HCG PCT! Help needed!

[Primordial Performance]

This is totally incorrect. Im sorry Eric but it couldnt be further from the truth. You will find some studies on rats, although you wil not find 1 single study backing up HCG desensitization clinically, not 1.

It does not happen its bro-lore myth. The only time it will ever actually happen is if HCG is dosed higher than 5,00 iu's at a time.

If you would like to disagree with thats fine, all I can say is PROVE IT.

Sometimes logic takes awhile to set in. Look around and talk to Hormone Replacement Therapy (HRT) patients and ask how long their 500iu EXD protocol worked for them. It rarely keeps T levels in the normal range for any longer than a couple months.

-Eric

 

[Primordial Performance]

How exactly does HCG inhibit GNRH? HCG stimulates the pituitary, in turn stimulating GNRHR, which is the receptor for GNRH.

hCG does not stimulate the pituitary. It bypasses it entirely. This article talks about that a bit - Health and fitness articles: Opioid-Modulation for preventing AAS induced HPTA supression

hCG will inhibit GHRH and LH release by negative feedback. Saying hCG increases GHRH is like saying LH increases it. hCG is mimetic of LH.

FYI, hCG is heterodimeric, with an alpha subunit identical to that of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and beta subunit that is unique to hCG.

Also the point im trying to make is that taking HCG during the time you are waiting to start your SERM is very important because at this time that same direct stimulation will provide the material the testicles need to make testosterone. By not taking it during this time you are allowing down regulation of that effect, since the suppress AAS in your system will be be suppressing the pituitary. You are also allowig your testicels to be suppressed by the still roaming AAS, when you worked so hard to keep them alive the entire cycle. Im sorry but it does not make any sense to me at all. Stoping HCG 4 days before SERM treatment should be plenty of time.

brolore here.

I like PP I think you have great products. Especially Pre-max and Sustain Alpha. I think these can be a great addition to any post cycle therapy (pct). I just dont agree with this HCG protocol thats all.

You will agree with it when you learn more about it.

I know our products are great. Thank you.

-Eric

 

[Primordial Performance]

I read, was very informative.

Problem is, when running Primobolan, Test Acetate, Materon and Tren - its nearly impossible for me to get the timing right.

Someone else recommended one 5000iu shot of HCG on monday, and one on friday. Another has said 1,000 IU EOD for 8 days.

Whats ur opinion?

I have 7mls left of the Test Ace/Tren and Masteron blend.

I have 7 mls Primobolan.

I have an idea but I need some help organising this.

If you havent started the cycle yet, then run hCG 250iu E4D during the cycle.

-Eric

 

[kmid]

primordial, hope you can give some advice in my thread 'low testosterone'?

 

[THE-DET-OAK]

you can sit there like a big shot if you want and act like i dont know what im talking about but your absolutely wrong in your article every step of the way. I will prove you wrong step by step but it may take me some time to put my articles together.

Keep in mind I corrected myself and said HCG stimulates, or up regulates the GNRH receptor. Thats what GNRHR is.

Now lets first get out of the way your ridiculous theory of stopping HCG a full 2 weeks before SERM treatment "so the testes can re-sensitize". The following document on HCG will show 2 things.

#1 HCG is virtually undetectable within 72 hours.

#2 That the decrease in serum T levels after continuous use of HCG has ABSOLUTELY nothing to do with desensitisation. The ONLY thing it has to do with is the negative feedback loop from the increased T levels due to Human Chorionic Gonadotropin (HCG). Simply your testicles refract and stop producing as much cause there is plenty in your system. The are not "desensitized". Youhave not provided one oounce of clinial proof that your theory of "desensitization even exist, after i have REPEATEDLY asked you to do so.

The purpose of running it during the cycle is to maintain sensitivity only. Getting hCG well out of the system allows the testes 1-2 weeks to re-sensitize again. The half-life of hCG is about 2-3 days.

Clinical Pharmacology - HCG:

The action of HCG is virtually identical to that of pituitary LH, although HCG appears to have a small degree of FSH activity as well. It stimulates production of gonadal steroid hormones by stimulating the interstitial cells (Leydig cells) of the testis to produce androgens.

Thus HCG sends the same message and results in increased testosterone production by the testis due to HCG's effect on the leydig cells of the testis. HCG therapy uses the body's own biochemical stimulating mechanisms to increase plasma testosterone level.

Following intramuscular injection, an increase in serum HCG concentrations may be observed within 2 hours; peak HCG concentrations occur within about 6 hours and persist for about 36 hours. Serum HCG concentrations begin to decline at 48 hours and approach baseline (undetectable) levels after about 72 hours.
HCG is not a steroid and is administered to assists the body in the continuing production of its own natural testosterone as a result of LH signals stimulating production of testosterone by the testis.

This LH stimulates the production of testosterone by the testes in males. Thus HCG sends the same message as LH to the testes and results in increased testosterone production by the testes due to HCG's effect on the leydig cells of the testes. In males, hCG mimics LH and helps restore and maintain testosterone production in the testes. If HCG is used for too long and in too high a dose, the resulting rise in natural testosterone will eventually inhibit its own production via negative feedback on the hypothalamus and pituitary.
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-DET-OAK]

Here is my "Bro-lore" from Dr. Crisler

"But theres another metabolic reason to employ this protocol. The P450 Side Chain Cleavage enzyme, which converts CHOL into pregnenolone at the initiation of all three metabolic pathways CHOL serves as precursor (the sex hormones, glucocorticoids and mineralcorticoids), is actively stimulated, or depressed, by LH concentrations. It is intuitively consistent that during conditions of lowered testosterone levels, commensurate increases in LH production would serve to stimulate this conversion from CHOL into these pathways, thereby feeding more raw material for increased hormone production. And vice versa. Thus the addition of HCG (which also stimulates the P450scc enzyme) helps restore a more natural balance of the hormones within this pathway in patients who are entirely, or even partially, HPTA-suppressed."

There are numerous studies backing up his claim, I guess you will figure it out when YOU learn more about HCG.

I will back later to prove how HCG up regulates the GNRH receptor.

 

[THE-DET-OAK]

If you havent started the cycle yet, then run hCG 250iu E4D during the cycle.

-Eric

This is just atrocious to me, you recommend a dose MUCH lower than your OWN reference supports.

 

[THE-DET-OAK]

HCG densensitization from DR. Michael Scally

HCG desensitization DOES NOT occur clinically. Anyone who says it does, does not know the literature, is trying to advance a myth, and probably believes in the hCG diet! Can hCG desensitization occur? Absolutely. There are many animal models demonstrating this effect, but, again, this effect is NOT seen clinically in FDA approved doses or less. Is there evidence for hCG desensitization in humans for hCG doses higher than FDA approved levels? Indirectly, a single (just one thats why you couldnt post any back up to your claim) study in does over 5,000 IU exploring testicular response to hCG administration reveals a leveling of T production.

hCG administration does stimulate estradiol and progesterone production. In fact, the estradiol rise occurs before the T rise.

The article "van Bergeijk L, Gooren LJ, van der Veen EA, de Vries CP. Effects of short- and long-term administration of tamoxifen on hCG-induced testicular steroidogenesis in man: no evidence for an oestradiol-induced steroidogenic lesion. Int J Androl 1985;8(1):28-36,: cited as support does nothing of the sort. This is a vain attempt to confuse the issue and by hopefully presenting a peer-reviewed article to win the argument. It ain't gonna work!

According to the abstract, the study examines the effect of tamoxifen hCG-induced testicular steroidogenesis. They do not use a model of hCG desensitization. The study is exploring a "local" effect of estradiol on T production. In fact, if you even give the slightest thought the study is about hCG desensitization, the study would not work!!! Duh . . . If the cells were desensitized to hCG, they would not produce estradiol or T, thus NO study on tamoxifen effects.


Another study (abstract below) cited by another forum is "Tang P-Z, Tsai-Morris CH, Dufau ML. Regulation of 3{beta}-Hydroxysteroid Dehydrogenase in Gonadotropin-Induced Steroidogenic Desensitization of Leydig Cells. Endocrinology 1998;139(11):4496-505." THIS IS A STUDY IN RATS!!! This expert is so desperate to prove him/herself. they cite rat studies. If we were to translate this study to humans, which is fraught with so many pitfalls, the easiest method is by dose (IU/kg). The dose for the rats is 100-125 IU/kg. For a 75 kg human, this would be 7,500 IU or more. A dose more than FDA approved, used clinically, and what they claim to cause hCG desensitization.


3{beta}-hydroxysteroid dehydrogenase/{Delta}5-{Delta}4 isomerases (3{beta}-HSD) are enzymes that catalyze the conversion of {Delta}5 to {Delta}4 steroids in the gonads and adrenal for the biosynthesis of sex steroid and corticoids. In gonadotropin-desensitized Leydig cells, from rats treated with high doses of human CG (hCG), testosterone production is markedly reduced, a finding that was attributed in part to reduction of CYP17 expression. In this study, we present evidence for an additional steroidogenic lesion induced by gonadotropin. Using differential display analysis of messenger RNA (mRNA) from Leydig cells of rats treated with a single desensitizing dose of hCG (2.5 {micro}g), we found that transcripts for type I and type II 3{beta}-HSD were substantially (5- to 8-fold) down-regulated. This major reduction, confirmed by RNase protection assay, was observed at the high hCG dose (2.5 {micro}g), whereas minor or no change was found at lower doses (0.01 and 0.1 {micro}g). In contrast, 3{beta}-HSD mRNA transcripts were not changed in luteinized ovaries of pseudopregnant rats treated with 2.5 {micro}g hCG. The down-regulation of 3{beta}-HSD mRNA in the Leydig cell resulted from changes at the transcriptional level. Western blot analysis showed 3{beta}-HSD protein was significantly reduced by hCG treatment, with changes that were coincidental with the reduction of enzyme activity and temporally consistent with the reduction of 3{beta}-HSD mRNA but independent of LH receptor down-regulation. The reduction of 3{beta}-HSD mRNA resulting from transcriptional inhibition of gene expression, and the consequent reduction of 3{beta}-HSD activity could contribute to the inhibition of androgen production in gonadotropin-induced steroidogenic desensitization of Leydig cells. The gender-specific regulation of 3{beta}-HSD by hCG reflects differential transcriptional regulation of the enzymes to accommodate physiological hormonal requirements and reproductive function

In case the readers did not notice this is the same study PP is referencing in its atricle to back up its "desensitization theory".......................

 

[THE-DET-OAK]

Doses of 250iu E3D with Dr. Scally

I am a proponent of hCG use during testosterone replacement therapy (TRT) or cycling. The question is the dose. I have written often that 250 IU is inadequate. I prefer 500 IU SC Q3D throughout the AAS administration. I do think that it aids it bringing the testes back online. However, this does not mean to stop hCG after stopping AAS. One must have a sense of the testes response to hCG. Also, from the posts I have read, the HPTA is not in an environment for functioning after AAS administration. The half-lives of the AAS must be taken into consideration.

The first phase of the HPTA protocol examines the functionality of the testicles by the direct action of hCG. hCG raises sex hormone levels directly through the stimulation of testis and secondarily decreases the production and level of the gonadotropin LH. The increase in serum testosterone with the hCG stimulation is useful in determining whether any primary testicular dysfunction is present.

This initial value is a measure of the ability of the testicles to respond to stimulation from the hCG. Demonstration of HPTA functionality is by an adequate response of the testicles to raise the serum level of T well into the normal range. If this is observed the hCG is discontinued. The failure of the testes to respond to an hCG challenge is indicative of primary testicular failure.

In the simplest terms, the first half of the protocol is determine testicular production and reserve by direct stimulation with hCG. If one is unable to obtain adequate (normal) levels successfully to the first half there is little cause or reason to proceed to the second half.






During AAS administration, the purpose of hCG can be to maintain testes size, testosterone synthesis, and/or spermatogenesis. They are not the same. For simplicity, cycling is to maintain testosterone synthesis. Do you want this to be at a near maximal rate or minimal rate? The answer to this will provide the answer for the hCG dose.

The use of 250 IU is a waste of time and money. I am willing to administer 500 IU Q3D (every three days), although, 1000 IU Q3D is probably more worthwhile. Remember, the idea is to STIMULATE MAXIMALLY T synthesis, not tickle it!!! During PCT, I use hCG 2,000-2,500 IU QOD. hGH has been shown to stimulate T synthesis.

 

[moremuscleplease]

If I was running this particular cycle and wanted to do a post cycle therapy (pct) after I would wait till the end of the 4th week beginning of the 5th week. that will give your body time to have most of the aas close to being completely out of your system. Then I would start taking 1 mg arimidex every day, every 3rd or 4th day I would be using hcg at 1500 for three weeks. I wouldn't use the nolva unless I had a problem mid cycle I'm not a fan of it post cycle and I don't like clomid at all.

 

[THE-DET-OAK]

Dr. Scally specializes in ASIH (anabolic steroid induced hypogonadism)

He has helped thousands of patients recover their HPTA. What is your reason for going aginst his writings that 250iu E4D is a waste of time an money?

You are not allowed to use the desensitization crap until you can actually prove that it happens IN MALES.

Please do not resort to posting studies on animals because i have numerous studies showing that the action of HCG is specie's specific.

This time instead of just giving me your opinion you can actually back up your recommendations with some sort evidence.

 

[THE-DET-OAK]

If I was running this particular cycle and wanted to do a post cycle therapy (pct) after I would wait till the end of the 4th week beginning of the 5th week. that will give your body time to have most of the aas close to being completely out of your system. Then I would start taking 1 mg arimidex every day, every 3rd or 4th day I would be using hcg at 1500 for three weeks. I wouldn't use the nolva unless I had a problem mid cycle I'm not a fan of it post cycle and I don't like clomid at all.

This is an ancient protocol, if you would like to use this yourself that is fine, but please keep it to yourself.

 

[moremuscleplease]

I just wouldn't use it during my cycle. The reason I would use it this way is because I know that it works its cost effective. I've done cycles many different ways and I find it to be very effective. mind you most of the guys I know and train with now don't even bother coming off at all anymore. Any thing that I am willing to post up is because I've tried it and not just thought about it, or read an article or two.

 

[THE-DET-OAK]

I just wouldn't use it during my cycle. The reason I would use it this way is because I know that it works its cost effective. I've done cycles many different ways and I find it to be very effective. mind you most of the guys I know and train with now don't even bother coming off at all anymore. Any thing that I am willing to post up is because I've tried it and not just thought about it, or read an article or two.

HCG is suppressve to your endogenous T production.

All your doing with your adex is crashing your estrogen, not a smart move at all my man.

 

[moremuscleplease]

I'll try and find the study again man but the one that I read was talking how arimidex has the ability to increase your natural test leves by up to 50% in the first 3 days of administering. That is the reason that I usually opt for that and the hcg all I've ever read is that it will increase your natural production in the short term but if used long or too high a dose will surpress it. But I will for sure read your info sources. I don't claim to be an expert I just wish to offer up what I have tried and read to have worked as well as what I have learned from my trainer. I'm just here to learn and try to help as well.

 

[THE-DET-OAK]

arimadex DOES NOT raise T production it only raises T levels for a short period of time.

Think of it as a tetor totter, its not letting your T convert to estrogen so therefore T levels will be automatically higher. Your body will eventually regulate this action by halting T production.

The reason why adex can be used for post cycle therapy (pct) is because you are erasing ALL of your estrogen. Your body needs estrogen, most of the receptors are in your joints, this is why your joints will hurt during this time. Estrogen is also responsible for some brain function so haveing 0 will give you headaches.

Your body then realizes it has no estrogen, the only way it can produce more is by creating T to convert to estrogen. SO moderate doses will not help the HPTA recover, but high doses and letting your estro crash will.

although this works it is not good for you at all.

The best way would be to use an Aromatase inhibitor (AI) along with a SERM to recover. The problem with adex and letro is their action will be SUBSTANTUALLY inhibited by the use of a SERM in conjunction. This is why Aromasin is the recommended Aromatase inhibitor (AI) to use during SERM therapy. Aromasin is not affected by the use of a SERM.

 

[Primordial Performance]

HCG desensitization DOES NOT occur clinically. Anyone who says it does, does not know the literature, is trying to advance a myth, and probably believes in the hCG diet! Can hCG desensitization occur? Absolutely. There are many animal models demonstrating this effect, but, again, this effect is NOT seen clinically in FDA approved doses or less. Is there evidence for hCG desensitization in humans for hCG doses higher than FDA approved levels? Indirectly, a single (just one thats why you couldnt post any back up to your claim) study in does over 5,000 IU exploring testicular response to hCG administration reveals a leveling of T production.

hCG administration does stimulate estradiol and progesterone production. In fact, the estradiol rise occurs before the T rise.

The article "van Bergeijk L, Gooren LJ, van der Veen EA, de Vries CP. Effects of short- and long-term administration of tamoxifen on hCG-induced testicular steroidogenesis in man: no evidence for an oestradiol-induced steroidogenic lesion. Int J Androl 1985;8(1):28-36,: cited as support does nothing of the sort. This is a vain attempt to confuse the issue and by hopefully presenting a peer-reviewed article to win the argument. It ain't gonna work!

According to the abstract, the study examines the effect of tamoxifen hCG-induced testicular steroidogenesis. They do not use a model of hCG desensitization. The study is exploring a "local" effect of estradiol on T production. In fact, if you even give the slightest thought the study is about hCG desensitization, the study would not work!!! Duh . . . If the cells were desensitized to hCG, they would not produce estradiol or T, thus NO study on tamoxifen effects.


Another study (abstract below) cited by another forum is "Tang P-Z, Tsai-Morris CH, Dufau ML. Regulation of 3{beta}-Hydroxysteroid Dehydrogenase in Gonadotropin-Induced Steroidogenic Desensitization of Leydig Cells. Endocrinology 1998;139(11):4496-505." THIS IS A STUDY IN RATS!!! This expert is so desperate to prove him/herself. they cite rat studies. If we were to translate this study to humans, which is fraught with so many pitfalls, the easiest method is by dose (IU/kg). The dose for the rats is 100-125 IU/kg. For a 75 kg human, this would be 7,500 IU or more. A dose more than FDA approved, used clinically, and what they claim to cause hCG desensitization.


3{beta}-hydroxysteroid dehydrogenase/{Delta}5-{Delta}4 isomerases (3{beta}-HSD) are enzymes that catalyze the conversion of {Delta}5 to {Delta}4 steroids in the gonads and adrenal for the biosynthesis of sex steroid and corticoids. In gonadotropin-desensitized Leydig cells, from rats treated with high doses of human CG (hCG), testosterone production is markedly reduced, a finding that was attributed in part to reduction of CYP17 expression. In this study, we present evidence for an additional steroidogenic lesion induced by gonadotropin. Using differential display analysis of messenger RNA (mRNA) from Leydig cells of rats treated with a single desensitizing dose of hCG (2.5 {micro}g), we found that transcripts for type I and type II 3{beta}-HSD were substantially (5- to 8-fold) down-regulated. This major reduction, confirmed by RNase protection assay, was observed at the high hCG dose (2.5 {micro}g), whereas minor or no change was found at lower doses (0.01 and 0.1 {micro}g). In contrast, 3{beta}-HSD mRNA transcripts were not changed in luteinized ovaries of pseudopregnant rats treated with 2.5 {micro}g hCG. The down-regulation of 3{beta}-HSD mRNA in the Leydig cell resulted from changes at the transcriptional level. Western blot analysis showed 3{beta}-HSD protein was significantly reduced by hCG treatment, with changes that were coincidental with the reduction of enzyme activity and temporally consistent with the reduction of 3{beta}-HSD mRNA but independent of LH receptor down-regulation. The reduction of 3{beta}-HSD mRNA resulting from transcriptional inhibition of gene expression, and the consequent reduction of 3{beta}-HSD activity could contribute to the inhibition of androgen production in gonadotropin-induced steroidogenic desensitization of Leydig cells. The gender-specific regulation of 3{beta}-HSD by hCG reflects differential transcriptional regulation of the enzymes to accommodate physiological hormonal requirements and reproductive function

In case the readers did not notice this is the same study PP is referencing in its atricle to back up its "desensitization theory".......................

So your saying that you believe 500iu E3D is superior to 250iu E4D like I recommend? Thats what you've been meaning to say the whole time?

Obviously, your going to get different opinions from different authorities referencing different data from different studies.

I'm actually working with Dr. Scally right now on several articles. Ill ask him about why he thinks there is no desensitization in the leydigs from hCG, because it certainly occurs in clinical practice and this is in hypogonadal men that dont have low testosterone levels to begin with!

If you want a human study, i suggest you check this out -
Low-Dose Human Chorionic Gonadotropin Maintains Intratesticular Testosterone in Normal Men with Testosterone-Induced Gonadotropin Suppression -- Coviello et al. 90 (5): 2595 -- Journal of Clinical Endocrinology & Metabolism

Notice how the 250iu is about 95% as effective as the 500iu. That should tell you something about the dose response relationship. I took this a step further with the increased sensitivity theory from frequency reduction, thus my recommendation for 250iu E4D.

-Eric

 

[THE-DET-OAK]

Listen you keep skurting the issue at hand. Its not the fact that you recommend too low of a dose, its more of a case that your entire article is based on the fact that desensitization occurs in clinical doses, and im sorry but it just doesnt. take desensitization away from you and the entire article needs to be re-written. I will look at your study in a minute but i have a feeling it will simply discuss the refractory period due to the biphasic pattern of HCG, I have studied this extensively.

things like using low doses because of desensitization, taking 2 weeks off of HCG before starting SERM treatment, that stuff goes out the window until you can prove desensitization.

 

[Swan]

The-det-oak owned this thread, if hcg was a immigrant girl trying to get her green card by marrying an american, she would have to choose the-det-oak to pass the "were a real couple" test

 

[THE-DET-OAK]

Ill ask him about why he thinks there is no desensitization in the leydigs from hCG, because it certainly occurs in clinical practice and this is in hypogonadal men that dont have low testosterone levels to begin with!-Eric

Like i said you keep saying this but have yet to produce 1 single shred of eveidence.

This is because it is hear say. It is a myth.

I would be polite when asking Dr. Scally about desensitization because he gets very offended when people try to advance that myth, that is one of his biggest problems with Dr. Crisler