HCG - The most important part of PCT

[Lazarus]

HCG - Unraveled By Eric M. Potratz

Eric M. Potratz has developed his education in the field of endocrinology and performance enhancement through years of research, counseling, and real world experience. Over the past five years he has been a private consultant for hundreds of athletes and bodybuilders alike, and is the founder & president of Primordial Performance.

PCT is a must upon cessation of steroid use. Many great PCT protocols have been outlined over the years, and many individuals have had success with following such protocols. Nevertheless, what works can always work better, and I intend to show you the most effective way to recover from AAS. This is especially the case for those that have had a lack of success following popular advice. In this article I will address the misunderstanding and misuse of Human Chorionic Gonadotropin (hCG) and show you the most efficient way to use hCG for the fastest and most complete recovery.

HCG unraveled –

Human Chorionic Gonadotropin (hCG) is a peptide hormone that mimics the action of luteinizing hormone (LH). LH is the hormone that stimulates the testes to produce testosterone. (1) More specifically 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 testes to stop producing testosterone, which causes 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, during PCT. Upon reviewing the science and basic endocrinology you will see 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 its purpose and its most efficient application. Many popular “steroid profiles” advocate using hCG at a dose of 2500-5000iu once or twice a week. These were the kind of dosages used in the historical (1960’s) hCG studies for hypogonadal men who had reduced testicular sensitivity due to prolonged LH deficiency. (21,22) A prolonged LH deficiency causes the testes to desensitize, requiring a higher hCG dose for ample stimulation. In men with normal LH levels and normal 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 their normal capacity.) (12-18) 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.

One term that is critical to understand is testosterone secretion capacity which is synonymous to testicular sensitivity. This is the amount of testosterone your testes can produce from any given LH or hCG stimulation. Therefore, if you have reduced testosterone secretion capacity (reduced testicular sensitivity), it will take more LH or hCG stimulation to produce the same result as if you had normal testosterone secretion capacity. If you reduce your testosterone secretion capacity too much, then no amount of LH or hCG stimulation will trigger normal testosterone production – and this leads to permanently reduced testosterone production.

To get an idea of how quickly you can reduce your testosterone secretion capacity from your average steroid 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)

Note: 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, when the testes may only appear 5-10% smaller, the testes ability to secrete testosterone upon LH or hCG stimulation can actually be significantly reduced to 98% of their normal production. (3-5) The point here is to not judge testosterone secretion capacity by testicular size.

The decreased testosterone secretion capacity caused by steroid use 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) Another study with men using low dose steroids 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) (INSL3 is an important biomarker for testosterone production potential and sperm production. 20)

These studies show that postponing hCG usage until the end of a steroid 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 at the end of a cycle, estrogen will be increased disproportionately to testosterone, which then causes further HPTA suppression (from high estrogen) while increasing the risk of gyno. (11) For example, high doses of hCG have been found to raise estradiol up to 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 testes (12,13,19 ) -- the last thing someone wants during recovery. While these negative effects of hCG can be partly mitigated by the use of a SERM such as tamoxifen, it will create further problems associated with using a toxic SERM (covered in another article).

In light of the above evidence, it becomes obvious that we must take preventative measures to avoid this testicular degeneration. We must protect our testicular sensitivity. 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 sensitivity is reduced, which appears to rapidly manifest within the first 2-3 weeks of steroid use. Also, it’s important to discontinue the hCG before you start PCT so your leydig cells are given a chance to re-sensitize to your body’s own LH production. (To help further enhance testicular sensitivity, the dietary supplement Toco-8 may be used)

A more convenient alternative to the above recommendation would be a twice a week shot of 200iu hCG, or possibly a once a week shot of 500iu. However, it is most desirable to adhere to a lower more frequent dose of hCG to mimic the body’s natural LH release and minimize estrogen conversion. If you are starting hCG late in the cycle, one could calculate a rough estimate for their required hCG ‘kick starting’ dosage by multiplying 40iu x days of LH absence, since the testes will be desensitized, thus requiring a higher dose. (ie. 40iu x 60 days = 2400iu HCG dose)

Note: If following the on cycle hCG protocol, hCG should NOT be used for PCT.

Recap –

For preservation of testicular sensitivity, use 100iu hCG ED starting 7 days after your first AAS dose. At the end of the cycle, drop the hCG two weeks before the AAS clear the system. For example, you would drop hCG about the same time as your last Testosterone Enanthate shot. Or, if you are ending the cycle with orals, you would drop the hCG about 10 days before your last oral dose. This will allow for a sudden and even clearance in hormone levels, while initiating LH and FSH production from the pituitary, to begin stimulating your testes to produce testosterone. Remember, recovery doesn’t begin until you are off hCG since your body will not release its own LH until the hCG has cleared the system.

In conclusion, we have learned that utilizing hCG during a steroid cycle will significantly prevent testicular degeneration. This helps create a seamless transition from “on cycle” to “off cycle” thus avoiding the post cycle crash.

References -

1. Glycoprotein hormones: structure and function.
Pierce JG, Parsons TF 1981
Annu Rev Biochem 50:466–495

2. Low-Dose Human Chorionic Gonadotropin Maintains Intratesticular Testosterone in Normal Men with Testosterone-Induced Gonadotropin Suppression
Andrea D. Coviello, et al
J. Clin. Endocrinol. Metab., May 2005; 90: 2595 - 2602.

3. Luteinizing hormone on Leydig cell structure and function.
Mendis-Handagama **
Histol Histopathol 12:869–882 (1997)

4. Leydig cell peroxisomes and sterol carrier protein-2 in luteinizing hormone-deprived rats
** Mendis-Handagama, et al.
Endocrinology, Dec 1992; 131: 2839.

5. Effect of long term deprivation of luteinizing hormone on Leydig cell volume, Leydig cell number, and steroidogenic capacity of the rat testis.
Keeney DS, et al.
Endocrinology 1988; 123:2906–2915.

6.The Effects of Gonadotropin Suppression and Selective Replacement on Insulin-Like Factor 3 Secretion in Normal Adult Men
Katrine Bay, et al
J. Clin. Endocrinol. Metab., Mar 2006; 91: 1108 - 1111.

7. Successful treatment of anabolic steroid–induced azoospermia with human
chorionic gonadotropin and human menopausal gonadotropin
Dev Kumar Menon, et al.
FERTILITY AND STERILITY VOL. 79, SUPPL. 3, JUNE 2003

8. Testicular responsiveness to human chorionic godadotrophin during transient hypogonadotrophic hypogonadism induced by androgenic/anabolic steroids in power athletes
Hannu et al.
J. Steroid Biochem. Vol. 25, No. 1 pp. 109-112 (1986)

9. Comparison of testosterone, dihydrotestosterone, luteinizing hormone, and follicle-stimulating hormone in serum after injection of testosterone enanthate of testosterone cypionate.
Schulte-Beerbuhl M, et al 1980
Fertil Steril 33:201–203

10. Effects of chronic testosterone administration in normal men: safety and efficacy of high dosage testosterone and parallel dose-dependent suppression of luteinizing hormone, follicle-stimulating hormone, and sperm production.
Matsumoto AM, et al 1990
J Clin Endocrinol Metab 70:282–287

11. Effect of human chorionic gonadotropin on plasma steroid levels in young and old men.
Longcope C et al
Steroids 21:583–590 (1973)

12. Regulation of peptide hormone receptors and gonadal steroidogenesis.
Catt KJ, et al
Rec Prog Horm Res 1980; 36:557–622

13. Effect of human chorionic gonadotropin on the endocrine function of Papio testes
GV Katsiia, et al
Probl Endokrinol (Mosk), Sep 1984; 30(5): 68-71.

14. Reproductive function in young fathers and grandfathers.
Nieschlag E, et al.
J Clin Endocrinol Metab 55:676–681 (1982)

15. The aging Leydig cell III Gonadotropin stimulation in men.
Nankin HR, et al. 1981
J Androl 2:181–189

16. Reproductive hormones in aging men. I. Measurement of sex steroids, basal luteinizing hormone, and Leydig cell response to human chorionic gonadotropin.
Harman **, et al. 1980
J Clin Endocrinol Metab 51:35–40

17. Prolonged biphasic response of plasma testosterone to single intramuscular injections of human chorionic gonadotropin.
Padron RS, et al. 1980
J Clin Endocrinol Metab 50:1100–1104

18. Gonadotrophins and plasma testosterone in senescence. In: James VHT, Serio M, Martini L, eds. The endocrine function of the human testis.
Mazzi C, et al. 1974
New York: Academic Press, Inc.; 51–66

19. Androgen biosynthesis in Leydig cells after testicular desensitization by luteinizing hormone-releasing hormone and human chorionic gonadotropin.
Dufau ML, et al.
Endocrinology 105 1314–1321 (1979)

20. Insulin-Like Factor 3 Serum Levels in 135 Normal Men and 85 Men with Testicular Disorders: Relationship to the Luteinizing Hormone-Testosterone Axis
K. Bay, S. et al
J. Clin. Endocrinol. Metab., Jun 2005; 90: 3410 - 3418.

21. Stimulation of sperm production by human chorionic gonadotropin after prolonged gonadotropin suppression in normal men.
Matsumoto AM, et al 1985
J Androl 6:137–143

22. Human chorionic gonadotropin and testicular function: stimulation of testosterone, testosterone precursors, and sperm production despite high estradiol levels.
Matsumoto AM, et al. 1983
J Clin Endocrinol Metab 56:720–728

HCG article

[Lazarus]

HCG (Human Chorionic Gonadotropin)

Scientists first recognized a specific hormone now called Human Chorionic Gonadotropin (HCG) in the 1920’s (1). HCG is no doubt one of the most misused, misunderstood and underutilized tools in bodybuilding pharmacology we have available. HCG is not a steroid, but a naturally occurring peptide hormone, produced by the embryo in the early stages of pregnancy and later by the trophoblast (part of the placenta) to help control a pregnant woman’s hormones (1). This makes the uterine lining ready for implantation of the fertilized egg. HCG is a glycoprotein composed of 237 amino acids and has a mass of 36.7kDa. HCG basically “acts” as Leutenizing Hormone (LH) in your body. LH is a Gonadotropin. They were first extracted from the human in 1958; more precisely the pituitary glands. A gonadotropin is any substance that stimulates the gonads (ovary, testes). It is heterodimeric (initiates prophase of mitosis) with an alpha subunit identical to LH (luteinizing hormone), FSH (follicle stimulating hormone) and TSH (thyroid stimulating hormone). LH is as stated above is called a gonadotropin because it stimulates the gonads (testes). It is produced in the pituitary cells and is made up of a beta chain of 115 amino acids and an alpha chain of 89 amino acids. In the testes, the LH binds to receptors on the leydig cells which in turn stimulates the synthesis and secretion of testosterone. Like LH, FSH is also called a gonadotropin. It consists of a beta chain of 115 amino acids and an alpha chain of 89 amino acids, the same as LH. Production and release of FSH is controlled by GnRH (gonadotropin releasing hormone). FSH stimulates testicular growth and supports the function of sertoli cells, which are needed for sustaining maturing sperm cells. TSH is also known as a thyrotropin and is secreted by cells in the anterior pituitary glands. TSH is comprised of a beta chain of 112 amino acids and an alpha chain of 89 amino acids. The alpha chain is the same as that found in the two other pituitary hormones, LH and FSH, and HCG as well. TSH is produced when the hypothalamus releases TRH (thyrotropin releasing hormone). TRH then causes the pituitary gland to release
TSH. TSH make the thyroid gland produce triiodothyronin (T3) and thyroxine (T4), which controls the body’s metabolism.

HCG is clinically used to induce ovulation and treat ovarian disorders in women, as well stimulate the testes hypogonadal (underproduction of testosterone) men. It is also used in the treatment of undescended testicles in young males. HCG offers no potential performance enhancement in female athletes, but does prove to be very useful in male athletes especially those that use AAS. As stated above HCG in males is similar to LH, because they are similar and LH binds to receptors on leydig cells stimulating synthesis and secretion of testosterone, the use of HCG would be an added bonus to ASS users even if there is a lack of endogenous LH. Since HCG increases the body’s natural testosterone levels its use during long or extremely high dosed cycles can be most beneficial were the effects on the hypothalamus causes a depressed signal to the testicles. The result of the depressed signal leads to what is known as testicular atrophy (shrunken nuts). The use of HCG will send an artificial signal to the testes (again, as if it were actually LH), thus preventing (to some degree) atrophy. It not only helps to maintain testicular size and condition but it will also help in restoring testicles back to their original size. At a time when below normal androgen levels (due to ASS use) could become costly. Restarting natural testosterone production as quickly as possible is of a special concern in males at the end of a cycle of AAS. The price paid by bodybuilders for failing to raise natural test levels is the loss of most if not all the hard earned muscle you have gained, the main cause is cortisol. Cortisol sends a message to the muscles that is opposite to that of testosterone. If cortisol is not dealt with (because of an extremely low testosterone level) it will quickly strip away the new and hard earned muscle you have just gotten.

Some users find that they have better gains and quicker recovery while using HCG during a cycle of AAS. This first claim is more than likely due to the fact that the body has a high level of natural testosterone as well as that provided by the use of AAS, and the second may be somewhat justifiable, as stimulating the testes to secrete testosterone intermittently may aid recovery. Perhaps this is due to the maintenence of a higher level of Inter-Testicular-Testosterone (ITT) provided by the intermittent use of HCG, which should greatly aid recovery of the hypothalamic-testicular-pituitary-axis. An average dose of HCG during a cycle is between 500iu to 1000iu every week to every other week while on a cycle. In one study I looked at, a single injection of 6000IU of HCG elevated test levels for 6 days. That's why a lot of people recommend taking it every 3-5 days. We'd have more stable blood levels, though if we shot it more frequently. Remember, it's non-estrified and a water-based injectable, after all. In that same study I just spoke of, 1500IU of HCG shot test levels up between 250 and 300%. Taking it all at once however will cause an increase in estrogen levels caused by the aromatization of normal testosterone, the result may be a case of gynecomastia for the user (3).

As regards HCG's use of Post-Cycle-Therapy (PCT), smaller and more frequent doses after a cycle of AAS would give the best results with the least amount of side effects. A dose of 250iu to 500iu everyday (ed) for 2 to 3 weeks is plenty and should very little from person to person (3). The Physicians Desk Reference recommends 500iu/day, as did the late, great, Dan Duchaine. The smaller doses are sufficient enough to begin reversal of testicular atrophy and used in conjunction with nolvade, will help the already present problem of recovery without raising the levels of estrogen to high and increasing the risk of gynecomastia in the user. Lower doses of 250iu to 500iu also avoid the further risk of down regulating LH receptors in the testes. The old saying more is better definitely does not apply to the use of HCG. You don’t want to finish PCT after using too much HCG only to find out your back at the beginning again. Your best bet is to start at 250iu or 500iu ed for 5 or 6 days, and if you don’t notice anything happening (nuts dropping and getting bigger) up the dose slightly. Small doses like 500iu two days a week isn’t going to cut it like some people think. The only thing small doses of HCG ay be useful (sublingually)for is reducing symptoms of benign prostatic hyperplasia (7). Yeah, thats right, you can probably reduce some symptoms of an enlarged prostate with the use of small doses of HCG.

As stated above the cycles of HCG should be in the 2 to 3 week range with a least one month off in between, you could stretch your cycle out to four weeks without any major concern if you are using lower doses. One should however take care when using HCG as prolonged use could repress the body’s natural production of gonadotropins permanently, but this is mostly just pure speculation as it does not have yet to be reported nor has there been a case of an overdose. To be on the safe side shorter cycles of HCG seem to be that of the norm. Most users cycle HCG near the end of a steroid cycle, you should start your HCG therapy on the last week of your cycle. For best results you should also run nolva while you run HCG as taking HCG by itself will do little to nothing and gyno even though rare may also flair up. Once the HCG cycle is finished you continue with your usual clomid or nolvadex (preferably the latter) for pct as it is more effective when used in conjunction HCG for pct. With an AAS cycle of 6 to 10 weeks HCG may not be necessary unless extreme doses of AAS were used or there is an existing problem of testicular atrophy or you are running a heavy oral only cycle. AAS cycles of 12 or more weeks should have HCG as a part of post cycle plan.

Since HCG is used to stimulate testosterone production, side effects can be the same as those associated with AAS, although gyno may be more common. Possible side effects of HCG use are water and sodium retention after higher doses are used. This is usually a result of higher androgen production. It may cause gyno (again if doses are too high).. Any athletes worried about failing urine test because of low levels of epitestosterone may find that using a dose of 500iu of HCG will increase epitestosterone levels. However the problem with HCG is that it is also banned by the IOC and can also be detected in a urine test, the half life of HCG is approximately 4 to 5 days. Another possible downside to HCG is that it to can be suppressive to natural testosterone because it takes the place of LH. Since LH is manufactured in the pituitary because of the response of GnRH (gonadotropin releasing hormone) which in turn is secreted by the hypothalamus. Because the HCG mimics LH and is being supplied exogenously the hypothalamus will be given a signal to still stop producing GnRH, so no natural LH will be produced (5). This is why it should always be used with a compound such as nolvadex. So although HCG is essential after long or heavy cycles, it should not be used without an ancillary such as (specifically) nolv. Also HCG therapy should be discontinued at least 2 weeks prior to stopping the use of nolva, or it may suppress natural testosterone itself (5). This should not be a problem if you are running it towards the end of your cycle of AAS and before pct.

Steroid.com forum-thread

[O.N.]

article By William Llewellyn

Understanding Post Cycle “T� Recovery

The Hypothalamic-Pituitary-Testicular Axis, or HPTA for short, 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 purposes of our discussion here 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 counter-balance things, by providing negative feedback signals (primarily to the hypothalamus and pituitary) to lower the secretion of testosterone when too much of this hormone is sensed. Synthetic steroids, of course, suppress testosterone the same way. This quick background of the testosterone-regulating axis is necessary to furthering our discussion, as we need to first look at the underlying mechanisms 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 discussed above, the big roadblock to a restored HPTA after we come off the drugs is surprisingly not the level of LH itself. This problem is made clearly evident in a study published in Acta Endocrinologica back in 1975(1). Here blood parameters, including testosterone and LH levels, were monitored in male subjects whom were given testosterone enanthate injections of 250mg weekly for 21 weeks. 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 is to be expected. Things looked very different, however, once the steroids had been withdrawn (see Figure I). 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 started. This lack of correlation makes clear that the problem in getting androgen levels restored is not the level of LH, but in fact testicular atrophy and desensitization to this hormone. After a period of inactivation the testes have apparently lost mass (atrophied), making them unable to perform the workload required by heightened levels of LH.

Post-Cycle LH Levels



Post Cycle Testosterone Levels

Figure I. LH and Testosterone measurements starting 1 week after the last injection of 250mg of testosterone enanthate (pretreated measures were 5 mU/ml and 4.5 ng/ml respectively). Note that between weeks 1 and 5, as testosterone levels are declining due to the cessation of exogenous androgen administration, LH levels are already rebounding. From weeks 5 to 10 testosterone levels are at or very near baseline, to spite the substantial LH levels by this point. No significant increase in testosterone is noted until after the 10-week mark.
HCG


So we now see, contrary to the dominating opinion of the times, that anti-estrogens alone will do little to raise testosterone levels in the early weeks of the post-cycle window. This leaves us to focus on a very different level of the HPTA in order to hasten recovery: the testes. For this we will need the injectable drug HCG. If you are not familiar with it, HCG, or Human Chorionic Gonadotropin, is a prescription fertility agent that mimics the bodies own natural LH. Although the testes are equally desensitized to this drug as LH (they both work through the same mechanism), we are administering it as a measured drug and are therefore not constrained by the limits of our own LH production. We similarly can use HCG to provide a bolus dose of LH (of our choosing), which works only to augment the recovering LH levels we already have in the body. In essence we are looking to shock them with an overwhelmingly high level of LH activity, coming from both endogenous and exogenous sources. We want it to reach a level far above what our body, even when supported by anti-estrogens, could possibly do on its own. The result can be a rapid restoration of original testicular mass and functioning, which would allow normal levels of testosterone to be output much sooner than without such an ancillary program. What we are looking at now is HCG actually being the pivotal post-cycle drug, while anti-estrogens are relegated to a supportive role at best.

[Testy]

After reading all the posts in this thread and reviewing a mates recent blood tests i cannot stress enough that HCG or any other forum HMG etc must always be used during your steroid cycle.

It is by far the most important tool you can have in getting back to normal testosterone levels ASAP.

Recently a young friend of mine finished a 10 week cycle, its only his second cycle and he is 20yrs old.
Before blood tests had his ranges all within normal for his age i cant remember the figures but they were 18+ from memory in total testosterone.
Clinical ranges are usually from 8-32.
If you score below 8 you qualify for HRT.

After he was off cycle for 6 weeks, made use of nolvadex and shit loads of tribulus he scored 6.8 total testosterone thats less than clinical and would qualify him for HRT.

Now on the other hand as some of you know i completed a very very long cycle as HCG was not available to me so i stayed on until i had it.
After 9 months on cycle on more than 1000mg per week, my recovery was back to normal in 45days with a test level of 20.98 and free test of 483.
2 months after that without supplementation 18 and i cant recall the free but it was still decent.

Several cycles later HCG is always used during my cycles now at 250IU every 5 days and recovery is perfect and i feel great.

Do yourself a favour wait until you can get HCG if not best of luck maybe make use of some of the PP products, they seem to look good and i will be trying them during my next PCT.

[Lazarus]

Couldn't agree more. Everything I've read and experienced endorses the view that HCG is a MUST.

[Testy]

HCG timing into PCT MY VIEW FROM ANOTHER FORUM POST I HAVE MADE:

based on the cycles I have done and all the info i have read....which by the way is shit loads as iam one of those obsessive compolisive need to know everything about steroids peptides bodybuilding drugs type guys.
I still say 250IU twice per week 4 days apart to 5 days apart.
continue past the last shot of test e.....WHY PAST THE SHOT?

When we look at the very first injection of Test e we see the LH levels reach near 0 on day 2-3. So why the fuck maintain testicular function for the entire cycle then just before you get off let the testosterone supress the nuts again for a few days.

i recommend this for example:
week 1-10: 500mg test E
HCG 250IU every 4-5days from week 1-11
Nolvadex 20mg week 10-15 or to next cycle, i preffer to use an anti e while off cycle to keep testosterone higher.

500mg test e final week will stay in the system for atleast 42days, some where in this time levels will become normal i'd say around day 23-25 so from day 1 of final shot HCG is only used for 7-10 more days test e will still be above normal from day 10-23/25 so for another 13 days test e is still active, it is in this time that nolva clomid etc start to raise LH and bomb we have a perfect recovery.

Other HCG protocals will still work and recovery will still be faster than no HCG use.
But as i have explained LH levels crash to near zero in 2-3 days form intial injection so why fuck with the science that is correct at the start of the cycle and muck around at the end.
Tell me why what iam saying is wrong?
Science tell's us its the right way.
Doctors as you know are not bodybuilders they dont have the same objective, i know they are talking about recovery, but i want perfect recovery, where in what i have said have i gone wrong i dont see it.
Only other thing i can see would be daily shots of HCG at 75-100IU could be even better than multiple larger shots, mimicing more natural LH release.

[mrt]

Who comes off nowdays

[Lazarus]

Well, in terms of long-term health, everyone should come off at some stage.

[O.N.]

The Role Of Anti-Estrogens


It is important to understand that anti-estrogens alone do not do much to restore endogenous testosterone release after a cycle. Normally they only foster LH by blocking the negative feedback of estrogens, and we now see that LH rebounds quickly without help anyway. Plus, post cycle there is not an elevated level of estrogen for anti-estrogens to block, as testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen levels will actually be lower here as a result, not higher.

Any estrogen rebound that occurs post-cycle likewise happens concurrently with a rebound in testosterone levels, not prior to it (note there is an imbalance in the ratio post cycle, but this is another topic altogether). We are seeing no mechanism in which anti-estrogenic drugs can really help here. We can see why this fact would not be difficult to overlook, however. The medical literature is filled with references showing anti-estrogenic drugs like Clomid and Nolvadex to increase LH and testosterone levels, and in normal situations these drugs do indeed increase endogenous androgen production by blocking the negative feedback of estrogens.

Combine this with the fact that just as many studies can be found to show that steroid use lowers LH levels when suppressing testosterone, and we can see how easy it would be to jump to the conclusion that post-cycle we need to focus on restoring LH. We would miss the true problem of testicular desensitization unless we were really looking into the actual recovery rates of the hormones involved. When we do, we immediately see little value in using anti-estrogenic drugs.

[UN Soldier]

The Role Of Anti-Estrogens


It is important to understand that anti-estrogens alone do not do much to restore endogenous testosterone release after a cycle. Normally they only foster LH by blocking the negative feedback of estrogens, and we now see that LH rebounds quickly without help anyway. Plus, post cycle there is not an elevated level of estrogen for anti-estrogens to block, as testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen levels will actually be lower here as a result, not higher.

Any estrogen rebound that occurs post-cycle likewise happens concurrently with a rebound in testosterone levels, not prior to it (note there is an imbalance in the ratio post cycle, but this is another topic altogether). We are seeing no mechanism in which anti-estrogenic drugs can really help here. We can see why this fact would not be difficult to overlook, however. The medical literature is filled with references showing anti-estrogenic drugs like Clomid and Nolvadex to increase LH and testosterone levels, and in normal situations these drugs do indeed increase endogenous androgen production by blocking the negative feedback of estrogens.

Combine this with the fact that just as many studies can be found to show that steroid use lowers LH levels when suppressing testosterone, and we can see how easy it would be to jump to the conclusion that post-cycle we need to focus on restoring LH. We would miss the true problem of testicular desensitization unless we were really looking into the actual recovery rates of the hormones involved. When we do, we immediately see little value in using anti-estrogenic drugs.

Very good and informative.

I used to have the view that so many novices have now, they think they need copious amounts of nolva and clomid post cycle, even for a short 4 week cycle lol! But yes I agree with goood ol ON here, and I have told people in the past that I used to just come clean off the gear with nothing at all, just plain old vitamins.......and patience. I don't have gyno at all, even coming off several grams of gear per week I did not get any gyno, and I tell you what nolva and clomid can make you feel pretty dam weird. I'm off the gear right now and I'm taking nothing at all, why? because I don't see any gyno, so why should I take anything.

[O.N.]

That's right UN you dont have gyno cause post cycle if your testosterone levels are crashed your estrogen levels are also crashed., unless you have testosterone in your system anti e's are pointless. it's like saying lets lower a hormone that is already low......why would you want to do that???

Anti e's are very effective when used when you are naturally producing testosterone.

[C_T]

how can estrogen be low in pct? and don't say hcg cause that would be lying.

[O.N.]

how can estrogen be low in pct? and don't say hcg cause that would be lying.

estrogen is created from testosterone so when you have very little testosterone you will have very little estrogen both hormones rise and fall together. There can be an imbalance but that is not the issue here post cycle the issue is if you come off steroids cold turkey (no hcg) you will have next to nothing in terms of testosterone thus estrogen will be low too.

And if you dont believe that well you might understand it further that is you know estrogen is a hormonal enemy of testosterone so do you really think if you have little to no testosterone from steroid use and not from hormonal problems that post cycle estrogen will spike to stop/slow testosterone recovery...hell no estrogen stays the hell away until levels normalise. Estrogen has no point in spiking or satying elevated and there is no hormones keeping it elevated or helping to produce more estrogen so it will also be low when testosterone is low.
If you have hormonal problems with estrogen then yes it can be higher and causing problems but you would know about these problems already as you would probably have low testosterone naturally and possibly estrogen issues gyno etc.

[RF1964]

I found this sometime ago on another site written by William Llewellyn..

Estrogen Rebound?
You’ve probably heard the term “estrogen rebound” so often that its existence is a given for you. Certainly, this phrase has become ingrained in the lore of the hard-core bodybuilding subculture, and the need for dealing with this phenomenon post-cycle, with anti-estrogens or aromatase inhibitors, is almost second nature. We are referring, of course, to the belief that estrogen levels become elevated for a period of time after steroids have been discontinued. The first several weeks post-cycle is undoubtedly a delicate window of time, with gynecomastia symptoms being a recurring problem for some people. This would seem to lend solid support for the belief that estrogen levels are becoming elevated. After all, when puffy nipples start poking out of your shirt, isn’t this just common sense? But how do we know that estrogen levels are actually running out of control in the post-cycle period, and by what mechanism would this occur? It turns out that a little investigation into the subject reveals some surprising answers, with the theory of estrogen rebound turning out to be less than entirely accurate.

The Source of Estrogen
To understand what’s going on post-cycle, it is first important to understand where estrogen comes from in men. This hormone is produced in our bodies largely through the aromatization of precursor steroids such as androstenedione and testosterone (these two steroids convert to the estrogens estrone and estradiol, respectively). It’s a process that takes place in both glandular (testes[1]) and extra glandular tissues (including adipose,[2] liver,[3] central nervous system[4] and skeletal muscle[5] tissue). Extraglandular tissues are actually the primary source for circulating estrogens in the male body, with a much smaller amount being accounted for by testicular secretion of this hormone.[6] As a result of this precursor/target hormone relationship, the availability of plasma androstenedione and testosterone are dominating factors controlling the level of estrogens in the body. That means, obviously, that if the levels of these precursor hormones drop, circulating estrogen levels will directly decline as a result.

Post-Cycle Estrogen
During the post-cycle window, of course, testosterone levels are suppressed. This restricts one of the main substrates used for the formation of estrogen in the body, which means we most certainly should not expect estrogen levels to be higher than they are normally. In fact, until testosterone production is restored to normal, estrogen levels should actually be a little lower than they were before the cycle. Studies published in 1993 with testosterone enanthate show the absence of a true “estrogen rebound” well.[7] In this male contraception trial, 28 subjects aged 22-40 years were given weekly injections of testosterone (200mg). Their hormonal profiles, including testosterone, estradiol, LH and FSH, were measured before, during, and after a 12-month period of steady therapy. Only the data from those men who had reached a state of azoospermia (suppressed sperm production) were actually included in the presented final data, giving us a good inside view of what your hormones should look like when recovering from strong endogenous testosterone suppression. The recovery period included in the investigation was six months, which was more than an ample window to chart hormonal parameters after drug withdrawal. The investigators noted that both estrogen and testosterone actually returned to pre-treatment values within the first month, and reported no unusual elevation in serum estrogen levels at all. In fact, the recovery pattern of estrogen mirrored that of testosterone very closely.

Androgen/Estrogen Imbalance
So, if estrogen levels are not elevated post-cycle, then what accounts for the individual who swears he is prone to symptoms of gyno during this period? The possible answer lies in the fact that it’s the ratio of estrogens to androgens that is most relevant to the formation of gynecomastia, not necessarily the total amount of estrogen present.[8] It turns out that androgens and estrogens play opposing roles in the growth of mammary tissue, and simply lowering the level of androgenic activity can be a trigger of this condition. Additionally, when looking at the two main sources of estrogens in the body, we find an interesting situation. Androstenedione is a hormone largely of adrenal origin,[9] which means that even as testicular steroidogenesis is diminished and testosterone suppressed, the body may still be left with pretty ample amounts of estrogen precursor hormones. Our extragonadal source of estrogen may therefore not be as drastically inhibited, causing an important and unwelcome shift in the estrogen to androgen ratio. With androgen levels not sufficient to counter estrogen’s activity in the breast, gyno could be triggered, even if levels of estrogen itself are normal or slightly suppressed. This possibility is illustrated well in a report published in the Journal of Clinical Endocrinology and Metabolism in 1980, concerning the spontaneous occurrence of gynecomastia in three elderly men one to 30 years after suffering from the mumps.[10] The men had serum testosterone concentrations of only about 20 percent of what is normal for men of their age, demonstrating a clear impairment of their bodies’ abilities to produce testosterone. Concentrations of androstenedione, estradiol and estrone, however, were within the range considered normal for healthy young men, with peripheral aromatization said to account for virtually all the estrogen produced in these subjects. The researchers suggested that the capacity of Leydig cells in the testes to secrete testosterone was impaired after mumps in the three men, but the capacity to form estrogen was not similarly impaired, since most estrogen is formed in extraglandular tissues. The resulting imbalance of androgen to estrogen ratio was likewise believed to be responsible for the onset of gynecomastia, which occurred even without high estrogen levels.

Drawing Conclusions
The above information suggests that estrogen rebound is, in fact, just another in a long line of misunderstandings in the bodybuilding world, an explanation quite off the mark of what is really happening in our bodies. If we want to be accurate, we are looking instead, of course, at a possible rebound imbalance in hormone levels. But what does this really mean to the average bodybuilder preparing to conclude his most recent steroid cycle? High estrogen levels or imbalanced estrogen/androgen ratio are going to be very similar to those in the individual prone to gynecomastia in a practical sense, so it should certainly not be interpreted as a recommendation to abandon anti-estrogens or aromatase inhibitors. These agents are indeed effective in preventing gynecomastia in either case, and well worth the money for that purpose. It does, however, allow us to look at the post-cycle window from a slightly different perspective. No longer are we to assume that estrogen is the main enemy during post-cycle recovery. In fact, we could logically conclude that this hormone may be offering less inhibition in the average post-cycle window than it does in normal physiological conditions. While there still may be reasons to include anti-estrogens in a well-thought-out recovery program, there no longer seems to be any reason to think estrogen suppression should be the sole focus of post-cycle therapy.
References

[1] Aromatase expression in the human male. Brodie A, Inkster S, Yue W. Mol Cell Endocrinol 2001 Jun 10;178(1-2):23-8
[2] Aromatization of androgens by muscle and adipose tissue in vivo. Longcope C, Pratt JH, Schneider SH, Fineberg SE. J Clin Endocrinol Metab 1978 Jan;46(1):146-52
[3] The aromatization of androstenedione by human adipose and liver tissue. J Steroid Biochem. 1980 Dec;13(12):1427-31.
[4] A review of brain aromatase cytochrome P450. Lephart ED. Brain Res Brain Res Rev 1996 Jun;22(1):1-26
[5] Aromatization by skeletal muscle. Matsumine H, Hirato K, Yanaihara T, Tamada T, Yoshida M. J Clin Endocrinol Metab 1986 Sep;63(3):717-20
[6] Origin of estrogen in normal men and in women with testicular feminization. MacDonald PC, Madden JD, Brenner PF, Wilson JD, Siiteri PK. J Clin Endocrinol Metab 1979 Dec;49(6):905-16
[7] Comparison between testosterone enanthate-induced azoospermia and oligozoospermia in a male contraceptive study. I: Plasma luteinizing hormone, follicle stimulating hormone, testosterone, estradiol, and inhibin concentrations EM Wallace, ** Gow, and FC Wu. J. Clin. Endocrinol. Metab. 77: 290-293
[8] Gynecomastia. Leung AK. Am Fam Physician 1989 Apr;39(4):215-22
[9] Proceedings: Adrenal androgens. 11. Blood androst-4-ene-3, 17-dione. Akane Y, Nawada S, Aiba H, Ueda T, Motomatsu T. Nippon Naibunpi Gakkai Zasshi 1974 Feb 20;50(2):34
[10] Androgen and estrogen production in elderly men with gynecomastia and testicular atrophy after mumps orchitis. Aiman J, Brenner PF, MacDonald PC. J Clin Endocrinol Metab 1980 Feb;50(2):380-6

[O.N.]

In fact, we could logically conclude that this hormone may be offering less inhibition in the average post-cycle window than it does in normal physiological conditions. While there still may be reasons to include anti-estrogens in a well-thought-out recovery program, there no longer seems to be any reason to think estrogen suppression should be the sole focus of post-cycle therapy.

Great post RF1964 more great info to help understand the process even further to what i have been trying to tell people.

[UN Soldier]

Just something basic here, I hear of guys pinning HCG Subcutaneously, but then on Pregynl HCG it says to pin it Intramuscularly, which is the best or correct way to do it?

[O.N.]

Just something basic here, I hear of guys pinning HCG Subcutaneously, but then on Pregynl HCG it says to pin it Intramuscularly, which is the best or correct way to do it?

either it works both ways IM is slighty more bio available but really wont make much difference.

[UN Soldier]

either it works both ways IM is slighty more bio available but really wont make much difference.

Okay excellent!

[Thrasha]

another question.
I am taking HCG 250iu every monday and thurs. I forgot to do it yesterday, should i take 40IU extra because of the missed day or is it fine just take normal 250iu?

[Heath29]

I would just keep taking as per normal. one day wont hurt you are still getting the same overall amount over a given time