I have commented on this study a number of times. It is a very poor study. I do agree that one could use the 250 IU as a starting point, but the study is NOT necessary to make that conclusion. See:
https://thinksteroids.com/community/posts/669461
In fact, my comments for the poorness and low quality of the study is reflected in the fact the study was repeated, but without exogenous T administration. See:
https://thinksteroids.com/community/posts/695687
Regardless, hCG TRT is a NON-STARTER. [THINK ABOUT IT!]
Michael Scally MD said:
Herein lies the rub! What is the purpose of the hCG administration: testes size, tweaking T level, maintaining testes function, etc. This question needs to be asked since the answer is different for each purpose.
In my experience, the use of hCG usually falls into the category of testes size and HPTA restoration after stopping AAS. As far as tweaking, which is what I see described often appears to be focused on optimizing the T level on weekly TRT injection. I find this to be, for the most part, hocus-pocus - an attempt at some magical number of T. Why not just optimize the injection dose.schedule? [I have read on one site that hCG has CNS effects causing "euphoria" not yet described but occurs somewhere in the brain. Guess Who?]
Your points about the limitations of the study are good observations --- namely, (1) that using T to suppress LH could interfere with ITT measurements, (2) that normal men should be used in the study if the purpose is to draw conclusions on the population of normal men, and (3) conclusions drawn about spermatogenesis are inappropriate without supplying spermatogenesis data. The updated study appears to address these points. Nonetheless, their conclusion regarding the use of HCG is the same in both studies: "
Doses of hCG far lower than those used clinically increase IT-T concentrations in a dose-dependent manner in normal men with experimental gonadotropin deficiency." While this paper may not be
necessary to justify using a low dose when starting HCG, it certainly doesn't hurt. After all, testicular desensitization
is a valid concern, particularly since there doesn't seem to be a study to support or refute its existence; the absence of evidence is not the evidence of absence.
Regarding HCG's use as TRT: While I've never used HCG, I see no reason why it isn't a viable option for people with secondary hypogonadism; if the problem is LH deficiency, HCG supplementation (particularly in low doses ED) seems like a good idea. My conclusion:
even if the majority of anti-aging clinics are just excuses for steroid-pushers, the OP got good advice this time.
The one aspect of his question that has not been addressed is the need / dosage for an AI. This would probably best be answered by any forum members that are actually using low-dose daily HCG instead of T.
Anyone here fitting this description care to comment? For all I know, an AI may not even be necessary if the HCG dosage is low enough. In theory, it would only be necessary if T spikes too high. Maybe this is typical of HCG, even in low doses. Hence, those with experience here should speak up.
On a side note: these low HCG doses probably aren't useful to those that have already expienced a lengthy testicular shut down. From what I've seen, these guys don't even respond to normal LH dosages, so why would they respond to similarly normal HCG dosages? I'm guessing this is probably why HAN and others have seen low dose HCG to be ineffective: they've been working with people whose testes have been shut down either by TRT or by steroid abuse.
