No Response to HCG


I recently came off a cycle, and my balls are now shrunken - but I
show no response to HCG - not at 250IU, 500 IU or 1500 IU.

My blood work shows that Estrogen is so low - it is undetectable (too much adex ;-o) - could this be the reason why I am not responding to HCG?

I have gotten my ball size back INSTANTLY in the past after a long cycle with only 250 IU of HCG- but not now…

If indeed it’s the E2 that is the problem and needs to be raised - what is
the quickest way of doing it? I have methyl testosterone and Sustanon 250 on hand - would
that aromatize quickly enough? or do I need some estrogen supplemention? Pills? Injection?

If you don’t know of any relationship between E2 and HCG - DON’T POST - the last thing
I need now is more confusion. This is freaking me out.

HCG signals the testes to produce testosterone, testosterone aromatises to estrogen to maintain a balance - so yes, HCG will increase your estrogen level too.

I understand that once before you got results immediately after using it but this is dependant on other factors. It is most certainly not the case that you will respond the same way to the same drug every time. Absolutely not, that would be far too easy wouldn’t it?

To answer the question which of the 2 drugs would aromatise quickest - it is of course the Methyl-Test (why in god’s name do you have this?) but it will also inhibit you further, essentially making this quite normal situation more of a problem.

Saying that - i didn’t catch on immediately but you are post cycle now aren’t you? You should have PREVENTED the atrophy with the HCG instead of waiting till post cycle to cure it - what do they say? Prevention is…?

What was the cycle you are recovering from?

Plus - Trust me, there will not be a single time in your life when you need Estrogen pills OR injections for fucks sake.

HCG acts directly on receptors located in the Lyedig cells. As far as I am aware they are not influenced by low estrogen levels but rather the opposite - high levels of estrogen can in fact have directly impact negatively on steroid formation. See the abstract below

Volume 64, Issue 9, September 1999, Pages 610-617

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

Tom O. Abney,


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.

Cymru - I do not see your reply - perhaps you can PM that to me if it’s of any relevance to the above issue I am having. THANK YOU! :slight_smile: