HCG according to theory should be ineffective. Discuss

[Juicin]

Everyone seems to like running HCG at the end of a suppressing cycle. Is it really that effective? According to my theory i would say not but i am not basing this off of anecdotal evidence or actual HCG testing.

So... We all know the negative feedback loop involving HPTA but if you dont, then here is a quick summary. The hypothalamus releases GnRH (gonadotropic releasing hormone) to the anterior pituitary through the hypophysial portal system. The pituitary in response to this hormone secretes LH (luteinizing hormone) and FSH (follicle stumulating hormone) whos target is the the leydig and sertoli cells of the testis respectively. LH causes testosterone production and FSH causes spermatogenesis. Testosterone circulates in blood bound to SHBG and has an effect at the hypothalamus and pituitary. Increased test inhibits GnRH at hypothalamus and LH at anterior pituitary. Thus the increased test from aas usage causes shutdown and we run pct

Now, HCG is a LHR (LH-receptor) agonist, which tricks the testis into producing testosterone.

This is where my theory comes in.

According to scientific data, when the GnRH causes LH and FSH secretion, there is a permissive action of FSH on LH receptors. The action of LH is dependent on FSH induction at Leydig cells. FSH increases LHR population in Leydig cells, thus increasing the response to LH.

Now it comes together.
At the end of a cycle, both LH and FSH secretion are minimal due to negative feedback loops. When we take HCG to mimic LH action of testosterone production are we really doing much considering the low concentration of FSH? My theory would say no, but again this is just theory.

Could an FSH analog increase the effectivness of HCG by permissive action during pct?

Anyway i thought this would be an interesting discussion.

What do you guys think?

 

[needtogetaas]

Good read. Looks like something I have seen before.

 

[Big_Joe]

Everyone seems to like running HCG at the end of a suppressing cycle. Is it really that effective? According to my theory i would say not but i am not basing this off of anecdotal evidence or actual HCG testing.

So... We all know the negative feedback loop involving HPTA but if you dont, then here is a quick summary. The hypothalamus releases GnRH (gonadotropic releasing hormone) to the anterior pituitary through the hypophysial portal system. The pituitary in response to this hormone secretes LH (luteinizing hormone) and FSH (follicle stumulating hormone) whos target is the the leydig and sertoli cells of the testis respectively. LH causes testosterone production and FSH causes spermatogenesis. Testosterone circulates in blood bound to SHBG and has an effect at the hypothalamus and pituitary. Increased test inhibits GnRH at hypothalamus and LH at anterior pituitary. Thus the increased test from aas usage causes shutdown and we run pct

Now, HCG is a LHR (LH-receptor) agonist, which tricks the testis into producing testosterone.

This is where my theory comes in.

According to scientific data, when the GnRH causes LH and FSH secretion, there is a permissive action of FSH on LH receptors. The action of LH is dependent on FSH induction at Leydig cells. FSH increases LHR population in Leydig cells, thus increasing the response to LH.

Now it comes together.
At the end of a cycle, both LH and FSH secretion are minimal due to negative feedback loops. When we take HCG to mimic LH action of testosterone production are we really doing much considering the low concentration of FSH? My theory would say no, but again this is just theory.

Could an FSH analog increase the effectivness of HCG by permissive action during pct?

Anyway i thought this would be an interesting discussion.

What do you guys think?

Your theory has a big glaring error. Testosterone levels do not suppress the hypothalamus, estrogen does. When aromatase converts testosterone into estrogen and the increasing levels of estrogen suppress the hypothalamus. So an AI is called for.

The reason one uses Hcg is to stimulate the leydig cells before the HPTA turns back on. Little balls don't work so well. That's why one should run it during cycle. If not near the end of the cycle. It's better to prevent shrinkage then to try and correct it after it has happened.

Love your balls and they will love you back.

 

[Juicin]

Your theory has a big glaring error. Testosterone levels do not suppress the hypothalamus, estrogen does. When aromatase converts testosterone into estrogen and the increasing levels of estrogen suppress the hypothalamus. So an AI is called for.

The reason one uses Hcg is to stimulate the leydig cells before the HPTA turns back on. Little balls don't work so well. That's why one should run it during cycle. If not near the end of the cycle. It's better to prevent shrinkage then to try and correct it after it has happened.

Love your balls and they will love you back.

I beleive you are wrong if i remember correctly. Estrogen increases testosterone production, hence the use of SERMs And testosterone does in fact feed back at the hypothalamus.

 

[SofaGeorge]

Theories are great, but they often don't hold much value. In reality, 600 iu HCG three days in a row then three days off for two weeks works great.

 

[the_alcatraz]

How many believe HCG is a little suppressive?

 

[Juicin]

run in long duration i would imagine it would be a little suppressive, that is supposing it actually works when shutdown. Increasing LH increases test which would shut one down. I never ran HCG but i know an ai should be used to combat aromatization. I wouldnt know though just talking hypothetically

 

[Roc86]

HCG doesnt really help with recovery ... its more effective for avoiding primary tesicular failure -- or "dormant nuts".

While on cycle using HCG or not your pituitary wont be releasing LH so fuck it --> give yourself a pinch of HCG E3D and keep the boys awake, then use Nolva and aromasin for PCT to get the Hypothalamus and pituitary in working order ASAP.

 

[Big_Joe]

I beleive you are wrong if i remember correctly. Estrogen increases testosterone production, hence the use of SERMs And testosterone does in fact feed back at the hypothalamus.

Maybe you should do a little more research. If estrogen increased testosterone production there would be an ever increasing amount of testosterone because of the aromatase enzyme. Aromatase converts testosterone into estrogen. If the amount of estrogen increases the amount of testosterone that would be a signal to produce more testosterone. Then aromatase would convert more testosterone into more estrogen that would produce more testosterone. So your idea that estrogen increases testosterone production can't be accurate.

And this is why your theory dosen't hold water. It's basic assumptions are wrong.

 

[Nelson Montana]

Your theory has a big glaring error. Testosterone levels do not suppress the hypothalamus, estrogen does. When aromatase converts testosterone into estrogen and the increasing levels of estrogen suppress the hypothalamus. So an AI is called for.

The reason one uses Hcg is to stimulate the leydig cells before the HPTA turns back on. Little balls don't work so well. That's why one should run it during cycle. If not near the end of the cycle. It's better to prevent shrinkage then to try and correct it after it has happened.

Love your balls and they will love you back.

It is not estro which supresses T, it's any exogenous influx and that includes HCG.

HCG doens;t cure anything, it just helps get the boys up and running and should not be used for too long or at too high of a dosage. This is where supps like UNLEASHED and Sustain also help recovery because they work WITH the body as opposeed to being a "false" elevation.

HMG may be a better option to HCG. I'm exploring that now.

 

[guarded_one]

Great Nelson...Keep us posted!

 

[Big_Joe]

It is not estro which supresses T, it's any exogenous influx and that includes HCG.

HCG doens;t cure anything, it just helps get the boys up and running and should not be used for too long or at too high of a dosage. This is where supps like UNLEASHED and Sustain also help recovery because they work WITH the body as opposeed to being a "false" elevation.

HMG may be a better option to HCG. I'm exploring that now.

I think there is a communication problem here. I never said that Hcg cures anything. And yes if you take testosterone you will stop producing testosterone. But your body has a mechanism to regulate the production of testosterone. That mechanism is the aromatase enzymes conversion to estrogen of testosterone. The signal that tells the hypothalamus to stop stimulating the pituitary is estrogen. This is what happens in a normal male. And is also why when you take an AI you get an increase in testosterone production.

Once you start injecting testosterone you get an increase in estrogen, that's one of the reasons people get gyno. It's the increase in estrogen that shuts you down. Not the increase of testosterone.

And to back up what I say with an outside source here is a link:
Hypothalamic-pituitary-gonadal axis in two men with aromatase deficiency: evidence that circulating estrogens are required at the hypothalamic level for the integrity of gonadotropin negative feedback -- Rochira et al. 155 (4): 513 -- European Journa

I'll make it easy for you and copy the important part.
"In men, the feedback of gonadotropins is regulated by estrogens that come from the aromatization of testosterone"

I'm actually surprised and dismayed that a person that reports to sell products that "work with the body" didn't understand this basic concept.

 

[access]

I think it's fair to also say that HCG doesn't cure anything or HCG doesn't aid recovery is also misleading. Going into PCT with your testes not in atrophy, thanks to low dose supplmentation of HCG on cycle is an obvious asset to recovery and a primary reason why we run HCG on cycle to begin with.

 

[Nelson Montana]

I think there is a communication problem here. I never said that Hcg cures anything. And yes if you take testosterone you will stop producing testosterone. But your body has a mechanism to regulate the production of testosterone. That mechanism is the aromatase enzymes conversion to estrogen of testosterone. The signal that tells the hypothalamus to stop stimulating the pituitary is estrogen. This is what happens in a normal male. And is also why when you take an AI you get an increase in testosterone production.

Once you start injecting testosterone you get an increase in estrogen, that's one of the reasons people get gyno. It's the increase in estrogen that shuts you down. Not the increase of testosterone.

And to back up what I say with an outside source here is a link:
Hypothalamic-pituitary-gonadal axis in two men with aromatase deficiency: evidence that circulating estrogens are required at the hypothalamic level for the integrity of gonadotropin negative feedback -- Rochira et al. 155 (4): 513 -- European Journa

I'll make it easy for you and copy the important part.
"In men, the feedback of gonadotropins is regulated by estrogens that come from the aromatization of testosterone"

I'm actually surprised and dismayed that a person that reports to sell products that "work with the body" didn't understand this basic concept.

You can save the not so subtle snide remarks. You're so wrong dude. You're reading that abstract incorrectly and I don't feel like explaining it to you. Gyno has NOTHING to do with supression. According to your thinking, as long as estro is low, the body will keep making T, and that's patently absurd.

 

[mus1cjunk1e]

I just want to chime in and say that without a doubt hcg does in fact aid in recovery. After a series of stupid cycles with no pct, I was shutdown hard. Months later my balls were still half size and hanging down far. I ran hcg at 1000iu EOD until a 5000iu vial was gone and started on nolvadex at 20mg a day. Within an hour or two of my first hcg shot my balls were back to full size. After I concluded the hcg shots, they stayed that way and were up closer to my body not hanging so low. I ran the nolvadex for 1 month. When that was over I was 90% recovered. Within another month I was 99% recovered (sex drive, ball size, etc).

So to say that both hcg and nolvadex are ineffective at recovering a supressed htpa is 100% completely wrong. I hear people bad mouthing nolvadex all the time on here saying it doesn't work and blah blah blah, and now I'm reading in this thread people saying hcg doesn't even actually help you recover. This is just wrong people. One month of nolvadex and 1 vial of hcg later and I was recovered when I had been shutdown/highly suppressed for months.

You guys can theorize all you want, I'm just telling you what actually worked for me. Just look at the quote in my sig for my thoughts on theory and actual reality.

 

[Big_Joe]

You can save the not so subtle snide remarks. You're so wrong dude. You're reading that abstract incorrectly and I don't feel like explaining it to you. Gyno has NOTHING to do with supression. According to your thinking, as long as estro is low, the body will keep making T, and that's patently absurd.

If you think that I am saying that low estrogen creates an unlimited increase in testosterone production you are not reading what I wrote correctly. What I said was increased levels of estrogen signal the hypothalamus to stop signaling the pituitary and thus the testicles stop producing testosterone. That's what this quote says "In men, the feedback of gonadotropins is regulated by estrogens that come from the aromatization of testosterone"

How you twisted it around to make it backwards I have no idea.

And it's not a snide remark it's exactly how I feel about the situation. Comments like "You are so wrong and I don't feel like explaining it to you" are just comments from someone that doesn't want to exemplify his ignorance but wants people to think he has all the answers. You haven't added any information to this thread at all.

And how you linked gyno to suppression is beyond be. Gyno comes from increased estrogen, most of the time, and that's what I said. Are you smoking or drinking something? I just don't see how you could draw the conclusions you did from what I wrote.

Here is another link for you:
Aromatase Inhibition in the Human Male Reveals a Hypothalamic Site of Estrogen Feedback -- Hayes et al. 85 (9): 3027 -- Journal of Clinical Endocrinology & Metabolism

And here is the important part:
"Anastrozole suppressed E2 equivalently in the NL (136 ± 10 to 52 ± 2 pmol/L, P < 0.005) and IHH men (118 ± 23 to 60 ± 5 pmol/L, P < 0.005). Testosterone levels rose significantly (P < 0.005), with a mean increase of 53 ± 6% in NL vs. 56 ± 7% in IHH men."

It's fairly clear that the use of an AI increases testosterone levels because of the suppression of the feed back loop, lower estrogen increases testosterone output. There is an inverse relationship between estrogen and testosterone in the male. And so others don't have to read the article E2 is estradiol.

So after reading this abstract how do you justify a statement like "According to your thinking, as long as estro is low, the body will keep making T, and that's patently absurd." This article supports everything I said and refutes what you said. In this study there is a lowering of estrogen and a concurrent increase of testosterone.

 

[SofaGeorge]

Nelson, how many trial runs have you made with HMG on yourself?