Proper use of HCG

[pirovoliko]

Ive spent a few days reading DET-OAK's thread "Standard PCT" which was great and a big thanks to him for that thread. A must read IMO and Made lots of sense and well informed and explained positions and advice. Most of the other HCG info on this forum is a bit widespread and buried in threads regarding personal cycles in general. So since I plan on using HCG in my future cycles I wanted to start another thread to try and centralize opinions and advice in one thread and get a good debate going on the proper use of HCG.

For everyone convenience, Ive cut and pasted the relevant HCG info from that thread here :

HCG for light cycles. Choose one of the following. #2 is best buts it not always practical for new guys.

#1 Use 500iu's of HCG every day for the 10 days leading up to 4 days before your SERM treatment.

#2 Use 500iu's a week of HCG for your entire cycle. Then use 500iu's every day for the 10 days leading up to 4 days before SERM treatment.

HCG for heavy cycles.

I consider any cycle with a progesterone, 3 or more compounds or any cycle that includes any compounds that are not in the light cycle category, a heavy cycle.

Use 1,000 iu's a week during the cycle. Do this for 5 consecutive weeks, take a week off and start again. If you get 5,000 iu bottles of HCG you will simply run 1,000iu's a week until the bottle is gone, then take a week off and start a new bottle. Do this the entire cycle.

Blast Phase Part 2 of HCG for heavy cycles. This phase should be ran in addition to the weekly dose during the heavy cycle.

Blast your HCG during the time period you are waiting for the suppressive compounds to leave your system. This is the time period starting the day after your last injection up until 4 days before SERM treatment. The blast Phase should consist of one of the following:

#1 500iu's every day.
#2 750iu's every day.
#3 1,000iu's every other day.
#4 1,500iu's every other day.

Since HCG directly stimulate's aromatization in the leydig cells some people can develop Gyno when taking high doses of HCG. You need to get a sense of how sensitive you are to HCG when determining how you want to run your blast phase. If you are sensitive start with every day dosing.

There are 3 reasons to run a blast phase of HCG

#1 To test the testicles to see if they are still able to produce testosterone at their maximum capacity. If they can not produce testosterone at their maximum capacity you have developed hypogonadism. It would be wise to get a blood test done during this time to see if the testicles are producing enough testosterone to get your testosterone levels within physiological range. If they are not, there is no point in SERM treatment at this time and more HCG is needed. When I say more, that may mean a higher dose for longer duration, or just a longer duration.

#2 By blasting during this time we are ensuring that our testosterone is within physiological range, thus attempting to prevent going catabolic.

#3 To stimulate the pituitary. This will provide the material the testes need to produce testosterone. [END].


NOW, other threads have conflicting opinions as to HCG use, including issues of dosage (Ive seen 500-2500 ius recommended weekly) and timing (either throughout the entire cycle and blasting pre-PCT, or just blasting Pre-PCT).

SO, lets assume a cycle of test with one other AAS, whether its primo, var, tren, or EQ for example. What are some opinions on proper dosage and timing of HCG for best results in order to maintain gains and restore function?

 

[THE-DET-OAK]

here is some more good info from Scally on HCG and PCT timing.

http://www.steroidology.com/forum/anabolic-steroid-forum/156877-hcg-desensitization-does-exist.html

 

[pirovoliko]

Nice addition. Thanks bro.

 

[Jesterz623]

Risks from over-use or over-dosage of HCG

By Daniel Gwartney, M.D.

Many young bodybuilders blindly begin taking anabolic-androgenic steroids (AAS), focused only on the immediate acquisition of greater strength and muscle mass. Without condoning AAS misuse in an unsupervised fashion, and standing against AAS abuse by adolescents, it is a testament to the effectiveness of AAS that the benefits can be achieved outside of the appropriate environment or dosing schedules. Unfortunately, this greatly increases the risk of adverse side effects.

This article addresses one of the most common adverse effects of supraphysiologic AAS use***8212;suppression of endogenous (natural) testosterone production and testicular atrophy (shrinkage), as well as a relevant and applicable finding recently presented in the scientific literature.This focus is not meant to diminish the impact of other potential adverse effects. It is meant to foster discussion that may lead to a better understanding of a predictable adverse effect common to an underserved population.

Testosterone is naturally produced within the testes, in specialized cells called "Leydig cells" after the German anatomist Franz Leydig who first identified them in 1850. An alternate term, "interstitial cells of Leydig" refers to
the same cells.The production of testosterone is regulated by a negative feedback loop system called the Hypothalamic-Pituitary-Gonadal axis, or HPG axis (testes are male gonads, ovaries are female gonads).1The hypothalamus and pituitary are two glands located near the brain stem. They release stimulatory "releasing hormones" when monitored hormones that regulate the metabolism are below a threshold concentration in the blood. When a monitored hormone exceeds the "ceiling" concentration, releasing hormones are no longer released until the hormone concentration falls into the lower range of normal.

So, to make it clearer, the negative feedback loop means when there is not enough testosterone in the blood, the brain releases the "GO" signal and when there is too much testosterone, the "GO" signal is shut off and no more testosterone is produced until the excess is cleared from the blood. The "GO" signal that directly affects the Leydig cells of the testes is a pituitary hormone called "LH." It is released when the hypothalamus detects a low testosterone concentration and the hypothalamus then releases its signaling hormone, "LHRH," that orders the pituitary to release LH. So, low testosterone leads to LHRH release, which leads to LH release, resulting in increased testosterone until the hypothalamus says "enough!"

When LH stimulates the Leydig cells, a series of enzymes are activated, creating testosterone from cholesterol. Most people fail to realize that cholesterol is the building block from which all steroids are created. This is why some cholesterol-lowering drugs also lower testosterone.2 LH is not very potent and is short acting. Thus, the HPG axis is triggered by fluctuations in testosterone multiple times daily. For the average man, the peak testosterone value is approximately 30 percent higher than the low value. Human chorionic gonadotropin (hCG) is approximately four times as potent as LH and stimulates the same receptors, generating a stronger response by the Leydig cells. Typically, hCG ***8212; a hormone produced by the placenta of a fetus during pregnancy***8212; is only present in pregnant women. It is used as part of a cocktail of hormones to treat women with fertility challenges.
HCG CUTS BOTH WAYS

There are several indications for hCG use in males: cryptorchidism (undescended testes), infertility and persistent hypogonadism secondary to androgen exposure (i.e., post-cycle recovery). hCG was once considered to be an automatic method for restoring natural testosterone production post-cycle. It is likely that most AAS users would recover natural testosterone production over time anyway. However, several cases emerged of persistent hypogonadism (low testosterone) despite hCG post-cycle treatment.3,4 Typically, these cases either resolved after many months or responded to hCG in conjunction with clomiphene, hMG, Nolvadex or an aromatase inhibitor. Recently, the use of triptorelin has proven effective in a limited number of refractory cases of AAS-induced hypogonadism (low testosterone post-cycle).4

Another trend among both aging-management practitioners and illicit AAS users is the use of low-dose hCG at the same time as testosterone or AAS.5,6The intent is to keep the testes stimulated during the period that they would normally be dormant due to the suppressive effect of testosterone replacement or supraphysiologic AAS use on the HPG axis.To be clearer (this is a lesson in endocrinology, after all***8212;expect a little bit of a mental workout), when the testes are shut down by testosterone/AAS, an appropriately scheduled low-dose hCG protocol may maintain testes size, function and hasten post-cycle/therapy recovery of natural testosterone production.

Most AAS users are convinced of the necessity of using hCG post-cycle; many during cycle as well. However, inappropriately dosed, hCG can actually impair natural testosterone production and even cause the Leydig cells to die off.6,7

That last sentence should have caused a double take. Use hCG wrongly, and not only do the testes stop making testosterone but the Leydig cells die in a process called apoptosis.This has been shown in animal studies and is consistent with the results observed in cryptorchid men treated with hCG.8

Briefly, hCG needs to be used sparingly and at low dose. High doses, and especially prolonged use (greater than 10 days) of high doses, initiate a series of biochemical reactions that result in a great amount of oxidative damage as well as starting the process of apoptosis (cell death).This agrees with observations made in men suffering from tumors that produce hCG. Men with these hCG-producing tumors see an increase in testosterone as well as other steroid hormones (17-hydroxyprogesterone, estradiol, etc.) when hCG concentration is low. When tumor-produced hCG results in a high concentration of hCG, testosterone concentration is actually lower than normal and the testosterone:estradiol concentration also falls.9

A trial compared dosing hCG at 1,500, 3,000 and 4,500 IU daily for three days. No difference among the doses was noted, suggesting that the maximal stimulation occurs at or below 1,500 1U.10 Repeated daily 1,500 IU dosing maintains the testosterone response, but it is not cumulative as testosterone is rapidly cleared. Also, hCG's effect is short-lived, with testosterone peaking within a day or two and then dropping. Compared to a single 1,500 IU injection, five daily injections of 300 IU resulted in a greater total testosterone increase.11 Another study showed a maximal testosterone increase at 5,000 IU in response to a single injection, but estradiol increased considerably more.12This is consistent with the experience some bodybuilders report of gynecomastia flaring up during hCG use.

Anecdotal reports from AAS-using men support dosing hCG at or below 500 IU for daily or alternate day use. Dr. John Crisler utilizes hCG for some of his patients on testosterone replacement therapy (allthingsmale.com) and his protocol describes 250 IU administered twice weekly***8212; two days and one day prior to testosterone injection if administered via injection. He has a established a therapeutic limit of 350 IU, noting an adverse increase in testicular aromatase and Leydig cell desensitization.5
THE NAC FACTOR

These practical observations lend credence to the findings of Dr. Aggarwal and colleagues reported in the journal Molecular and Cellular Endocrinology.8 Using rats, they followed the response and cellular effects of hCG administration over 30 days, compared to placebo.They noted that though testosterone initially increased over the first week, by the end of the month there was a significant decrease in circulating (blood) testosterone. Also, the signaling system of the Leydig cells was not generating as strong a response to hCG. Aggarwal et al. noted in an earlier study that hCG induced a significant rise in oxidative stress within the Leydig cells. In fact, when compared to the control group, the Leydig cells had greater lipid peroxidation (damage), reduced glutathione (a major antioxidant) and reduced enzymes and capacity of the antioxidant system. This was associated with a marked increase in the signals that promote apoptosis. Additionally, signals that protect against apoptosis were reduced in the hCG-treated animals' Leydig cells.

Recognizing the role and potency of glutathione in protecting against oxidative damage, Aggarwal's group provided N-acetylcysteine (NAC) to certain groups of rats to look at the effect of NAC given once weekly or twice weekly- either with out without hCG. So, some rats received nothing; others received NAC once weekly; others received NAC twice weekly; others received only hCG daily; others received hCG daily and NAC once weekly and lastly, a group received hCG daily and NAC twice weekly.

NAC is a modified amino acid that is a direct precursor to glutathione. By itself, it had no significant effect upon the rats or the Leydig cells. However, during the oxidative stress induced by hCG, NAC was able to restore Leydig cell function such that it was as responsive and was not spiraling into an apoptotic state- BUT ONLY WHEN DOSED TWICE WEEKLY.8 As the hCG insult was being administered daily, and glutathione is used up during ongoing oxidative damage, it is understandable that the once-weekly NAC dosing was unable to sustain Leydig cell status under the repeated hCG attack. It would have been of interest to see if more frequent NAC dosing could have provided any further benefit.

Glutathione reduces oxidative damage by allowing itself to be oxidized, rather than essential molecules responsible for keeping cells alive and functioning. It is like a bodyguard that jumps in front of a bullet. After being "shot," glutathione can be regenerated by an enzyme called glutathione reductase. Unfortunately, the pace of regeneration can easily be outstripped by the rate of oxidative damage when a cell is stimulated to a higher rate of function. A similar pattern of oxidative damage in the testes of rats has been noted with the administration of D-aspartic acid.13 It has been noted that glutathione can be increased through supplementation with NAC, lipoic acid and vitamin D; other products also can positively affect glutathione content in the body.14

Thus, it appears that the research of Aggarwal provide a basis for a deeper understanding of the effects of hCG on the Leydig cells, and a method of reducing the desensitization to hCG treatment over a period exceeding approximately 10 days. In agreement with the observations of bodybuilders and aging management clinicians, the benefits of hCG are obtained when used with discretion in moderation. Proper treatment to protect or restore testes function appears to require no more than 350-500 IU per day, with as little as 250 IU twice a week being capable of offering benefit. Even under this limited stimulation, oxidative damage is likely to increase, making it reasonable to suggest the inclusion of NAC, alpha-lipoic acid and vitamin D in the nutritional support protocol during this time. Even when hCG is not being administered, these are practical supplements to take for health purposes, though they are not likely to have a noticeable effect on testosterone production. It is worth noting that there is a documented association between vitamin D and testosterone values in older men.15

The take-home message is that short-term hCG for post-cycle treatment will likely achieve maximal effect near 1,500 IU, though elevated aromatase activity will induce unwanted estrogen-related adverse effects.The Leydig cells will face undue oxidative stress, and if such a dose were maintained for greater than one week, apoptosis and reduced testosterone production may ensue. Optimal dosing appears to be within a range between 250-500 IU, administered two to five times weekly with antioxidant support (NAC, lipoic acid and vitamin D). Even done correctly, there remains a risk of long-term suppression with the use of high-dose AAS that does not respond to hCG or other post-cycle therapy. Bodybuilders should not disregard this potential risk, as it may lead to lifetime dependence upon testosterone replacement or testosterone deficiency if it goes undiagnosed or untreated.

 

[pirovoliko]

jesterz,
great contribution and welcome to ology.

 

[stb1041]

good info on hcg. thanks

 

[THE-DET-OAK]

Sorry to be debbie downer but whoever wrote this put in there a bunch of crap that isn't backed up at all and to be perfectly honest, the whole article is worthless.

Risks from over-use or over-dosage of HCG

By Daniel Gwartney, M.D.

 

[THE-DET-OAK]

This is from Scally and he basically tears apart every study that entire article was based on. HCG desensitization has never once been proven clinically and as a matter of fact stable elevated serum TT due to HCG has been shown in 2-6 year studies................................ if it did exist, that couldn't happen.

I was hoping to obtain the full-text document, but no luck. If anyone has it, either post of forward. This article from 1982 does not show hCG desensitization. In fact, the article states, These data indicate that continuous long term hCG administration stimulated T levels in HH. The only note for partial desensitization is a delayed "kinetic" response to hCG administration from 24 to 48 hours! It is also of interest this was over 23 months, almost 2 years with a three times per week schedule. This is a long time, yet they state the above there continued to be T production. It would be nice to know what the hCG concentration is at this schedule after almost 2 years. The following abstract that used an every 6 day schedule over a year found a consistent T production. Moreover they note that maximal T production occurs 58 hours after injection.


D'Agata R, Vicari E, Aliffi A, Maugeri G, Mongiol A, Gulizia S. Testicular Responsiveness to Chronic Human Chorionic Gonadotropin Administration in Hypogonadotropic Hypogonadism. J Clin Endocrinol Metab 1982;55(1):76-80.

Steroidogenic responsiveness to long term hCG administration (1500 U three times a week for 23 months) was characterized in 8 males with hypogonadotropic hypogonadism (HH). During hCG treatment, testosterone (T), which was in the prepuberal range under basal conditions, rose considerably to the upper end of the normal range and remained at that level during the 23 months of observation. A 2.5-fold increase was observed in serum levels of 17{beta}-estradiol (E2) an increment less than seen with T. The increment in 17{alpha}-hydroxyprogesterone was also lower than that in T throughout the study; thus, the 17{alpha}-hydroxyprogesterone to T ratio, despite continuous hCG administration, remained low. Serum androstenedione was slightly increased during hCG therapy. No significant changes were observed in serum levels of dehydroepiandrosterone. These data indicate that continuous long term hCG administration stimulated T levels in HH, with a relatively small change in E2. The kinetics of the T and E2 responses to 2000 U hCG, evaluated after 23 months of therapy, indicated that the testicular response was markedly reduced. No increment in T levels was observed at 24 h; the maximal response occurred at 48 h. This pattern of T response supports the idea that partial testicular desensitization occurs in HH patients receiving chronic treatment with hCG.


Balducci R, Toscano V, Casilli D, Maroder M, Sciarra F, Boscherini B. Testicular responsiveness following chronic administration of hCG (1500 IU every six days) in untreated hypogonadotropic hypogonadism. Horm Metab Res 1987;19(5):216-21.

The observation that the testosterone (T) response to a single intramuscular injection of hCG is prolonged suggests that currently used regimens (2-3 injections per week) to stimulate endogenous androgen secretion in hypogonadotropic hypogonadism (HH) patients have to be reassessed. Moreover, during the last few years, Leydig cell steroidogenic desensitization has been found after massive doses of hCG. The aim of the present investigation, carried out in 6 HH patients who showed no signs of puberty, was to study the effect of 1500 IU hCG administered every six days over a period of one year to induce the onset of pubertal development. To evaluate the kinetics of the response of T, 17 alpha-hydroxyprogesterone (17 alpha-OHP) and 17 beta-oestradiol (E2), blood samples were taken basally and 1, 2, 4 and 6 days after drug injection. This dynamic study was performed after the first injection and after the 4th and 12th month of treatment. During this one year time period, a progressive increase in testicular size was observed. Comparing plasma T levels (mean +/- SE) before the first injection (11.2 +/- 4.7 ng/dl) with the corresponding values at the 4th (38.7 +/- 10.5 ng/dl) and 12th months (99.5 +/- 19.9 ng/dl) of therapy, a progressive and significant increase was observed. T reached a maximum elevation 58 hours after hCG injection at the 4th month (198.3 +/- 42 ng/dl; P less than 0.01) and at the 12th month (415.6 +/- 62.6 ng/dl; P less than 0.05), whereas it remained unchanged following the first hCG injection.(ABSTRACT TRUNCATED AT 250 WORDS)

 

[Jesterz623]

Oak you've clearly got a lot of knowledge and experience and I've referenced a ton of your contributions in building my understanding of aas and related hormones.. Does the article you cited suggest that there are in fact no risks of long term hcg use?

issues I have with the study quoted are that:
1) the participants suffered from hypogonadotropic hypogonadism; thus they have no naturally occurring LH, and aren't prone to the negative feedback loop mentioned above.
2) (I'm assuming) the participants were adolescents of puberic age and not adults, whose chemistry is clearly different.

 

[THE-DET-OAK]

Oak you've clearly got a lot of knowledge and experience and I've referenced a ton of your contributions in building my understanding of aas and related hormones.. Does the article you cited suggest that there are in fact no risks of long term hcg use?

Yea sorry to come off like a dick i had a bad day.

issues I have with the study quoted are that:
1) the participants suffered from hypogonadotropic hypogonadism; thus they have no naturally occurring LH, and aren't prone to the negative feedback loop mentioned above.

This won't make a difference. A common misconception about HCG is that it "makes the HPGA move" it does not. It just stimulates the testes, and also tells the pituitary there is plenty of LH, so HCG itself is suppressive to the HPGA taking the negative feedback loop out of the equation.

2) (I'm assuming) the participants were adolescents of puberic age and not adults, whose chemistry is clearly different.

It wouldn't matter what age they were to determine desensitization. Its a pair of balls and either they continually accepted stimulation or they didn't, and they did.

If anything performing the study on men that were older would just show that you would need more HCG, not less.

 

[THE-DET-OAK]

Edit

There is some stimulation at the pituitary but it irrelevant to the question.

also keep in mind both Scally and Chrisler refer to the same study

 

[bigsixx]

What about introducing Human Chorionic Gonadotropin (HCG) for lets say, the last 4 weeks of cycle at low doses then blasting the ten days after last pin?
Just a question, please dont tear me a new one lol