Some questions about PCT

[skywalk]

- To prevent estrogen rebound after PCT, should aromasin or femara be run throughout PCT, or do you stop them after your last pin?
- how long after PCT should you wait before doing all your bloodwork? or should it be done immediately after PCT?

 

[Michael Scally MD]

What is this "estrogen rebound"? From all that I read it is more BS.

As far as labs, I recommend getting a LH & TT at some point during SERM use and one month or more after stopping all meds. I have stated before that AI use does not provide an accurate picture of HPTA restoration. For that reason, I do NOT use an AI.

 

[skywalk]

What is this "estrogen rebound"? From all that I read it is more BS.

As far as labs, I recommend getting a LH & TT at some point during SERM use and one month or more after stopping all meds. I have stated before that AI use does not provide an accurate picture of HPTA restoration. For that reason, I do NOT use an AI.

thanks Dr Scally.
noted on the LH and TT during, and 1month+ after cessation of all meds.

what about cholesterol and liver enzymes? how soon before I test for those? thanks

 

[Dr JIM]

FYI SW, rebound has a rather explicit meaning in the bioscience, it refers to a "system" overreaction once a suppressive stimulus is removed. In this instance, if AI's exhibited rebound, upon their discontinuation E-2 levels should eventually climb ABOVE pretreatment baseline values. This has not been shown to occur with AI's BUT it has been reported as factual on a several forums.

 

[Pericles]

There may be no estro rebound from a powerful AI like A dex or Letro because they completely shut down production, but there can be from Nolva or other SERM's.

Also, for those that use HCG at the end of a cycle, there will be tons of estro that needs mitigation (IE I always use an AI at that time).

 

[Dr JIM]

E-2 levels do not "rebound" and EXCEED (or overshoot) pretreatment baseline levels upon the discontinuation of either SERM's or AI''s. Moreover since there's no evidence to support the assertion, I suspect it's bro dogma propagated through AAS forums.

 

[foreveryoung]

E-2 levels do not "rebound" and EXCEED (or overshoot) pretreatment baseline levels upon the discontinuation of either SERM's or AI''s. Moreover since there's no evidence to support the assertion, I suspect it's bro dogma propagated through AAS forums.

I wonder about this... I believe the school of thought is that the body is trying to reach a level of estrogen in the system so that aromatase production is ramped up in the presence of an AI so that when the AI is discontinued the higher aromatase levels then cause a rebound effect

 

[Dr JIM]

FY
Your assumption is on spot because this is exactly what happens biochemically in classic "rebound". Because the "system" has been suppressed for a given period of time, accumulation of substrate, enzyme or cofactors may occur. Consequently, once the suppressive substance is removed the "system" increases it production ABOVE baseline exhausting those compounds amassed until a equilibrium is reached whereupon it returns to prior levels.
However neither of these occur with AI's or SERM's probably because testosterone may be metabolized into DHT, E-2 or enter the cell unchanged. In other words substrate does not accumulate because two other courses are available if aromatase is blocked (testosterone or DHT) Moreover the DHT AND E-2 are relatively minor metabolic pathways accounting for a combined 20% of testosterone end product metabolism, the remainder enters the cell as testosterone.

 

[Dr JIM]

For clarification, there are circumstances where the withdrawal of either AI's or SERM's result in an absolute increase in E-2 levels yet the tT;E-2 RATIO remains unchanged.
For instance after the effective treatment of hypogonadism E-2 levels may raise above baseline AND remain at that level. Such as a patient whom starts hypogonadal therapy using either an AI or a SERM with an initial tT and E-2 level of 207 ng/dl and 24 pg/ml respectively (one of my patients). After effective treatment the drug is removed once the tT level improves to 413ng/dl and an E-2 of 42 pg/ml. Indeed E-2 levels have increased above baseline but on a pro rata basis with tT. However FURTHER increases of E-2 are not observed as a CONSEQUENCE of discontinuing either the AI or SERM therapy.
A related situation may occur with cycling, for example cycling T-prop while using an AI simultaneously can reduce the E-2 level and INCREASE the tT;E-2 ratio remarkably. However once the cycle or AI are stopped obviously E-2 will increase since aromatase is no longer being blocked. Moreover if appropriate PCT is not instituted, AI discontinuation may appear responsible for a further elevation of E-2 when the culprit is actually the adrenal glands, since LH has a limited influence on it's estrogen production.
Best

 

[Michael Scally MD]

I wonder about this... I believe the school of thought is that the body is trying to reach a level of estrogen in the system so that aromatase production is ramped up in the presence of an AI so that when the AI is discontinued the higher aromatase levels then cause a rebound effect

In a word, hogwash. Can you direct me to any evidence that aromatase levels are dependent upon estrogen? Just how is this mechanism supposed to occur? Further, the "school of thought" as you state is a bit out there (trying to say it nicely).

 

[foreveryoung]

In a word, hogwash. Can you direct me to any evidence that aromatase levels are dependent upon estrogen? Just how is this mechanism supposed to occur? Further, the "school of thought" as you state is a bit out there (trying to say it nicely).

ok, thanks Dr S and Dr J

 

[Dr JIM]

Excellent point Dr S. since aromatase levels are "genetically" pre--determined.