HCG info...no broscience please

[TrojanMan60563]

I talk to my endo today about taking HCG while on TRT to keep my "boys" working while on TRT for the sake of easier recovery if I stop TRT, or if I decide to not pull out (knock someone up). He said it can be run at lower dose i.e. 250/500iu forever if I wanted as a form of therapy. I spoke to him in more depth about how it works and what he told me makes me question why people that cycle steroids take it during a cycle to speed up recovery. He told me the pituitary gland sends luteinizing hormone to stimulate leydig cell production of testosterone which in return increases sperm count as well. In my case where I have something preventing this from happening naturally means that if I took HCG it would mimic natural function of this process however once the HCG stops I go right back to where I was prior.

So in someone that is cycling running HCG doesn't fool your pituitary gland into thinking you're low. It is just taking place of the glands function. So the gland is still going to shut down its production of the luteinizing hormone while on cycle even with HCG. So my question is why is HCG often ran low dose during a cycle when it really doesn't aid in recovery? It would seem to me that it would maybe benefit you if your pituitary gland were to be fully recovered and functional at the end of PCT and the end of HCG therapy. I can see how if your balls are still full and producing test and sperm it would be an easier transition.

Can someone shed some light here please? Because the practice of running HCG on cycle seems pointless after this talk with my endo today. Unless maybe you're trying to have a kid.

 

[heavyiron]

HCG increases the mass of your testes to output testosterone sooner. The ease of recovery is directed at your testes not pituitary.

You will recover without HCG but it may take a bit longer.

 

[hypo_glycemic]

^ just had a long conversation with my endocrinologist on the same topic today. I was prescribed HCG today

 

[TrojanMan60563]

HCG increases the mass of your testes to output testosterone sooner. The ease of recovery is directed at your testes not pituitary.

You will recover without HCG but it may take a bit longer.

HCG sends a fake LH signal to the testes leydig cells which stimulated your testes to produce testosterone/sperm. The leydig cells are not affected by the use of steroids. It is the pituitary gland that stops sending LH to signal the testes to work properly. So my understanding is you're not shutting down your testes on cycle you are interupting the LH being sent from the pituitary gland that tells your testes to work. So post cycle if your pituitary isn't recovered as soon as HCG is stopped the testes are no longer being stimulated. Based on this information I don't understand why low dose HCG is ran during a cycle to speed up recovery. It would seem that a drug to stimulate the pituitary to function would be the ticket.

 

[TrojanMan60563]

^ just had a long conversation with my endocrinologist on the same topic today. I was prescribed HCG today

Did he lower your test dose?

 

[hypo_glycemic]

No. I'm still at 200 mg's. 3 weeks ago I scored 198 ng/dl.. Lowest ever. I have a pituitary disorder. Prescribed 2 IU a day.

 

[TrojanMan60563]

No. I'm still at 200 mg's. 3 weeks ago I scored 198 ng/dl.. Lowest ever. I have a pituitary disorder. Prescribed 2 IU a day.

So on 200mg EW you were at 198? I wonder where it all goes.

 

[heavyiron]

HCG sends a fake LH signal to the testes leydig cells which stimulated your testes to produce testosterone/sperm. The leydig cells are not affected by the use of steroids. It is the pituitary gland that stops sending LH to signal the testes to work properly. So my understanding is you're not shutting down your testes on cycle you are interupting the LH being sent from the pituitary gland that tells your testes to work. So post cycle if your pituitary isn't recovered as soon as HCG is stopped the testes are no longer being stimulated. Based on this information I don't understand why low dose HCG is ran during a cycle to speed up recovery. It would seem that a drug to stimulate the pituitary to function would be the ticket.

HCG basically is LH in laymens terms. Without LH stimulation to your testes they "shut down" they will atrophy and stop producing teastosterone in the presence of steroids. ITT levels drop. When HCG is added to steroids the mass of the testes increase, they produce T again which raises ITT levels dose dependantly.

Steroids shut down pituitary output AND therefore your testes. Both are shut down on cycle. HCG keeps the testes outputting T. Once the cycle is over you use a SERM to help restart the pituitary which then does not have to wait for the testes to increase in mass and output T. The testes are ready to go. This allows a bit faster recovery. HCG is not absolutely needed though. You will recover without it.

 

[TrojanMan60563]

HCG basically is LH in laymens terms. Without LH stimulation to your testes they "shut down" they will atrophy and stop producing teastosterone in the presence of steroids. ITT levels drop. When HCG is added to steroids the mass of the testes increase, they produce T again which raises ITT levels dose dependantly.

Steroids shut down pituitary output AND therefore your testes. Both are shut down on cycle. HCG keeps the testes outputting T. Once the cycle is over you use a SERM to help restart the pituitary which then does not have to wait for the testes to increase in mass and output T. The testes are ready to go. This allows a bit faster recovery. HCG is not absolutely needed though. You will recover without it.

HCG by itself can shut down your testes by stopping the natural LH signal from the pituitary.

 

[heavyiron]

HCG by itself can shut down your testes by stopping the natural LH signal from the pituitary.

That's why it's recommended you stop administering HCG when the AAS are clearing and then begin SERM treatment. However while on AAS, HCG stimulates the testes to output testosterone. If you want to see a study that demonstrates HCG causes ITT levels to rise while on steroids I will dig it up for you.

 

[jshel12]

HCG basically is LH in laymens terms. Without LH stimulation to your testes they "shut down" they will atrophy and stop producing teastosterone in the presence of steroids. ITT levels drop. When HCG is added to steroids the mass of the testes increase, they produce T again which raises ITT levels dose dependantly.

Steroids shut down pituitary output AND therefore your testes. Both are shut down on cycle. HCG keeps the testes outputting T. Once the cycle is over you use a SERM to help restart the pituitary which then does not have to wait for the testes to increase in mass and output T. The testes are ready to go. This allows a bit faster recovery. HCG is not absolutely needed though. You will recover without it.

So Heavy, if your on trt and no longer want children and in your 30's or 40's is there any real reason to be on hcg besides testes size?

 

[heavyiron]

So Heavy, if your on trt and no longer want children and in your 30's or 40's is there any real reason to be on hcg besides testes size?

Its a debate within the anti-aging community. Some docs believe that HCG does more than just elevate T and will elevate mood and libido more than just T alone. From a practical standpoint probably not.

 

[Roaddkingg]

This is interesting.
I'd like to follow this conversation. I have always used HCG on cycle.
My new thought on this is(and I am currently doing) stating the HCG early ie first wk and run up until four days before PCT begins with the last 2 pins being 1500iu's.
500iu's 2x wkly throughout.
Thoughts?

 

[hypo_glycemic]

So on 200mg EW you were at 198? I wonder where it all goes.

My total T is raising from when I initially had my BW done a month ago from 200 mg of Cyp a week TRT.. It was brought to my attention from my endocrinologist that my pituitary has a deficiency in producing hormones. I have an appointment on the 10th to discuss things moving forward. I'll post my labs tonight showing the deficiency and informalities.

 

[TrojanMan60563]

That's why it's recommended you stop administering HCG when the AAS are clearing and then begin SERM treatment. However while on AAS, HCG stimulates the testes to output testosterone. If you want to see a study that demonstrates HCG causes ITT levels to rise while on steroids I will dig it up for you.

I know it keeps the testes producing test, but it stops when the HCG stops. So where is the benefit of using it during a cycle, and not just part of the PCT? Prolonged use of HCG can have negative effects like desensitizing the leydig cell response to LH which means you'll never fully recover. Knowing that AAS doesn't affect the leydig cells they will always respond to HCG treatment unless you desensitize yourself. I'm thinking HCG and clomid make a great PCT but I don?t see any logic in use during a cycle, and think it might even be a bad idea.

 

[heavyiron]

I know it keeps the testes producing test, but it stops when the HCG stops. So where is the benefit of using it during a cycle, and not just part of the PCT? Prolonged use of HCG can have negative effects like desensitizing the leydig cell response to LH which means you'll never fully recover. Knowing that AAS doesn't affect the leydig cells they will always respond to HCG treatment unless you desensitize yourself. I'm thinking HCG and clomid make a great PCT but I don?t see any logic in use during a cycle, and think it might even be a bad idea.

On cycle steroids stop the testes from producing Testosterone. The testes then begin to atrophy and ITT levels drop. The benefit of HCG on cycle is the mass of the testes is kept normal allowing normal output of T dose dependently. As you enter PCT while the AAS are clearing you may still administer HCG to keep the testes producing T. Once the AAS ester clears HCG will likely supress pituitary output just like the steroids so using HCG then is counter-productive. However you could run the HCG the last 3 weeks of the cycle including while the AAS is clearing (something I have recommended for years if a guy is short on HCG).

Desensitization is largely misunderstood in my experience. There is a refractory period when follow up HCG injections are administered within a day or two of each other. This may cause hCG-induced steroidogenic refractoriness of Leydig cells but if you wait a few extra days the Leydig cells respond well to additional HCG.

Keep in mind there is a lot we don't understand about how all the various responses work so this discussion is probably over simplified. Other factors like E2 are likely the real culprit which inhibit androgen production in the testes which then lends support to using an AI during any administration of aromatizing compounds including HCG. In other words guys may be blaming HCG for difficulty recovering when in fact it may be high levels of E2.

The potential roles of estrogens in regulating Leydig cell development and function: A review

References and further reading may be available for this article. To view references and further reading you must purchase this article.

Tom O. Abney, , a

a Department of Physiology and Endocrinology, Medical College of Georgia, Augusta, Georgia 30912, USA

Available online 10 September 1999.

Abstract
It is generally agreed that estrogens, principally estradiol-17β, are synthesized by and act in the testis of mammals, including humans. The site of estradiol synthesis in the testis is generally believed to begin in the Sertoli cell and switch to the Leydig cell during neonatal development where a gonadotropin-regulated aromatase is present. Numerous studies suggest that the primary target cell of estradiol in the testis at all ages is the Leydig cell. In fact, the Leydig cell is known to possess an estrogen receptor that binds estradiol in the classic manner. The mechanism of estradiol action and the role of its receptor in the testis, however, remain unresolved. In Leydig cells, estradiol appears to induce several alterations that are dependent in large part on the developmental stage of the Leydig cell. In the fetal and neonatal testes, estradiol appears to block the ontogenic development of Leydig cells from precursor cells. There is also evidence that estradiol similarly blocks the regeneration of Leydig cells in the testis of mature, ethane dimethylsulfonate-treated animals. Evidence indicates that the precursor cell possesses high levels of estrogen receptors relative to that of the Leydig cell. It is postulated that estradiol is a paracrine factor involved in regulating the interstitial population of Leydig cells. Evidence also indicates that estradiol acts directly in the mature testis to block androgen production. It appears to do so by inhibiting the activities of several steroidogenic enzymes involved in testosterone synthesis. Although the more conventional receptor-mediated mode of action is feasible, several studies have suggested that this action might entail direct competitive inhibition of key steroidogenic enzymes by estradiol. In summary, the net biologic effect of estradiol in the testis appears to be inhibition of androgen production, either by limiting development and growth of the Leydig cell population or through direct action in the Leydig cell.