BR,
A SERM will create normal or higher levels of LH and FSH, typically higher. This will allow the testes to physically recover. But this does not address the transition to normal stimulation of the pituitary by the hypothalamus. The SERM must be tapered off of course. The levels of estrogen need to be low-normal for the resumption of GnRH. This is where the problem is.
I think that things will always go better when E2 levels are lower, in the lower 20’s [pg/ml <54]. This is why I want guys to land on lower E2 levels during PCT, then take 0.5 mg/ml per week to support this transition and to avoid an HPTA repressive estrogen rebound.
SERMs are HPTA repressive, AIs are not. It is better to transition onto an AI before getting natural than from a SERM.
The amount of adex used needs to match the serum testosterone levels. More correctly, the level of bio-available testosterone as I assume that SHBG bound T cannot aromatize to E.
Adex should be introduced as one tapers off of T then the adex needs to be reduced to as ones T levels drop towards normal levels. We do know that for guys who are natural and needing E levels reduced, a pre-TRT condition, that adex0.5mg/week produces good results. A guy who is estrogen rebounding after PCT with T levels that are repressed resembles the situation of older guys with lower T and elevated E who do well on low does adex.
When one has symptoms of elevated E, and when elevated E levels are probable [after a cycle or non-ideal PCT], then it does not make much sense to do an E2 lab as a first action. The lab will show levels that are above optimal, or elevated [in the 30’s pg/ml], and perhaps even high. E levels do not need to be high to kill libido when combined with lower levels of T. I suggest that one take a trial adex dose. One can then expect to feel significant improvements in libido.
Libido seems to be the fastest responder and is thus an ideal guide to dosing. After 3 weeks on that, one can then, if desired, get a serum E2 test. Now - what to do with that number? If one accepts the rule of thumb from TRT - that E2=22pg/ml is ideal then one needs to adjust the adex dose. Dose response is quite linear.
The new dose is the old dose scaled by the current E2 level divided by 22pg/ml. This really works well in TRT settings. In TRT, things are quite steady state. With a transition out of PCT things are not steady state. That makes fine level dose adjustment of adex a bit problematic.
Back on track - one can establish an adex dose, and then the first lab, if done, can drive a corrected dose instead of simply producing an E2 level that cannot really lead to a very good dosing decision. Estimated adex doses can be scaled by body weight vs a 160 pound reference. So a 240 pound guy might be better off with a PCT exit dose of .75mg/week instead of 0.5mg/week.
For TRT, the first dose approximation can also be scaled up if there is a large %BF - not something that is expected in this forum. I have had really good results with my TRT consults using this first dose and lab driven linear dose change calculations, and with first dose scaling by BW [and BF].
The only hiccup is when a guy is an adex over-responder and need to then take 1/4th or 1/8th of the expected doses.
These are then going through an estrogen crash with the expected symptoms. This cannot be avoided and does imply that front loading adex when one has never used adex before can have a negative outcome for a few.
It is well known that SERMs increase estrogen levels and that is the main reason to taper off of SERMs. In some cases the SERM taper is not enough to avoid problems.
hCG dosing needs to be discussed, as some of the doses discussed on the WWW, and here on T-Nation in the past have been too high. This can down regulate LH receptors which could make the transition off of PCT go bad. 250iu hCG SC EOD is known to typically be a replacement dose for ones normal LH induced testicular activity.
One might then expect that a low dose such as that would not drive testicular estrogen production rates higher than ones natural baseline testicular estrogen production. This does assume that for a given baseline level of testosterone production, that estrogen production is the same for stimulation of the testes by LH+FSH or hCG.
And as you suggest, guys need to be aware that high doses of hCG will create higher levels of T–>E aromatization in the testes.
When I suggest that the PCT exit level of adex be continued for an indeterminate amount of time then tapered to zero… I do not know how long that should be. Perhaps 4-5 weeks. I expect that many will soon feel that they are ok and will be done with it.