Historically I’d long recommended against using HCG at all in PCT. My methods, which included that avoidance, were borne out as working well in very many users over many years.
Lately, I’d started thinking that maybe I’d gone too far, that really the principal (but not sole) inhibitory effect of added testosterone production is from increased estrogenic effect, and so if this is properly under control, a moderate dose of HCG could be okay in PCT.
However, I now strongly suspect I was wrong.
Besides the increased testosterone being somewhat inhibitory, which itself should not be too great a problem, there is evidence of HCG itself being directly inhibitory.
Unless and until there is actual evidence of ongoing HCG use in PCT not reducing LH production in practice, I’m back to recommending against it.
[quote]Bill Roberts wrote:
Unless and until there is actual evidence of ongoing HCG use in PCT not reducing LH production in practice, I’m back to recommending against it.
[/quote]Recommending against it during PCT or at all BR?
I guess I missed the part where you were back to recommending it during PCT. I assume you’re still a proponent of on cycle usage.
As for me Im not using it any more or likely ever again, its the most gyno inducing compound I’ve ever used
RG, it’s a combination of checking the research of effect on HCG on the hypothalamus as well as a personal finding. The personal finding by itself would only be suggestive, but in combination with there indeed being a mechanism for HCG to suppress LH production it makes more sense to go back to my much-more-longstanding recommendation.
I thought you might be interested in these blood test results. They are from a bodybuilder who it appears is suffering from primary ASIHG. He had been injecting around 2000iu of hCG EOD - a total of 15 shots in an attempt to kick start his testes. As you can see from the results LH and FSH are very high so maybe hCG is not directly inhibitory? I would be grateful for your thoughts
Each person needs to go by his own results when he has them. I would never say differently.
For this lifter, his protocol did not cause him a problem with LH/FSH.
The function of the hypothalamus in regulating LHRH production is quite complex. I really don’t remember these days everything I’d once learned on it – there are a great number of inputs.
It might very well be, for example, that if testosterone is low as with this lifter, then the HCG is not necessarily inhibitory in terms of yielding low values but results might be completely different with both being high, or with HCG being high and testosterone being normal.
There is also the consideration that in primary hypogonadism, there is not a pre-existing situation of low LH output. Whereas the steroid user who is coming out of a cycle is in that situation.