Important HPTA and HCG question

Gambale

New Member
Hello, I have some doubt about HCG and HPTA, can someone kindly help me with these doubts? Now I try to explain.

What I know is that HCG mimics leutenizing hormone (LH). LH stimulates the Leydig cells in the testicles to produce testosterone. This action also causes the testicles to return to normal size and function if they were suppressed due to exogenous testosterone.

There is a problem, HCG at high doses or for long periods down-regulate and/or desensitize Leydig cell receptors to LH so when you stop HCG your testicles will atrophize again. The question is: is this true and if yes, how can we avoid this? What dosages and times should be followed?

Second, when you are on AAS or TRT your hypothalamus stops producing GnRH, → your pituitary stops producing LH and FSH, → Leydig cells stop producing Testosterone and sertoli cells stop producing sperm → your testicles atrophy.

When I use SERMs in PCT the pituitary gland restarts LH and FSH production and this should induce the testicles to restart testosterone and sperm production as before. The question is: Do the testicles after an AAS cycle respond to the LH / FSH that are reproduced by the pituitary gland as before the cycle and slowly resume their previous sizes and functionality or since they have become atrophied they have become less sensitive to LH/FSH and to bring them back to size and functionality before the cycle, should HCG be used and then SERM used for a period to maintain the sensitivity and dimensions/functionality obtained from HCG?

Thank you very much to all those who will answer my questions.
 
There is a problem, HCG at high doses or for long periods down-regulate and/or desensitize Leydig cell receptors to LH so when you stop HCG your testicles will atrophize again.

Where are you getting this information?
Which specific studies have you read that state this?
 
Where are you getting this information?
Which specific studies have you read that state this?
I'm guessing, I ask you based on your knowledge and experience if this is true or false. Some talk about Down-regulation and/or desensitization of LH receptors in the testicles by HCG and I would like to understand better.
 
This is an excellent study on down-regulation modeling. This paper has some good modeling graphs. The doses used for PCT will not result in down regulation.

"The model we developed allows us to simulate arbitrary dosing schemes. The example we provide shows an informal way to obtain a maximum response while using the minimum amount of drug. The simulated testosterone levels show that to reach a target testosterone concentration of 25 nmol/liter [~720 ng/dL], a dose of 1000 IU of rhCG every other 4 days would be sufficient. A higher 2500 or 5000 IU dose would produce a slightly higher response, but the highest dose will produce a lesser response according to the model. Clearly, the predicted pattern of decreased response at high doses and the pronounced rebound effect at treatment cessation is intriguing. The extrapolation to a clinical setting certainly deserves confirmation."

Gries JM, Munafo A, Porchet HC, Verotta D. Down-regulation models and modeling of testosterone production induced by recombinant human choriogonadotropin. J Pharmacol Exp Ther 1999;289(1):371-7. Down-Regulation Models and Modeling of Testosterone Production Induced by Recombinant Human Choriogonadotropin
 
This is an excellent study on down-regulation modeling. This paper has some good modeling graphs. The doses used for PCT will not result in down regulation.

"The model we developed allows us to simulate arbitrary dosing schemes. The example we provide shows an informal way to obtain a maximum response while using the minimum amount of drug. The simulated testosterone levels show that to reach a target testosterone concentration of 25 nmol/liter [~720 ng/dL], a dose of 1000 IU of rhCG every other 4 days would be sufficient. A higher 2500 or 5000 IU dose would produce a slightly higher response, but the highest dose will produce a lesser response according to the model. Clearly, the predicted pattern of decreased response at high doses and the pronounced rebound effect at treatment cessation is intriguing. The extrapolation to a clinical setting certainly deserves confirmation."

Gries JM, Munafo A, Porchet HC, Verotta D. Down-regulation models and modeling of testosterone production induced by recombinant human choriogonadotropin. J Pharmacol Exp Ther 1999;289(1):371-7. Down-Regulation Models and Modeling of Testosterone Production Induced by Recombinant Human Choriogonadotropin
Thank you for sharing, so for example:
On the cycle, a dose of 200IU every other 2 days or 250IU every other 3 days.
Post cycle, a dose 500-1000 iu every other 4 days.
All these possible doses don't cause down-regulation or desensitization in any way, right?
 
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