
32. The effects of opiates on androgen binding in the forebrain of the rat. PJ Sheridan and JM Buchanan
Int J Fertil, January 1, 1980; 25(1): 36-43. 33. Morphine exerts testosterone-like effects in the hypothalamus of the castrated male rat. CICERO, T. J., MEYER, E. R., GABRIEL, S. M., BELL, R. D. AND WILCOX, C. E. Brain Rae. 202: 151-164, (1980)
dihydrotestosterone and testosterone not suppressive to the pituitary like estrogens
34. Studies of gonadotropin-releasing hormone (GnRH) action using GnRH receptor-expressing pituitary cell lines. Kaiser UB, Conn PM, Chin WW. Endocr Rev. 18:46–70. (1997)
Estrogen decreases gonadotrope receptors for GrRH.
35. Patterns of LH secretion in castrated bulls during intravenous infusion of androgenic and estrogenic steroids: Pituitary response to exogenous luteinizing hormone-releasing hormone. M.J. D’occhio et al. Biology of reproduction 26, 249-257 (1982)
36. Demonstration of progesterone receptor mediated gonadotrophin suppression in men. Brady B, Anderson RA, Kinniburgh D, Baird DT 2002. J Endocrinol 3(Suppl):OC37
37. Bagatell CJ, Dahl KD, Bremner WJ. 1994 The direct pituitary effect of testosterone to inhibit gonadotropin secretion in men is partially mediated by aromatization to estradiol. J Androl. 15:15–21.
38. Sherins RJ, Loriaux DL. 1973 Studies on the role of sex steroids in the feedback control of FSH concentrations in men. J Clin Endocrinol Metab. 36:886–893
39. Santen RJ. 1975 Is aromatization of testosterone to estradiol required for inhibition of luteinizing hormone secretion in men? J Clin Invest. 56:1555–1563
40. Influence of nandrolondecanoate on the pituitary-gonadal axis in males. JW Bijlsma, SA Duursma, JH Thijssen, and O Huber. Acta Endocrinol (Copenh), September 1, 1982; 101(1): 108-12.
Both progestin (nandrolone) and testosterone more effective at reducing LH/FSH and causing azoospermia.
41. Endocrine approaches to male fertility control. UA Knuth and E Nieschlag; Baillieres Clin Endocrinol Metab, February 1, 1987; 1(1): 113-31.
42. Aromatization Mediates Testosterone's Short-Term Feedback Restraint of 24-Hour Endogenously Driven and Acute Exogenous Gonadotropin-Releasing Hormone-Stimulated Luteinizing Hormone and Follicle-Stimulating Hormone Secretion in Young Men. J. A. Schnorr, M. J. Bray, and J. D. Veldhuis
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43. Short-Term Aromatase-Enzyme Blockade Unmasks Impaired Feedback Adaptations in Luteinizing Hormone and Testosterone Secretion in Older Men; Johannes D. Veldhuis and Ali Iranmanesh
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44. Effects of Aromatase Inhibition in Elderly Men with Low or Borderline-Low Serum Testosterone Levels
Benjamin Z. Leder, Jacqueline L. Rohrer, Stephen D. Rubin, Jose Gallo, and Christopher Longcope
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45. Comparative Assessment in Young and Elderly Men of the Gonadotropin Response to Aromatase Inhibition. Guy G. T’Sjoen, Vito A. Giagulli, Hans Delva, Patricia Crabbe, Dirk De Bacquer, and Jean-Marc Kaufman. J. Clin. Endocrinol. Metab., Oct 2005; 90: 5717 - 5722.
46. Pharmacokinetics and Dose Finding of a Potent Aromatase Inhibitor, Aromasin (Exemestane), in Young Males. Nelly Mauras, John Lima, Deval Patel, Annie Rini, Enrico di Salle, Ambrose Kwok, and Barbara Lippe
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47. Differential Regulation of Gonadotropin Secretion by Testosterone in the Human Male: Absence of a Negative Feedback Effect of Testosterone on Follicle-Stimulating Hormone Secretion
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Title: Odg: Terapija poslije ciklusa - PCT
Post by: Nitrom on September 27, 2009, 12:45:08 AM
Mislim da je dovoljno,ko nije svatio poentu posle ovolikih textova bolje da se ni ne upusta u ovu materiju :P  :clap:

imas pm inace  :rolleyes01:
Title: Odg: Terapija poslije ciklusa - PCT
Post by: sele137 on October 22, 2009, 11:06:30 PM
MALE MEDICAL FERTILITY TREATMENT: HCG + PHARMACEUTICAL URINARY LH + FSH
TO INCREASE SPERM COUNT THROUGH SPERMATOGENESIS
 

National Medical Clinic, Inc. physicians provide a Male Medical Fertility Treatment consisting of the administration of Human Chorionic Gonadotropin (HCG), Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH) to increase male fertility (sperm count) or spermatogenesis in hypogonadotropic men when the pituitary gland is not secreting sufficient FSH, or is deficient in the production of both LH and FSH, such that spermatogenesis does not occur.

The purpose of HCG treatment with regard to male infertility is to increase spermatogenesis in hypogonadotropic men deficient in FSH, or is deficient in the production of both LH and FSH. The use of pharmaceutically manufactured gonadotropin LH combines with HCG to replace insufficient LH secretion by the pituitary. FSH is available mixed with LH in the form of Pergonal® or Menopur®, and other more purified forms of gonadotropins, as well as in a pure forms as recombinant FSH (Gonal F, Follistim). This treatment combines pharmacy compounded or manufactured HCG with pharmaceutically manufactured gonadotropin LH and FSH to induce spermatogenesis in hypogonadotropic men when the pituitary gland is not secreting sufficient LH, FSH or is deficient in the production of both LH and FSH such that spermatogenesis does not occur.

Hypogonadism is a medical term for a defect of the reproductive system that results in lack of function of the gonads (ovaries or testes). The gonads have two functions: to produce hormones (testosterone, estradiol, antimullerian hormone, progesterone, inhibin B), activin and to produce gametes (eggs or sperm). Deficiency of sex hormones can result in defective primary or secondary sexual development, or withdrawal effects (e.g., premature menopause) in adults. Defective egg or sperm development results in infertility.

Follicle-stimulating hormone (FSH) is a hormone synthesized and secreted by gonad tropes in the anterior pituitary gland. FSH regulates the development, growth, pubertal maturation, and reproductive processes of the human body. FSH and Luteinizing hormone (LH) act synergistically in reproduction. In males, FSH enhances the production of androgen-binding protein by the Sertoli cells of the testes, and is critical for spermatogenesis.

In males, FSH enhances the production of androgen-binding protein by the Sertoli cells of the testes, and is critical for spermatogenesis. FSH regulates the reproductive processes of the human body. Both LH (or HCG as a medication substitute for naturally produced LH) and FSH must be present for spermatogenesis.

Luteinizing hormone (LH) is a hormone produced by the anterior pituitary gland. LH is a glycoprotein. Each monomeric unit is a sugar-like protein molecule; two of these make the full, functional protein. Its structure is similar to the other glycoproteins, follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), and human chorionic gonadotropin (hCG). The protein dimer contains 2 polypeptide units, labeled alpha and beta subunits that are connected by two disulfide bridges:

In both males and females, LH is essential for reproduction. In the male, LH acts upon the Leydig cells of the testis and is responsible for the production of testosterone, an androgen that exerts both endocrine activity and intratesticular activity such as spermatogenesis.

The release of LH at the pituitary gland is controlled by pulses of gonadotropin-releasing hormone (GnRH) from the hypothalamus. Those pulses, in turn, are subject to the estrogen feedback from the gonads. LH levels are normally low in men during childhood. During the reproductive years typical male LH levels are between 5-20 mIU/ml. Physiologic high LH levels are seen during the LH surge. They typically they last 48 hours.

Persistently high LH levels are indicative of situations where the normal restricting feedback from the gonad is absent, leading to a higher pituitary production of both LH and FSH. High levels of LH and FSH in men may indicate gonadal dysgenesis, Turner Syndrome, castration testicular failure or CAH. Congenital adrenal hyperplasia (CAH) refers to any of several autosomal recessive diseases resulting from mutations of genes for enzymes mediating the biochemical steps of production of cortisol from cholesterol by the adrenal glands (steroidogenesis). Most of these conditions involve excessive or deficient production of sex steroids. Diminished secretion of LH can result in failure of gonadal function (hypogonadism), which is a medical condition that is typically manifested in males as failure in production of normal numbers of sperm.

LH is available mixed with FSH in the form of Pergonal or Menopur), and other forms of gonadotropins . More purified forms of gonadotropins may reduce the LH portion in relation to FSH. Recombinant LH is available as lutropin alfa (Luveris). All these medications have to be given parenterally. They are commonly in infertility therapy to stimulate follicular development, notably in IVF therapy. HCG medication is often used as a substitute for LH because it activates the same receptor. HCG medication is derived from urine of pregnant women, less costly, and has a longer half-life than LH.

Spermatogenesis is the process by which male spermatogonia develop into mature spermatozoa. Spermatozoa are the mature male gametes in many sexually reproducing organisms. Spermatogenesis produces mature male gametes, commonly called sperm but specifically known as spermatozoa, which are able to fertilize the counterpart female gamete, the oocyte, during conception to produce a single-celled individual known as a zygote. This is the cornerstone of sexual reproduction and involves the two gametes both contributing half the normal set of chromosomes (haploid) to result in a chromosomally normal (diploid) zygote.

Spermatogenesis takes place within several structures of the male reproductive system. The initial stages occur within the testes and progress to the epididymis where the developing gametes mature and are stored until ejaculation. The seminiferous tubules of the testes are the starting point for the process, where stem cells adjacent to the inner tubule wall divide in a centripetal direction-beginning at the walls and proceeding into the innermost part, or lumen-to produce immature sperm. Maturation occurs in the epididymis and involves the acquisition of a tail and hence motility.

Hormonal control of spermatogenesis varies among species. In humans the mechanism are not completely understood, however it is known that initiation of spermatogenesis occurs at puberty due to the interaction of the hypothalamus, pituitary gland and Leydig cells. If the pituitary gland is removed, spermatogenesis can still be initiated by follicle stimulating hormone and testosterone.

Follicle stimulating hormone (FSH) stimulates both the production of androgen binding protein by Sertoli cells, and the formation of the blood-testis barrier. Androgen binding protein is essential to concentrating testosterone in levels high enough to initiate and maintain spermatogenesis, which can be 20-50 times higher than the concentration found in blood. Follicle stimulating hormone (FSH) may initiate the sequestering of testosterone in the testes, but once developed only testosterone is required to maintain spermatogenesis. However, increasing the levels of follicle stimulating hormone will increase the production of spermatozoa by preventing the apoptosis of type A spermatogonia. The hormone inhibin acts to decrease the levels of follicle stimulating hormone.

The Sertoli cells themselves mediate parts of spermatogenesis though hormone production. They are capable of producing the hormones estradiol and inhibin. The Leydig cells are also capable of producing estradiol in addition to their main product testosterone.

In this male infertility treatment follicle stimulating hormone (FSH) is administered to treat male infertility by increasing the both the production of androgen binding protein by Sertoli cells, and the formation of the blood-testis barrier. After the androgen binding protein initiates the sequestering of testosterone in the testes and thereby causes testosterone concentration in levels high enough to initiate and maintain spermatogenesis, the LH and HCG stimulate the testes to increase the production of testosterone to maintain spermatogenesis. And spermatogenesis is the process of creating sperm. This treatment requires that a patient present with a insufficient levels of naturally produced LH or FSH or deficient in both LH and FSH. The gonadotropins FSH and LH in combination with HCG induces spermatogenesis in hypogonadotropic men.
This medical protocol does not include the administration of recombinant FSH to induce spermatogenesis. However, a medical treatment that includes the use of recombinant FSH may be indicated if the administration of the urinary FSH gonadotropin does not increase both the production of androgen binding protein by Sertoli cells, and the formation of the blood-testis barrier. The increase in testosterone production alone by LH or HCG is not sufficient to cause spermatogenesis in hypogonadotropic men. There must also be an FSH induced increase both the production of androgen binding protein by Sertoli cells, and the formation of the blood-testis barrier to increase the production of the androgen binding protein, which initiates the sequestering of testosterone in the testes and thereby causes testosterone concentration in levels high enough to initiate and maintain spermatogenesis. It is at this time that the increased production of testosterone resulting from the stimulation of the testes by administration of HCG and LH is essential to maintaining spermatogenesis

HCG is approved for use in cases of hypogonadotropic hypogonadism (hypogonadism secondary to a pituitary deficiency). It is used to stimulate the testes of men who are hypogonadal or lack sufficient testosterone production.

Diagnosis of Oligozoospermia

No single medical treatment has proven to be consistently reliable in increasing sperm count for patients diagnosed with Oligozoospermia or low sperm count. A diagnosis of Oligozoospermia is based on a symptom wherein a sample of semen contains less than 20 million spermozoa per ml of ejaculate.

Increasing Spermatogenesis in Hypogonadotropic Men

"Like urinary FSH, recombinant FSH in combination with HCG seems to induce spermatogenesis in hypogonadotropic men" See Drug Treatment of Male Fertility Disorders by Gerhard Haidl, et al. and specifically the discussion of HCG therapy therein. This article is located at URL: http://www.asiaandro.com/1008-682X/2/81.htm (Source: Wikipedia).

The Decline in Gonadal Stimulating Pituitary Hormone LH (Luteinizing hormone)

The natural decline in male testosterone production that occurs with aging is attributed to a decline in the gonadal stimulating pituitary hormone LH (Luteinizing hormone). As a result of the hypothalamus secreting less gonadoropin-releasing hormone (GhRH), which stimulates the pituitary gland to produce LH, the pituitary gland produces declining amounts of LH. This decrease in the pituitary secretion of LH reduces the stimulation of the gonads or male testes and results in declining testosterone and sperm production due to the decreased function of the gonads.

The decreased stimulation of the testes by the pituitary's diminished secretion of LH can also cause testicular atrophy. HCG stimulates the testis in the same manner as naturally produced. HCG Therapy is administered medically to increase male fertility by stimulating the testes to produce more sperm cells and thereby increase sperm count or Spermatogenesis.

How HCG Therapy Increases Plasma Testosterone Level in Hypogonadotropic Men

HCG therapy uses the body's own biochemical stimulating mechanisms to increase plasma testosterone level during HCG therapy. It is used to stimulate the testes of men who are hypogonadal or lack sufficient testosterone.

The male endocrine system is responsible for causing the testes to produce testosterone. The HPTA (hypothalamic-pituitary-testicular axis) regulates the level of testosterone in the bloodstream. and . The hypothalamus produces gonadotropin-releasing hormone (GnRH), which stimulates the pituitary gland to release Luteinizing hormone (LH).

LH released by the pituitary gland then travels from the pituitary via the blood stream to the testes where it triggers the production and release of testosterone. Without the continuing release of LH by the pituitary gland, the testes would shut down their production of testosterone, causing testicular atrophy and stopping natural testosterone produced by the testes.

As men age the volume of hypothalamus produced gonadotropin-releasing hormone (GnRH) declines and causes the pituitary gland to release less Luteinizing hormone (LH). The reduction if the volume of LH released by the Pituitary gland decreases the available LH in the blood stream to stimulate the testes to produce testosterone.

In males, HCG mimics LH and increases testosterone production in the testes. As such, HCG is administered to patients to increase endogenous (natural) testosterone production. The HCG medication administered combines with the patient's own naturally available LH released into the blood stream by the Pituitary gland and thereby increases the stimulation of the testes to produce more testosterone than that produced by the Pituitary released LH alone. The additional HCG added to the blood stream combined with the Pituitary gland's naturally produced LH triggers a greater volume of testosterone production by the testes, since HCG mimics LH and adds to the total stimulation of the testes.

In this treatment HCG is administered to men to promote an increase in sperm production (spermatogenesis) by the testes. HCG combined FSH or both LH and FSH is also used to increase male spermatogenesis and medically treat male infertility.



Title: Odg: Terapija poslije ciklusa - PCT
Post by: sele137 on January 27, 2010, 04:51:57 PM
PCT” What is it and Why do we need it


Veterans’ Consensus Statement on Post-Cycle Recovery©

Anabolic/androgenic steroids are used widely in human and veterinary medicine, and are increasingly useful to the training methods of elite athletes. Benefits of the intelligent use of anabolic/androgenic steroids include enhanced quality of life and the promise of greater longevity, as well as marked improvements in body composition, strength, and stamina. However, anabolic/androgenic steroids produce their benefits by interfering with the endocrine system, a complex system of glands and brain structures that are normally kept in an homeostatic state of balance by the action of countless subtle, sensitive feedback mechanisms. The perturbation in normal endocrine function that is introduced by the use of anabolic/androgenic steroids can, through these feedback mechanisms, elicit compensatory endocrine responses, such as up- or down-regulation of essential enzyme stores or of receptor molecules, in order to maintain homeostasis. When these compensatory mechanisms persist into the post-cycle era after steroids have been withdrawn, unwanted effects can occur, such as fatigue, depression, loss of sex drive, loss of size and strength, and others. Fortunately, both prophylactic and restorative measures that the athlete can take in this situation are now fairly well known.

Many athletes have agreed that androgenic/anabolic steroids render appreciable gains for a limited time only. As said gain period differs between individuals, this CS will refrain from any recommendations to the optimum time of such therapy but discuss methods of restoring optimum normal endocrine function.

It should be noted that the longer a cycle lasts past the eight-week mark, the harder testosterone recovery becomes. The best way of gauging ones hormonal milieu and planning compensatory measures is to have blood tests done prior to and following cessation of AAS therapy. For the purpose of this Consensus Statement and the awareness of a lack of testing athletes, the following universally accepted post cycle hormone status is assumed:

a) Luteinizing Hormone (LH): low to none, Luteinizing Hormone Releasing Hormone (LHRH): low to none
b) Testosterone (T): low
c) Estrogen (E): high in relation to T
d) Cortisol (C): high
e) Red Blood Cell (RBC) count: falling

While all of these hormone measurements are assumed on the low end of the scale, biochemical individuality will ultimately determine where a person’s levels fall. So assumption of low to substandard levels will not always be true in everyone.

1. What are the goals of testosterone recovery?

The return of hormonal balance is but one goal of this program. To create a transitional period of minimized muscle loss and sustained and/or increased motivation is another.

2. Detailed Recommendations
If the athlete is ready to come off and is still taking long acting esters he shall switch to short acting drugs in order to have complete control of exogenous hormone levels. A “waiting period” for esters to clear is unacceptable and provides for a slow slide into the post cycle catabolic state. This period of short acting supplements shall last for a minimum of 2 weeks.

a) Luteinizing Hormone and shrunken testicles

H C G
If the testis have atrophied, the introduction of H C G at 1000iu x 14 days is necessary. To prevent this atrophy from happening, the use of H C G at 500-1000iu x 4-7 days every 2-3 weeks of the AAS cycle is recommended. This will provide exogenous LH and must only be used to restore/keep proper testicle size.
Week 1-2: H C G, 500-1000iu ed

C l o m i d
The practice of using Clomid at 50mg throughout the AAS cycle or 100mg a day for 3-5 days every 4th week has been used successfully to maintain proper testicle size.

b) Low testosterone and lack of motivation

The introduction of exogenous hormones to compensate for the low endogenous testosterone levels may help to keep loss of drive, strength and muscle at bay but may also slow the recovery process. The below drug and application was chosen for its limited impact on the HPTA

D i a n a b o l
Studies and empirical evidence have shown Dianabol to be beneficial to keep Cortisol in check and provide some intermediate relief from the symptoms of low testosterone via an increase of dopamine, IGF-1, and Central Nervous System stimulation. The heightened dopamine will combat Prolactin and help raise the levels of endogenous Human Growth Hormone. Other studies point to a lack of LH suppression when taken first thing in the morning. It shall be noted that only a low dose upon rising is recommended in order to avoid further disruption of the HPTA
Week 1-6: 10mg dbol am, ed

c) High Estrogen and suppressed Hypothalamus- Pituitary- Testicular- Axis (HPTA)

Estrogen acts as the primary messenger of testosterone production. Testosterone is aromatized into estrogen, which signals the Hypothalamus to stop producing the proper testosterone release hormones. Estrogen must be kept low.

A r i m i d e x
A powerful aromatize inhibitor shall be part of every cycle. For testosterone recovery it is used to keep the testosterone/ estrogen balance in favor of testosterone. It is also of help to keep any additionally occurring estrogen from dbol and Androgel low to none. Studies have shown a 54% increase of testosterone in eugonadal patients
Week 1-10: ½-1mg ed
C l o m i d
Universally accepted as THE testosterone recovery tool. It blocks estrogen from the HPTA and stimulates the production of LHRH. LHRH then initiates the production of LH, which in turn signals the testis (if not atrophied) to produce testosterone.
Week 3-5: 100mg ed
Week 6-8: 50mg ed
N o l v a d e x
A volume of research and empirical evidence suggest the usefulness of this estrogen blocker for recovery. Its action is very similar to Clomid but may be better suited for individuals who experience side effects from Clomid.
Week 1-8: 20mg ed

d) High Cortisol, suppressed HPTA and catabolism

Cortisol is catabolic. It is the enemy of all anabolism and must be kept in check. While it is blocked when under the influence of AAS, it is free to attach to the Anabolic Receptors (AR) once the steroids leave. Due to this blockage Cortisol tends to accumulate and increase when on. A low level is desirable however since it is important for other vital functions such as control of inflammation. Balance is the key.

V i t a m i n C
At 3-5g before heavy workouts, it keeps the exercise induced rise of Cortisol in check
Always: 3-5g before workouts

D H E A
A useless pro-hormone as far as anabolism is concerned, this substance is great to keep Cortisol within normal levels. There is a correlation between high Cortisol and low DHEA levels.
Week 1-6: 150mg am and pm

H u m a l o g
It is well known that insulin possesses powerful anti Cortisol/anabolic properties, specially when used at times when Cortisol is high, such as early morning and post workout.
It is of utmost importance to be educated about insulin and its proper use. However, this CS defers to other available research material for more detailed recommendations and cautionary measures.
A minimum of 10g of dextrose/Maltodextrin per iu with a high carb/mixed glycemic index meal 45 min after insulin injection is suggested as a rough guide line for Humalog use only.
Perfect with dextrose/malto and Creatine.
Week 1-5: 10iu am and 10iu post workout
Caution: DO NOT EXCEED THESE RECOMMENDATIONS

D e x t r o s e a n d M a l to d e x t r i n
It is neither a supplement nor a drug, but these carbohydrates have a very high glycemic index and keep Cortisol levels low by increasing endogenous insulin or keep blood sugar normal when used with exogenous insulin. They also provide excellent energy for heavy workouts. In order to not gain unwanted fat, dextrose and/or maltodextrin shall be ingested during your workout and with your post workout shake only.
Always: 100g with workout water and 100g with post workout shake

e) Red Blood Cell Count and Stamina

E P O
Causes the bone marrow to increase red blood cell production and may have anabolic, fat burning and rejuvenating benefits.
It is of utmost importance to be educate about EPO and its proper use. However, this CS defers to other available research material for more detailed recommendations and cautionary measures.
Week 8: 500-1,000iu ed for 7-10 days
Caution: DO NOT EXCEED THESE RECOMMENDATIONS

C r e a t i n e
The use of Creatine has shown to increase ATP metabolism and cellular water storage among many other things. This is very beneficial because it provides for heightened nutrient storage and a slight increase in anabolism as well as workout stamina. Perfect with dextrose/maltodextrin/.
Always: 5g with workout water and 10g with post workout shake

V i t a m i n B - 1 2 & I r o n
Prolongs the life of your RBC and may be beneficial for increased oxygen transport
Week1-8: 1,000mcg ed

Miscellaneous beneficial drugs, supplements and recommendations

H G H
Administration of exogenous HGH has been shown to help maintain an anabolic environment until natural testosterone levels have reached a satisfactory level.
Week 1-8: 2iu at mid morning and 2iu at mid afternoon

Z i n c
Assists with testosterone production and is always low in weight lifting subjects. Do not consume with calcium for ease of absorption
Week1-8: 50mg ed

M a g n e s i u m
Has too many benefits for weight lifters to list
Week 1-8: 800mg every evening

V i t a m i n B - 6
Assists with testosterone production, keeps Prolactin in check and is very relaxing
Week 1-8: 200mg every evening

M e l a t o n i n
May improve sleep pattern and help increase HGH. With this supplement, the less you take the more it works.
Always: 1.5mg at nite

D e p r e n y l
Known as one of the most favorite life extension drug this dopamine enhancer provides anti-depressant properties as well as possible IGF-1 increase. Do not take with Bromocriptine.
Week 7 & 8: 5mg eod in the morning

E p h e d r a
Ephedrine HCL and related products such as Clenbuteral or Nor-ephedrine (NYC) may offer limited anti catabolic and workout stimulating benefits.
Use as preferred, but do not combine with insulin due to similarities of hypoglycemic and Eph induced over stimulation episodes

N o o t r o p i c s
A course of these "smart drugs" may be beneficial to improve blood flow to the brain and HP. No specific drug, combination of drugs and/or drug course recommendations shall be made due to varying individual preferrences

W o r k o u t a n d c a l o r i c r e s t r i c t i o n
Workouts shall be brief and focus on retaining your newly gained strength after a week long layoff. A power lift routine may be advantages at this stage. Calorie intake shall match expenditure; a calorie-restricted diet shall commence only upon complete recovery of natural testosterone production.

3. Final word

This program is based on empirical evidence, research and experimentation and represents the maximum effort to recover one’s testosterone production. Some of the above supplements and drugs may not be required or may not agree with every individual and advances in medicine may provide newer and more useful drugs for the testosterone recovery following steroid therapy.
Furthermore, it must be noted that a period of 8 weeks of abstinence from all drugs (vitamins and supplements excluded) is the minimum time recommended and that a blood test to assess actual testosterone recovery act as the only gauge for the timing of the next hormone therapy.

Anabolic/androgenic steroids wisely used have many benefits, but they produce their benefits by perturbing the natural course of endocrine function, something that can have consequences for the athlete in terms of enduring dysregulation of said endocrine function upon the cessation of anabolic use. Fortunately, both prophylactic and restorative measures that the athlete can take to restore endocrine function and prepare the way for the next cycle of anabolics are fairly well known.

Ovdje ima dosta stvari sa kojim se ne bi slozio kao sto je doziranje i vrijeme na nekim stvarima ili uopste uzimanje nekih stvari kao sto je Dianabol za vrijeme PCT-a ali tekst je relativno interesantan za pocetnika...ako neko zeli da rabi nesto od ovoga neka prvo pita za doziranje i sl!!!
Title: Odg: Terapija poslije ciklusa - PCT
Post by: zzz on January 27, 2010, 05:17:57 PM
vitamin c 3-5g pre treninga?
Title: Odg: Terapija poslije ciklusa - PCT
Post by: sele137 on January 27, 2010, 09:55:22 PM
vitamin c 3-5g pre treninga?

Ja bi to podjelio na ujutro, prije treninga!!!
Title: Odg: Terapija poslije ciklusa - PCT
Post by: sele137 on January 27, 2010, 09:58:30 PM
CORTISOL BY CHRIS ACETO

Learning to control this muscle-eroding hormone will increase your muscle mass

Do you feel sore, tired, irritable or weak? Have you noticed that your gains have plateaued? These could be signs that your cortisol levels are out of whack.
Cortisol is a stress hormone that’s truly the antithesis of testosterone: whereas testosterone supports muscle building, excess cortisol kills it. Besides tearing down muscle tissue and preventing the body from storing carbs as muscle glycogen, cortisol actually lowers testosterone. It also interferes with testosterone’s ability to bind to its receptors within muscle cells and induce an anabolic effect. When testosterone levels drop, not only does it become harder to build muscle and recover, but oestrogen tends to have a stronger effect in the body. Oestrogen is correlated with water retention, and it also makes shedding bodyfat a lot more difficult.

Cortisol levels can be elevated for a variety of reasons — training itself can induce this rise. It’s important that bodybuilders learn how to control their cortisol levels to keep making the best gains. If you suffer from the symptoms mentioned earlier, institute the following suggestions to help get your cortisol levels under control.

1. Stay on top of your workout nutrition As mentioned, cortisol rises when you train — it’s a natural reaction. One of the best ways to avoid excessively elevated cortisol levels is to be disciplined with your postworkout nutrition. By supplying your body with exactly what it needs as soon as the work-out is done, you’ll jump-start your recovery and help blunt cortisol spikes.
After your workout, take in 30-50 grams (g) of whey Protein with 60 to 100 g of carbs. Maltodextrin is easy, but you can take in other fast-digesting carbs such as rice cakes, white bread or cold cereal. You can also add 5 g of branched-chain amino acids (BCAAs) to the mix, or take them before you work out — BCAAs before exercise help maintain testosterone levels and can be used to fuel muscles. Leucine, one of the BCAAs, also spikes insulin levels through a different mechanism than carbs, and insulin helps in the suppression of cortisol. Whey provides building blocks that help prevent catabolism — muscle breakdown — and preventing catabolism is directly related to lower cortisol levels. Finally, the carbs in this combo spike insulin to further offset Protein breakdown.

2. Control your workouts Training volume can have a direct impact on cortisol levels. If you’re overtraining, you’re taking your body past the point where you can make the best gains. Follow these rules to make the most of your muscle-building regime.
• Limit weight training to four sessions per week. Training more frequently prevents the body from attaining a full recovery.
• Keep sessions to about an hour. When you perform too many sets and exercises in a given session, you can break down your muscle tissue too much. Limiting the length of your training sessions helps avoid this.
• Emphasise multijoint movements. Exercises such as squats, deadlifts and bench presses are the most effective at stimulating muscle growth while helping to limit total training volume. They also best stimulate growth hormone (gh) and testosterone, which can help blunt cortisol.
• Avoid excessive pumping and finishing movements. When you perform numerous sets and reps of these types of exercises, you can raise your cortisol levels too high without stimulating as much muscle growth. Try to keep pumping and finishing movements to no more than three sets per bodypart at the end of the workout.

3. Be careful with your cardio If cardio exercise burned only bodyfat, then you could hop on a bike and cycle your way into the record books as the most ripped human ever. The problem is, though, that prolonged and excessive cardio causes an increase in cortisol, and this situation can begin to prioritise muscle tissue as an energy source, tearing it down instead of helping to build it.NO FUCKING CARDIO IN PCT  :nonono:


4. Eat six meals a day The benefits of eating multiple meals per day are numerous. Besides allowing you to stay lean, a diet strategy of smaller and more frequent meals has been shown to keep cortisol levels lower than less-frequent feedings. Multiple meals — at any calorie level — will result in greater cortisol control than less-frequent meals, and we know keeping cortisol in check yields less fat, more muscle, better recovery and more energy. Strive to take in six meals per day throughout all phases of your training programme.

5. Take vitamin C This water-soluble vitamin cushions the negative effects of free radicals, compounds that are released with training. Free radicals target tissues such as muscles, weakening them and increasing inflammation and breakdown. When this happens, cortisol levels spike. By providing your body with antioxidants, such as vitamin C, you can help control cortisol. One study showed that a daily dose of 1,000 milligrams (mg) helped weightlifters keep cortisol under control.

6. Supplement with vitamin E This fat-soluble vitamin offers many versatile benefits. Primarily, vitamin E helps combat the oxi-dative stress of training and dieting. Like vitamin C, vitamin E is also helpful at combating free radicals. Large amounts of vitamin E have been shown to decrease creatine kinase activity, a marker for muscle-fibre injury. That’s what happens when you train. It’s the irony of trying to get big: you tear down your muscles to rebuild them and make them grow bigger. Taking 800 international units of vitamin E daily may help to prevent severe breakdown, which, in theory, should allow you to recover more quickly from your training.

7. Try phosphatidylserine Phosphatidylserine (PS) is a phospholipid, a quasi fat that is derived from soya beans. PS has been shown to help control cortisol levels. When you take 800 mg immediately after training, it saves muscles by blunting the total amount of cortisol released by your body. In theory, you can train like a madman and rapidly recover if you follow up the hard training with this anticortisol supplement. Another benefit is that when you keep cortisol levels under control, it’s easier for your muscles to “carb up”. With escalating cortisol levels, muscles experience a downgrade in their ability to take up carbs and deposit them as stored muscle glycogen.

8. Eat (or supplement with) garlic This bulbous flavourful herb common to Asian, Mediterranean and Middle Eastern cooking has a long-deserved retion as a health food. Recent research has shown that garlic along with a high-casein diet altered the body’s hormonal status, yielding lower levels of stress hormones such as cortisol. Other studies have shown that garlic may help increase testosterone levels. In general, the higher your testosterone levels, the lower your cortisol levels. So supplement with garlic powder — 450 mg twice daily with meals — or with a garlic supplement that provides about 4 mg of allicin with casein Protein shakes. This may help keep cortisol to a minimum.

9. Get your glutamine You knew it had to show up here, right? Recent studies have pooh-poohed glutamine’s beneficial effects on cortisol levels, but I disagree. There are many other studies that take a pro-glutamine view in muscle building. Glutamine works to spare BCAAs, and keeping BCAAs high helps keep cortisol levels from rising. In addition, glutamine pushes water into muscles, and hydrated muscles remain anabolic. Several studies show that supplemental glutamine can help keep cortisol levels in check.
Glutamine can help suppress the amount of cortisol circulating in blood. Glutamine also increases gh levels, combating cortisol’s catabolic effects. For a beneficial effect on cortisol levels, athletes may need a lot more glutamine than amounts that are often suggested. I recommend taking 5 to 10 g before and another 5 to 10 g after training to help reduce cortisol levels.

10. Add arginine to your supplement regime Arginine is now touted as a nitric oxide inducer; yet, it remains an effective gh releaser. Arginine may also have effects on cortisol levels. When gh levels rise, which naturally occurs with sleep, cortisol levels fall. As you get older, the sleep-induced gh boost just isn’t what it used to be, which allows cortisol levels to rise. Rising cortisol makes it harder for your body to grow, to hold mass and to get lean. Take 9 to 12 g of arginine before bed without carbs to increase gh levels and to blunt cortisol.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: sele137 on January 27, 2010, 10:18:38 PM
Regular bloodwork being done by the AS using bodybuilder is an indispensable part of our routine.

It is not wise to leave these type of things to chance and just hoping that "everything will return to normal for me". Even if you continue to cycle after seeing some problem areas in your bloodtest results, you will at least be able to work on clearing these up before you do so.

Also, as I have mentioned before, High Cholesterol can be the silent killer that catches up with us later when we don't keep an eye on it. Most guys worry a lot about their nads coming back, or proper testosterone levels, or even their sperm count if they want children someday.

We don't see nearly as much concern for our cholesterol levels though.

Below is a brief discussion of the components of a blood profile and what the indicators reveal in terms of bodily functions.

Such information may help you to see at a glance what is going on in your body when you get a copy of your results. At the least you will be able to more intelligently discuss your situation with your doctor.

I am not a Physician but this information is generic in nature regarding the functions of the liver and kidneys as seen in bloodwork profiles.

It is not meant to be used for self-diagnosis and is only for personal interest.

Too many factors come in to play with bodybuilding to attribute elevated levels to impaired function of a particular organ without precise and qualified investigation by a Physician

> Blood Glucose

Steroids can change our sensitivity to insuline and especially certain ones such as Human Growth Hormone, the direct use of Insuline, as well as others. Checking this level will help monitor your insuline sensitivity.

> Blood Urea Nitrogen (BUN)

This reading will help a physician to determine the function of the kidneys in terms of urea filtration in the kidneys. Steroids have the potential of damaging the filtration system of your kidneys.

> Creatinine

This again checks the function of the kidney's by way of its ability to clear the by-product creatinine from the system. These levels could also be high due to creatine usage as the by-product of creatine usage is creatinine. It is important to have a doctor who you trust and whom you can reveal all the particulars to.

> BUN/Creatinine Ratio


Again, this is a predictor of kidney problems whether they be temporary or permanent.

> Total Protein

Blood excesses MAY indicate kidney damage. It is important to note that in some of these areas of indicators bodybuilders may have levels that are higher in a transient way rather than a permanent way. Also, whenever I have used creatine, my levels of creatinine were higher but their was no indication otherwise of kidney damage. It was just a by- product of the creatine usage. This is one reason that I advocate that bodybuilders use Physicians that are familiar with Sports Medicine and the various peculiarities that go with supplementation but which may only be fleeting changes in blood chemistry.

> Albumin

Can indicate Kidney damage.

> Globulin

Again can indicate the possibility of Kidney damage.

> Albumin/Globulin Ratio

Aspects pertinent to kidney function.

> Total Bilirubin


Liver damage is sometimes indicated by high levels of bilirubin.

> Alkaline Phosphatase

High levels of this can be a marker for liver damage.

> GGTP  

This is the most reliable and specific marker for liver damage and can be stubborn in bringing down if total recovery is even possible. In some cases such as chemical induced hepatitis and other instances of damage it may remain elevated indefinitely. The liver is a very resilient organ but it does have its limitations.

> AST(SGOT)

A marker for muscle/liver damage.

> ALT(SGPT)

Also a marker for liver damage.

> LDH

An indicator for muscle/liver/coronary problems. I keep a close eye on this one as I think that it is more indicative of real problems than the changing nature of my cholesterol levels which are only temporary.

> Cholesterol


This helps your doctor to decide if you are in the realm of coronary risk. The elevation of cholesterol even if temporary is a pretty inescapable aspect of AS usage. I eat very clean with respect to saturated fats at all times. Also, I do a lot of cardio off cycle and on cycle, unless gains are crucial. Additionally, I use a niacin supplement, guggul, and Chinese rice yeast to spike my healthy cholesterol which in turn "fights" the unhealthy cholesterol.

> HDL and LDL Cholesterol Levels

It is important to have a proper balance of these two. The HDL(good cholesterol) helps keep the LDL in balance but the HDL is often driven down with AS usage. HDL less than 35 is not good and can have serious implications in terms of health consequences.

> Cholesterol/High Density Lipoprotein (HDL)

The HDL level is looked at here to assess the risk of coronary artery damage in conjunction with any other relevant findings that would confirm that.

> Triglycerides

If these levels are high it could also be an indicator of coronary damage. Other factors such as high sugar consumption and alcohol could also be the culprit.

> Total Testosterone

Helps to assess the function of our natural testosterone production and depending on how long one has been off the cycle it may indicate whether your levels are functioning normally again or not. Long term usage without proper cycling or long durations of excessively high dosages of AS can permanently alter these levels in a negative way.

> Cortisol

Much can be said about how cortisol levels change in the athlete as he/she trains, but generically these levels are watched to look for adrenal problems or to indicate over- training.

Again remember that diet, heavy training and subsequent muscle breakdown, deep tissue massage, prolonged levels of mental stress, overtraining, creatine usage, recent antibiotic usage, tylenol, and other factors can also temporarily alter blood levels of various these indicators.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: sele137 on February 13, 2010, 09:31:07 PM
Changes in the Endocrinological Milieu After Clomiphene Citrate Treatment for Oligozoospermia: The Clinical Significance of the Estradiol/Testosterone Ratio as a Prognostic Value

NAOKI ITOH, TAUI TSUKAMOTO, AKIHITO NANBU, HITOSHI TACHIKI, TOSHIKAZU NITTA,
KEIGO AKAGASHI, HIROSHI MARUTA, AND YOSHIAKI KUMAMOTO

From the Department of Urology, School of Medicine, SapporoMedicalUniversity, Sapporo, Japan.

 ABSTRACT:

We have already reported that the rate of increase in the estradiol/testosterone ratio (E2/T ratio) following human chononic gonadotropin (hCG) injection has prognostic value in the treatment of oligozoospermia. It was found that the rate of Increase in the E2/T ratio was statistically greater in the therapeutically ineffective cases compared to the therapeutically effective cases. The present study was planned in order to elucidate the relationship between the changes in the endocrinological milieu, especially the change in the E2/T ratio, and the therapeutic efficacy when clomiphene citrate was administered. Thirty-eight oligozoospermlc patients were administered 25mg of clomiphene citrate daily for 3 months. Sixteen of the 38(42.1%) cases showed improvement of more than 10 x 1 0/ml in sperm concentration. The rate of increase in the E2/T ratio of the effective cases (0.90 ± 0.43) during the administration of clomiphene citrate was statistically (P = 0.02) lower than that of the ineffective cases (1.44 ± 0.80). The rate of increase in the E2/T ratio during clomiphene citrate treatment showed a statistically positive correlation (r= 0.542) with the rate of increase following hCG injection performed before clomiphene citrate treatment. The rate of increase in follicle-stimulating hormone (FSH) in the Ineffective cases (2.16 ± 1.01) was statistically higher than in the effective cases (1.50 ± 0.43). The rate of increase in insulin-like growth factor-i (IGF-1) in the seminal plasma that was secreted by Sertoli cells was statistically higher in the effective cases (1.98 ± 1.23) than in the ineffective cases (1.19 ± 0.45). Based on these results, it is surmised that the relatively increased E2 level during clomiphene citrate treatment suppressed Sertoli cell function, and the serum FSH was elevated as a result. We concluded that the rate of increase in the E2/T ratio during clomiphene citrate treatment has prognostic value, and performing the hCG test before this treatment may be helpful in predicting the endocrinological milieu after It. If the rate of increase In the E2/T ratio following hCG injection Is high, treatment should consist of a combination of clomiphene citrate and an aromatase inhibitor to decrease the E2/T ratio.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: sele137 on April 11, 2010, 10:38:59 AM
Injecting HCG - Intramuscularly or Subcutaneously?

Q: I have heard some people say to inject HCG intramuscularly and some say subcutaneously. Which one is it?

A: One should always inject hCG subcutaneously. The simplest reason is the comfort of the injection; less trauma to tissues; and decreased risk of infection. SC v IM are equally effective. As far as the kinetics of the injections one would expect them to be fairly similar. the reason why testosterone preparations last a longer time is due to the depot (oil) in which they are injected. hCG is soluble in water and will therefore be absorbed quickly. Other considerations are the weight of the individual. There are clinical indicators to monitor while taking hCG. If the hCG is being used for HPTA normalization a serum testosterone ashould be obtained while taking hCG and not after. this is critical and important for successful HPTA normalization.

Weissman, A., S. Lurie, et al. (1996). "Human chorionic gonadotropin: pharmacokinetics of subcutaneous administration." Gynecol Endocrinol 10(4): 273-6.

The objective of the present study was to evaluate the pharmacokinetics of human chorionic gonadotropin (hCG) following different regimens of subcutaneous and intramuscular single-dose administration. Two hypogonadotropic hypogonadal volunteers received hCG injections without prior ovarian stimulation. The regimens included a single dose of 10,000 IU hCG either subcutaneously or intramuscularly, or 5000 IU hCG intramuscularly. Serum beta-hCG concentrations were measured periodically up to 13 days after hCG administration. Each of the three regimens exhibit a similar pharmacokinetic profile and the highest serum beta-hCG concentrations were achieved with a dose of 10,000 IU administered subcutaneously. Seven days after hCG administration beta-hCG was detectable only after subcutaneous or intramuscular administration of 10,000 IU, but not after a single intramuscular injection of 5000 IU. From the preliminary results of the study it is suggested that a single intramuscular dose of 5000 IU hCG might be sufficient to trigger ovulation, but for luteal-phase support a higher dose may be needed. Subcutaneous administration of hCG for the induction of ovulation or luteal-phase support in gonadotropin-induced cycles is feasible and might offer a better tolerance and cost-effectiveness of infertility treatments, leading to their further simplification.

Trinchard-Lugan, I., A. Khan, et al. (2002). "Pharmacokinetics and pharmacodynamics of recombinant human chorionic gonadotrophin in healthy male and female volunteers." Reprod Biomed Online 4(2): 106-15.

The pharmacokinetics and pharmacodynamics of recombinant human chorionic gonadotrophin (rHCG) were investigated in three studies of healthy volunteers. After single intravenous doses of 25, 250 and 1000 microg, rHCG and urinary HCG (uHCG) showed linear pharmacokinetics described by a bi-exponential model, although the area under the curve (AUC) for uHCG was ~29% lower than for rHCG. After intramuscular or subcutaneous administration (absolute bioavailability, 40-50% for both), rHCG pharmacokinetics could be described by a first-order absorption, one-compartment model. During multiple subcutaneous dosing, the amount of HCG increased by approximately1.7-fold. A comparison of liquid and freeze-dried rHCG and freeze-dried uHCG showed pharmacokinetic bioequivalence. In down-regulated male subjects, single doses of 125 microg rHCG, given intravenously, intramuscularly or subcutaneously, produced comparable increases in serum testosterone, inhibin and 17beta-oestradiol, with little further increase during repeated subcutaneous administration (in female subjects, this produced a sustained comparable increase in serum androstenedione and testosterone concentrations). In conclusion, the pharmacokinetics and pharmacodynamics of rHCG are similar to those of uHCG and are not affected by the use of different formulations. In healthy subjects, rHCG produces pharmacodynamic responses consistent with HCG physiology and is suitable for use in the same clinical indications as uHCG. The secured source and high purity of rHCG may offer important advantages.

Burgues, S. and M. D. Calderon (1997). "Subcutaneous self-administration of highly purified follicle stimulating hormone and human chorionic gonadotrophin for the treatment of male hypogonadotrophic hypogonadism. Spanish Collaborative Group on Male Hypogonadotropic Hypogonadism." Hum Reprod 12(5): 980-6.

The efficacy and safety of highly purified follicle stimulating hormone (FSH) associated with human chorionic gonadotrophin (HCG) was studied in 60 men with hypogonadotrophic hypogonadism. Of these men, 16 suffered from Kallmann's syndrome, 19 from idiopathic hypogonadotrophic hypogonadism and 25 from hypopituitarism. Basal testosterone concentrations were found to be far below the normal range. At baseline, 26 patients were able to ejaculate and all of them showed azoospermia, while the remaining patients were aspermic. All patients self-administered s.c. injections of FSH (150 IU x three/week) and HCG (2500 IU x two/week) for at least 6 months and underwent periodic assessments of testicular function. Testosterone concentrations increased rapidly during treatment and all but one patient reached normal values. Testicular volume showed a sustained increase reaching almost 3-fold its baseline value. At the end of treatment, 48 patients (80.0%) had achieved a positive sperm count. The maximum sperm concentration during treatment was 24.5 +/- 8.1 x 10(6)/ml (mean +/- SEM). The median time to induce spermatogenesis was 5 months. Eleven patients reported adverse events, generally not related to treatment. Three patients experienced gynaecomastia. No local reactions at injection site were observed. In conclusion, the s.c. self-administration of highly purified FSH + HCG was well tolerated and effective in stimulating spermatogenesis and steroidogenesis in these patients.

Jones, T. H., J. F. Darne, et al. (1994). "Diurnal rhythm of testosterone induced by human chorionic gonadotrophin (hCG) therapy in isolated hypogonadotrophic hypogonadism: a comparison between subcutaneous and intramuscular hCG administration." Eur J Endocrinol 131(2): 173-8.

When human chorionic gonadotrophin (hCG) is used to stimulate testosterone synthesis and release in males with hypogonadotrophic hypogonadism, it is administered two or three times weekly by intramuscular injection. We have compared the pharmacokinetics of a twice weekly standard dose of hCG (5000 U) given for the first week by intramuscular injection and in the second week by self-administered subcutaneous injection. The patients studied had Kallmann's syndrome, isolated idiopathic hypogonadotrophic hypogonadism or post-traumatic isolated hypogonadotrophic hypogonadism. Salivary testosterone was collected twice daily at 08.00 h and 20.00 h, and serum testosterone was collected after 0, 24 h, 72 h, 120 h and 168 h each week. The cumulated serum and salivary testosterone levels were comparable on both intramuscular and subcutaneous hCG. In normal males there is diurnal variation in testosterone, with peak serum levels in the morning falling to a nadir in the evening. The exact nature and controlling factors of this circadian rhythm have not been established. In four of the subjects, the twice weekly hCG injections, either subcutaneous or intramuscular, produced a regular testosterone diurnal rhythm. The other four patients had fluctuations in testosterone but with no strict diurnal pattern. This study provides evidence that the luteinizing hormone-like action of hCG is necessary to prime the circadian rhythm but only a single bolus of hCG is sufficient to induce the rhythm in the absence of endogenous gonadotrophin production. In conclusion, self-administered subcutaneous hCG is safe and produces comparable levels of serum and salivary testosterone to that administered by the intramuscular route. Moreover, it was very well accepted by the patients and was preferred to conventional treatments. Human hCG in some patients with hypogonadotrophic hypogonadism produces normal physiological changes in daily testosterone levels.

Saal, W., H. J. Glowania, et al. (1991). "Pharmacodynamics and pharmacokinetics after subcutaneous and intramuscular injection of human chorionic gonadotropin." Fertil Steril 56(2): 225-9.

OBJECTIVE: The pharmacokinetics and efficiency of human chorionic gonadotropin (hCG) after subcutaneous (SC) injection was to clarify in comparison with the intramuscular (IM) mode of administration.

DESIGN: In a prospective study, the pharmacokinetics of hCG and the response of serum testosterone (T), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) after an IM and SC injection of 5,000 IU hCG were evaluated up to 144 hours in two randomized groups.

SETTING: The study was carried out in a clinical dermatology department providing tertiary care.

PARTICIPANTS: Twenty-four healthy male volunteers with a mean age of 22.7 +/- 4.3 years were divided into two groups.

INTERVENTIONS: Human chorionic gonadotropin (5,000 IU) was injected IM or SC.

MAIN OUTCOME MEASURE: Serum concentration of /b-hCG, T, LH, and FSH were evaluated after IM and SC administration of hCG. Differences between the two groups were determined by t-test.

RESULTS: Compared with IM administration of hCG, peak serum drug concentration was significantly delayed (P = 0.01) and serum half-life was prolonged (P = 0.01) after SC injection; however, T, LH, and FSH responses were identical.

CONCLUSIONS: Subcutaneous application of 5,000 IU hCG is as effective as IM administration in terms of steroidogenesis.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Lazic on April 11, 2010, 10:45:20 AM
spas  :clap:
Title: Odg: Terapija poslije ciklusa - PCT
Post by: @Bestia@ on October 02, 2010, 06:53:32 PM
zanima me da li se sa tribulusom krece odmah sutradan po davanju zadnje injekcije ili se saceka nedelju dana da istekne polu-zivot,a naisao sam i na podatak da se posle 2 nedelje od davanja zadnje injekcije enanthata krece sa tribulusom ??
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Lazic on October 02, 2010, 10:23:01 PM
zanima me da li se sa tribulusom krece odmah sutradan po davanju zadnje injekcije ili se saceka nedelju dana da istekne polu-zivot,a naisao sam i na podatak da se posle 2 nedelje od davanja zadnje injekcije enanthata krece sa tribulusom ??
ova druga solucija je bolja
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Pedja Petrovic on October 03, 2010, 05:51:24 PM
pa zar nisi to isto pitao kod mene na forumu i dobio odgovr? :dunno: :dunno:
Title: Odg: Terapija poslije ciklusa - PCT
Post by: BUKAS on October 03, 2010, 06:27:36 PM
To isto pitanje je pitao pre par meseci na trecem  forumu  i dobio isti odgovor
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Pedja Petrovic on October 03, 2010, 06:32:14 PM
 :boxed: :boxed:
Title: Odg: Terapija poslije ciklusa - PCT
Post by: aragorn on October 03, 2010, 06:55:47 PM
To isto pitanje je pitao pre par meseci na trecem  forumu  i dobio isti odgovor

Nikad nije dosta potvrda,a pogotovo kad je u pitanju tako opasna supstanca kao sto je tribulus... :lol:

Ko zna sta moze da mu se desi ako promasi sedmicu...mozda mu izraste jos jedan... :lol:
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Milan on October 03, 2010, 07:08:00 PM
Quote
mozda mu izraste jos jedan

nece znati jel od puberteta ili tribulusa  :evillaugh:
Title: Odg: Terapija poslije ciklusa - PCT
Post by: aragorn on October 03, 2010, 07:10:51 PM
nece znati jel od puberteta ili tribulusa  :evillaugh:

 :lol: :lol: :lol:
Title: Odg: Terapija poslije ciklusa - PCT
Post by: BUKAS on October 03, 2010, 07:20:17 PM
ahahhahaha da da inace decko ima 16 god
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Nitrom on October 30, 2012, 06:43:35 PM
Teoretsko pitanje...

gledajuci sve topice i dalje mi nije jasno preklapanje nolvadexa+ clomida u PCTU i njihova doza po danima

pa imam par pitanja


uzimajuci npr enanthat ,2 nedelje posle zadnjeg shota nema koriscenja nicega..tek nakon 14 dana krece nolva i clomid?

e sada koliko vidim sele preporucuje oko 4 nedelje pct-a....clomid ide ED ili EOD ?
nolva ide ED ?

Neko preporucuje vise jednog neko vise drugog..neko samo nolvu jer clomid izaziva neke psihoticne situacije?...

sta je najbolje od ta 2 i kako se dozira po DANU kroz 4 ned?  ...tj dali je x/x/x/x format u stvari dnevna doza po nedelji? ili su to dani u okviru jedne ned

cela prica mi je malo zbrkana....lewellyn je napisao power pct program ali tu postoji koriscenje HCG-a tako da ovde njega izuzmemo i pricamo samo o pctu sa nolvom i clomidom... misljenja i neki linkovi?
hvala  ;)
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Becks on October 30, 2012, 06:49:44 PM
Iskreno, ako je kura solo test, nema nikakve potrebe za clomidom i nolvom, bukvalno nista da ne uzmes oporavices se brzo. Ako hoces da potpomognes onda je dovoljan DAA ili ako si pri parama neki bolji test booster, ali nema potrebe.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Nitrom on October 30, 2012, 07:15:21 PM
ma nije bitan steroid,hajde da uzmemo da je bilo kakav dug estar,koji ostaje u krvi duze nego inace,i da je potreban oporavak..kakva bi shema isla

tj x/x/x/x  predstavlja dnevnu dozu po nedeljama 4 ned ?right
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Becks on October 30, 2012, 07:19:51 PM
ma nije bitan steroid,hajde da uzmemo da je bilo kakav dug estar,koji ostaje u krvi duze nego inace,i da je potreban oporavak..kakva bi shema isla

tj x/x/x/x  predstavlja dnevnu dozu po nedeljama 4 ned ?right

Tesko je dati genericki odgovor. U vecini slucajeva nema potrebe za clomidom i nolvom, a ja bih pre isao letrozol nego nolvu. I radio bih pct jedino posle neke kure od 30+ nedelja a koja je ukljucivala boga i oca. U stvari onaj ko i radi takve kure obicno radi cruise 4-8 nedelja pa ponovo na kuru, tako da pct ni ne postoji  :lol:
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Nitrom on October 30, 2012, 08:34:58 PM
ok ali dali znas koje se doze koriste i po kojoj shemi


ono zasto sve ovo pitam je nesto sto me interesuje zbog slucaja: neko je na kuri zbog navale gino morao da koristi nolvu during cycle..a sad treba i MORA da uradi pct..sta se desava sa nolvom tih 2 nedelje od zadnjeg uboda....dali se smanjuje izbacuje ili sta ,i kako se to radi u tim slucajevima..

u principu ono sto ja vidim je clomid ED 100/100/50/50   nolva 40/40/20/20   2 nedelje posle zadnjeg uboda dugog estra

kad su kratki estri pct ide odma pa mi je slika malo i jasnija
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Becks on October 30, 2012, 09:39:11 PM
ok ali dali znas koje se doze koriste i po kojoj shemi


ono zasto sve ovo pitam je nesto sto me interesuje zbog slucaja: neko je na kuri zbog navale gino morao da koristi nolvu during cycle..a sad treba i MORA da uradi pct..sta se desava sa nolvom tih 2 nedelje od zadnjeg uboda....dali se smanjuje izbacuje ili sta ,i kako se to radi u tim slucajevima..

u principu ono sto ja vidim je clomid ED 100/100/50/50   nolva 40/40/20/20   2 nedelje posle zadnjeg uboda dugog estra

kad su kratki estri pct ide odma pa mi je slika malo i jasnija

Clomid nece pomoci oko gyno. Nolva ce samo trenutno pomoci, tj verovatno znas nacin na koji deluje... Ja da sam poceo dobijati gyno, odmah bi krenuo sa letrozolom, sad opet zavisi do kojeg stepena je dosao gyno...
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Nitrom on October 31, 2012, 01:45:47 AM
ma kapiram te skroz ali nikako da se potrefimo oko sustine pitanja  :lol:
Title: Odg: Terapija poslije ciklusa - PCT
Post by: BUKAS on November 28, 2012, 06:35:04 PM
Ako mora ici ceo ciklus nolvu, a cisto sumnjam da tako nesto bi bilo potrebno, te dve nedelje naravno da ce da nastavi, ako ima potrebe, to treba uvek da se naglasi. Kad dodje vreme za pct, za kojim opet treba da ima potrebe, nolvu ne treba uzimati.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Mr.Paf on December 04, 2012, 12:26:29 AM
Ako mora ici ceo ciklus nolvu, a cisto sumnjam da tako nesto bi bilo potrebno, te dve nedelje naravno da ce da nastavi, ako ima potrebe, to treba uvek da se naglasi. Kad dodje vreme za pct, za kojim opet treba da ima potrebe, nolvu ne treba uzimati.

A ovo Buki ne vazi za Femaru...Ona se uzima za vreme ciklusa i 5 nedelja nakon poslednjeg uboda....??
Title: Odg: Terapija poslije ciklusa - PCT
Post by: BUKAS on December 04, 2012, 12:35:22 AM
Sve to zavisi od pojedinca do pojedinca. Femara je mnogo cudan lek, dobar ali isto tako moze da izazove dosta problema. U pct moze da se koristi, radi suzbijanja estrogena i oporavka hpta. Naravno, opet ponavljam, ako uopste ima potrebe za tim. Ali skok estrogena se tesko moze izbeci, tako da se neki generalni odgovor moze dati, ali opet sa rezervom. A sto se tice doziranja, tu ne postoji generalni odgovor nikako.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Jelisej on December 06, 2012, 02:26:33 AM
Ljudi, pa kakve vi to savete dajete? kao prvo HCG je obavezan na svakom ozbiljnijem ciklusu, samo sto je u onom tekstu doza nenormalno previsoka- taj tekst je zastareo. HCG ne treba dozirati preko 500 mcg, najbolja je doza 250 mcg svaki drugi dan. Sto se HCG tice on ne samo sto odrzava testise funkcionalne vec ima i druge pozitivne efekte- stimulise stitnu zlezdu i takodje nadbubreznu i usput ima i pozitivan efekat na pregnenolon.
Sto se tice atrofije testisa- same lejdigove celije cine mali dio povrsine testisa, tako testisi mogu biti atrofirani a da se to i ne primeti toliko u velicini.
Takodje prilikom ciklusa treba koristiti i antiestrogen tj AI da nebi E2 previse odlepio.
Za kuru posle ciklusa SERM je obavezan- bilo da je Clomid ili Nolva- takodje u samom orginalnom tekstu pisac preporucuje prevelike doze- 25mg svaki dan Clomida ili 50mg svaki drugi dan je sasvim dovoljno,  problem kod velikih doza je sto i Clomid i Nolva blokiraju estrogen u odredjenim tkivima Npr u mozgu i grudima ali moze doci do nagomilavanja estrofena u nekim drugim tkivima- pogotov kod tako ogromnih doza. Licno preporucujem uz SERM i malu dozu AI- po mom misljenju aromasin/exemestan je najbolji. Takodje neki test booster je dobro dosao a i antikortisol- najbolje je uzeti neki fosfolipid, a i takodje dodati tokoferol zato sto oni pojacavaju osetljivost testisa na LH.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: BUKAS on December 06, 2012, 01:14:45 PM
@Jelisej ti si natural zar ne?


Sve je to lepo u knjigama ali u praksi, stvari su drugacije.
Ozbiljne kure? Sta je po tebi ozbiljna kura?
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Jelisej on December 06, 2012, 02:01:23 PM
@Jelisej ti si natural zar ne?


Sve je to lepo u knjigama ali u praksi, stvari su drugacije.
Ozbiljne kure? Sta je po tebi ozbiljna kura?

Ja jesam natural i na 181 cm imam samo 76kg- obim ruke pisljivih 37 cm, potisak s klupe- maksimum nesto iznad 100 kg, mrtvo dizanje 155kg i to kad sam 100% spreman, dakle poprilicno jadna statistika.
Mogu ti dati jos "dokaza" ako treba da ti pomogne da ignorises moje misljenje/znanje.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: BUKAS on December 06, 2012, 02:03:25 PM
Ne ne nikako, nisam mislio da treba da te uvredim niti na bilo koji nacin osporim. Samo bih da ti skrenem paznju da generalni saveti u vezi ovih lekova ne smeju da postoje.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Jelisej on December 06, 2012, 02:12:20 PM
Pa nemozemo dozvoliti da ljudi sebi uniste endokrini sistem s nepravilnim koristenjem aas, a osim toga bez dobre "terapije posle kure" izgubit ce dosta i misicne mase.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: BUKAS on December 06, 2012, 02:37:44 PM
Puno teorije a malo ili nemanje prakse zna biti pogubno i po osobu i po onoga koji savete prima. (nista uvredljivo, samo sam se u to uverio 100x i po pitanju aas i drugih stvari)
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Becks on December 06, 2012, 03:21:19 PM
Pa nemozemo dozvoliti da ljudi sebi uniste endokrini sistem s nepravilnim koristenjem aas, a osim toga bez dobre "terapije posle kure" izgubit ce dosta i misicne mase.

I sa pravilnim koristenjem ce prirodna proizvodnja biti nula. Posle kure svakako se povrati brzo i bez hcg, clomida itd.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Jelisej on December 06, 2012, 11:42:15 PM
I sa pravilnim koristenjem ce prirodna proizvodnja biti nula. Posle kure svakako se povrati brzo i bez hcg, clomida itd.

Prvi dio je tacan; drugi dio se ne slazem- posle kure je potreban clomid/nolva ili sta vec- posto nije samo pitanje dali ce se HPTA povratiti vec i na koji nivo, sigurno nije dobro ako se neko ko je imao tt 700 ng/dl povrati na 600 ng/dl. Inace i sa dobrim "terapijom posle kure" desava se da neko se ne povrati kako treba, no dobro priznajem da nisam licno koristio AAS tako da je Bukas po tom pitanju u pravu, no ipak se nadam da ce ljudi zdravog razuma ako se vec odluce na "kuru" odratiti i dobru "terapiju posle", posto se igrati ruskog ruleta sa endokrinim sistemom nije pametno.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: BUKAS on December 07, 2012, 12:46:21 AM
Onome kome je stalo do sebe ce uraditi ono sto je potrebno, ovo potrebno treba naglasiti, onima kojima nije, radice kure 4-6 ned metana i 40mg nolve  :hitself:
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Milan on December 07, 2012, 08:19:47 AM
Koliko je iu 250/500mcg HCG-a?
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Jelisej on December 08, 2012, 12:16:20 AM
Koliko je iu 250/500mcg HCG-a?

Michael Scally i ja smo bili clanovi istog foruma, uglavnom on u onom tekstu ne spominje koliko HCG treba uzimati tokom samog ciklusa ali znam da je njegova preprucena doza bila previsoka kao prvo, kao drugo on je imao neke glupave proracune kad poceti koristiti HCG i sl. sto je u sustini glupost. Koristenje HCG-a tokom "terapije posle kure" nije bas najbolja ideja, iako zvuci dobro- isto kao sto teoretski za vreme kure
clomid bi bio bolje resenje od HCG-a ali za ogromnu vecinu u praksi to nije tako.

Uglavnom, necu vise komentarisati u ovoj sekciji foruma, a s druge strane nadam se da mi se nece bas svaka sitnica uzimati "na zub" posto mi koncentracija nije uvek na nivou, kao i kod vecine drugih ljudi pa se desi da omanem.
I jos jednom da napomenem- terapija posle kure je uvek obavezna.
Title: Re: Terapija poslije ciklusa - PCT
Post by: Milan on December 08, 2012, 03:50:28 AM
Ma jok nego trenutno prvi put uzimam hcg posle dugog ciklusa pa rekoh da ne izrazavaju mozda i u mcg.

Sent from my GT-S5830 using Tapatalk
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Jelisej on December 08, 2012, 02:32:43 PM
Tamo u tekstu sam ukucao mcg umesto IU- dakle trebalo je biti 250 IU HCG-a svaki drugi dan, posle nisam mogao izmeniti gresku.
Ovidrel je dolazio u pakovanjima na kojima se korsitio mcg, no nije me to zbunilo vec jednostavno cesto koristim mikrograme kao jedinicu pa sam "automatski" ukucao mcg.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: BUKAS on December 08, 2012, 03:48:49 PM
Imas preporuke 250iu svaki 5i dan. Al koja je prava uloga hcg-a u toku ciklusa? Cisto da dodjemo do nekog zakljucka i mozda do istog misljenja  :yes:
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Jelisej on December 08, 2012, 05:16:40 PM
HCG-u je osnovni zadatak da odrzava funkciju testisa i da spreci atrofiju, (iako na nekim tezim "kurama" ni HCG nemoze spreciti atrofiju). Sama atrofija je najtezi dio posla u "terapiji posle kure".
HCG ima jos prednosti jer stimulise rad stitne zlezde a i nadbubrezbe i usput podize i nivo pregnenolona- ovo se na "kurama" i ne primeti toliko no recimo ljudi na nadomjestku testosterona primete razliku.
Inace, ceste atrofije testisa polako ali sigurno unistavaju Leydig-ove celije sto postupno smanjuje nivo testosterona.
Nekad su bodibilderi HCG koristili posle kure, tj u TPK (terapiji posle kure), no to je bila velika greska i oni su sada vecinom na "nadomjestku testosterona"- evo malo brojki: bodibilder, 44 god- pre koristenja AAS pre nekih 20 god ima je TT oko 700 ng/dl, trenutno krece sa "nadomjestkom"- tt mu je bio 67 i 107 ng/dl u zadnja dva nalaza krvi. Ima poprilican broj takvih slucajeva, a bio bi daleko manji broj...
Inace- sto se HCG-a tice, cesto se spominje tzv "desenzitacija testisa na LH" prouzrokovana HCG-om no ja nisam cuo ni za jedan takav slucaj, tj i preko foruma koji je imao preko 30 000 clanova od kojih je 95% korisnika AAS u raspravi o HCG-u nijedan nije zapravo znao nikoga kojemu je HCG pruzrokovao desenzitaciju.
Uglavnom 250 IU svaki drugi dan bi trebalo biti dovoljno za vecinu kura, a vise  neznaci i bolje. 250 iU svaki 5 dan je malo (a i HCG ima half-life negde oko 3-4 dana, ako se ne varam), ljudi koji su na "HCG" monoterapiji koriste u proseku 1000- 1500, retko po 2000IU nedeljno s time da neki koriste svaki dan manje doze, neki svaki drugi dan, zavisi kako kome odgovara.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: BUKAS on December 08, 2012, 05:53:32 PM
Odlicno. Ima smisla korisiti u toku kure, obicno je kolicina 250-500iu na 5 dana. Sad za sam hcg ima mnogo prica, teorija itd.


Navescu svoj primer iskustva sa njim. U kuri sam ga koristio upravo kako sam gore opisao 250iu svaki 5i dan, kroz 8 nedelja. Testisi se nisu smanjivali skoro uopste. Sam libido nakon kure nije padao. Mogu reci da sam se najbrze oporavio tada. Nakon ciklusa sam nastavio koriscenje hcga nekih 1500 svaki drugi dan kroz 3 ned, i uzimao 50mg klomida 3 ned i osecao se kao jadnik. Kad sam sisao sa terapije, bilo je odlicno, nikakvih padova rapsolozenja, libida itd. Ali za te tri nedelje od klomida mi nije bilo ni do cega. Klomid sam tada koristio treci put i po treci put se uverio kako mi je stvarao losu "atmosferu" u glavi. Uglavnom sldeci "pct", iskren da budem ne znam kada ce da bude  :lol: , nece biti klomida, ali bice nekih drugih stvari, ali lekcina kao sto su ovi nece. Pa cu da vidim razliku.

Aktivan zivot 64h.

Da dodam, nakon 10 nedeljne kure ili 12 nedeljne nema potrebe da se pposeze za nekim velikim brojem lekova, a nekada ne mora ni za jednim. Duze kure zahtevaju drugaciji pristup.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Jelisej on December 08, 2012, 06:12:52 PM
Klomid je poznat po tome sto baca ljude u depresiju, medjutim nesto je efektivniji od nolve a nolva je nesto povezana s rakom tako da je mnogi zbog toga izbegavaju- no nolva izaziva daleko manje probleme.
Inace svi ti SERM-ovi u odredjenim tkivima blokiraju estrogen ali se on nagomilava u drugim- i mislim da je to jedan od razloga za probleme u emocijama. Mislim da mala doza AI uz SERM moze pomoci, jedino je problem da se ne doda previse jer to moze imati stetne posledice po kosti.
Opet, koliko god bio traumatican klomid je dokazano efektivan.
Inace, toremifen je takodje popularan SERM, no ja nisam imao "kontakata" s njim i slabo ga poznajem.
Inace HCG za veme "TPK" je dubiozna ideja, jer uglavnom mislim da hipofiza nece da luci LH dok se HCG ne "iscisti".
Interesantno je da si koristio klomid 3 nedelje- to je nekad bio "engleski" stil dok su amerikanci imali 4 nedelje SERM-a, posle su englezi poceli takodje 4 nedelje (kopirajuci amerikance) a u medjuvremenu su amerikanci presli na 6 nedelja.

Za krace kure, zaista nije potreban SERM za "TPK" ali sama teraija posle kure je ipak potreban, takodje ima jos kura gde nije SERM uvek potreban, npr za vecinu "DHT" kura, ali opet potreban je odredjena TPK.
Inace atrofija testisa se nemoze meriti po velicini- sama atrofija je cesto neprimetna a vec u drugoj nedelji je atrofija poprilicna tako da mislim da je HCG "dobar prijatelj".
Title: Odg: Terapija poslije ciklusa - PCT
Post by: BUKAS on December 08, 2012, 06:23:23 PM
Problem koji je mnogo zeznutiji je visok estrogen nakon kure, koji kao i visok kortizol usporavaju oporavak hpta. Slazem se da male doze Ai mogu da budu jako korisne. Uglavnom, najvise paznje treba upravo da se obrati na ova dva vraga. Resis problem sa njima 80% posla je uradjeno. 

Da i ovo moramo da rascistimo da pct ili aj na naski Tpk, ne treba da podrazumeva odmah koriscenje ovih lekova. Ima i drugih solucija za odradjivanje tpk.


Ameri kod njih sve mora da bude vece, duze itd.
Title: Odg: Terapija poslije ciklusa - PCT
Post by: Jelisej on December 08, 2012, 06:49:34 PM
Ovog puta se vec slazemo- tj sto se tice estrogena i kortisola. Uostalom fora i kod SERMA je to sto blokira receptore estrogena u mozgu, pa onda hipofiza luci LH da bi povecala nivo estrogena, tj mi zapravo varamo hipofizu. S druge strane sami AI su ustvari i superiorniji kao prvo a kao drugo na kod AI-je prednost sto mozes oceniti koliki je nivo estrogena (pomocu osmatranja erekcije)- no mana je kod AI sto njima treba vise vremena da pocnu da funkcionisu.
Kortizol je druga prica- u vecini "hitnih slucajeva" organizam se naslanja na nadbubreznu zlezdu tj na kortisol- ali i na sam adrenalin- tako da se posle kure ako je nivo testosterona mali organizam takodje koristi usluge nadbubrezne zlezde a ovo ima usporavajuci efekat oporavka, a i uglavnom deluje pogubno na misicnu masu.
Inace, van TPK anti-kortisol nije dobro koristit jer iako kortizol i testosteron jedan drugog smanjuju s druge strane, za dobar nivo testosterona je potreban i dobar nivo kortizola.

Sto se Amerikanaca tice- istina je da oni redovno preteruju i dan danas oni znaju da koriste po 100mg klomida svaki dan sto je glupost i moze cak imati obrnuti efekat od zeljenog, no s druge strane slazem se da je 6 nedelja minimum za TPK (posle duze kure). Takodje mislim da je dobro postepeno smanjivati dozu SERMA, radije nego jednostavno prestati (uglavnom vecina endokrinologa rade po ovom sistemu).