Evo, clanak je kopiran sa mesomorphosis. Skratio sam ga jer je dosta dugacak. Ovo je najbitnije.
Everything That’s Wrong With Your PCT by Eric M. Potratz
In the world of steroid users, it has become mandatory to follow post cycle therapy (PCT) upon cessation of steroid use. Many great PCT protocols have been outlined over the years, and many individuals have had great success with following such protocols. Nevertheless, what works can always work better. This is especially the case for those that have had a lack of success following popular advice. In this article I will address the major problems with popular PCT protocols and clarify exactly how we should use the items at our disposal for optimum recovery from AAS. Three main topics will be covered in this article –
hCG on cycle -- I will show you the best way to use HCG, which will protect your "testicular real-estate", and prime your HPTA for the fastest and most complete recovery possible.
SERMs. -- Drugs such as Clomid and Nolvadex are some of the most toxic drugs in a steroid-users cabinet. I will present the evidence of this toxicity and provide alternatives.
Peptides for PCT -- Peptides such as Growth Hormone and IGF-1 have much more of a role in PCT than most people realize. Besides preserving muscle gains, these hormones can actually help restore testicular function after a cycle.
HCG unraveled
Human Chorionic Gonadotropin (hCG) is a peptide hormone that is used in place of LH to stimulate hormone production from the gonads.1 LH is the primary signal sent from the pituitary to the testes, which stimulates the leydig cells within the testes to produce testosterone. When steroids are administered, LH levels rapidly decline. The absence of an LH signal from the pituitary causes the rapid onset of testicular degeneration. The testicular degeneration begins with a reduction of leydig cell volume, and is then followed by rapid reductions in intra-testicular testosterone (ITT), peroxisomes, and Insulin-like factor 3 (INSL3) – All important bio-markers and factors for proper testicular function and testosterone production.2-6,19 However, this degeneration can be prevented by a small maintenance dose of hCG ran throughout the cycle. Unfortunately, most steroid users have been engrained to believe that hCG should be used after a cycle. Though, we will learn that a faster and more complete recovery is possible if hCG is ran during a cycle.
Firstly, we must understand the clinical history of hCG to understand the most efficient way to use it. Many popular "steroid profiles" advocate an hCG dose of 2500-5000iu once or twice a week. These were the kind of dosages used in the historical hCG studies for hypogonadal men who had reduced testicular sensitivity due to prolonged LH deficiency.85,86 That is, testes desensitize when not presented with a sufficient LH signal. In men with normal LH levels and testicular sensitivity, the maximum increase of testosterone is seen from a dose of only ~250iu, with minimal increases obtained from 500iu or even 5000iu.2,11 (It appears the testes maximum secretion of testosterone is about 140% above base line.12-18) So, if you have allowed your testes to desensitize over the length of a typical steroid cycle, (8-16 weeks) then you would require a higher dose to elicit a response in an attempt to restore normal testicular size and function – but there is cost to this, and a high probability that you won’t regain full testicular function.
To get an idea of how quickly testicular degeneration occurs from your average multi-AAS cycle, consider this: LH levels are rapidly decreased by the 2nd day of steroid administration.2,9,10 By shutting down the LH signal and allowing the testis to be non-functional over a 12-16 week period, leydig cell volume decreases 90%, ITT decreases 94%, INSL3 decreases 95%, while the capacity to secrete testosterone decreases as much as 98%.2-6 It should be mentioned that visually analyzing testes size is a poor method of judging your actual testicular function, since testicular size is not directly related to the ability to secrete testosterone.4 This is because the leydig cells, which are the primary sites of testosterone secretion, only make up about 10% of the total testicular volume. Therefore, testicular size may appear normal on a cycle, but the testes ability to secrete testosterone upon LH or hCG stimulation can actually be significantly diminished.3-5
The decreased testosterone secretion capacity was well demonstrated in a study on power athletes who used steroids for 16 weeks, and were then administered 4500iu hCG post cycle. It was found that the steroid users were about 20 times less responsive to hCG, when compared to normal men who did not use steroids.8 In other words, their testosterone secretion capacity was dramatically reduced because they did not receive an LH signal for 16 weeks. The testes essentially became desensitized and crippled. Case studies with steroid using patients show that aggressive long-term treatment with hCG at dosages as high as 10,000iu E3D for 12 weeks were unable to return full testicular size.7 Other studies with men using low dose steroid implants for 6 weeks showed unsuccessful return of Insulin-like factor-3 (INSL3) concentration in the testes upon 5000iu/wk of HCG treatment for 12 weeks.6
These studies show that postponing hCG usage until the end of a cycle, increases your need for a higher dose of hCG, and decreases your odds of a full recovery. As a consequence to using a higher dose of hCG, estrogen will be increased disproportionately, which then causes further HPTA suppression while increasing the risk of gyno.11 For example, high doses of hCG are known to raise estradiol 165%, while only raising testosterone 140%.11 Higher doses of hCG are also known to reduce LH receptor concentration and degrade the enzymes responsible for testosterone synthesis within the testes12,13,19 (the last thing someone wants during recovery). While these negative effects of hCG can be partly mitigated by the use of a drug such as tamoxifen, it will create further problems associated with using a toxic SERM. (covered in the next section)
In light of the above evidence, it becomes obvious that we must take preventative measures to avoid this testicular degeneration. Besides, with hCG being so readily available, and such a painless shot, it makes you wonder why anyone wouldn’t use it on cycle. Based on studies with normal men using steroids, ~100iu HCG administered everyday was enough to preserve full testicular function and ITT levels, without causing desensitization typically associated with higher doses of hCG.2 It is important that low-dose hCG is started before testicular degeneration occurs, which appears to rapidly manifest within the first 2-3 weeks of steroid use.
Recap – For optimal preservation of testicular function during cycle, use 100iu hCG ED starting 3 days after your first AAS dose. Drop the hCG a week before the AAS clear the system. For example, you would drop hCG a week after your last Testosterone Enanthate shot. Or, if you are ending the cycle with orals, you would drop the hCG a week before your last oral dose. This will allow for a sudden and even drop in hormone levels, while initiating LH and FSH production from the pituitary, making for a seamless recovery.
A more convenient alternative to the above recommendation would be a weekly shot of 500iu hCG, throughout the entire cycle. Beyond this dose, one could calculate a rough estimate for their required hCG dosage by multiplying 40iu x days of LH absence. (40iu x 60 days = 2400iu HCG dose)
As an alternative to the on cycle hCG protocol, you could follow a plan based on modulation of the gonadotropin pulse generator.
Note: If following any of these protocols, hCG should NOT be used after the cycle.
