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Originally Posted by SWALE Interesting, William.
I am also concerned with lowering E's too far status post AAS, thereby unnecessarily extending the period of plaque deposition within the cardiovascular system.
The idea of employing AI's during PCT is certainly not a new one. But the idea that a more expensive and hard-to-obtain type of same is preferable completely unwarranted by the arguemetns provided in this paper.
I certainly would recommend all users of testosterone during AAS use maintain somewhat normal estrogen levels DURING the cycle, as this, by my experience, helps in restoring the system following the cycle.
And this leads to the best reason to NOT use an AI (once testosterone conversion has subsided to the point E's are no longer elevated), or finasteride, or any of the other nonsensical ideas this Robert's character has come up with: the underlying goal during PCT is to normalize the metabolic pathways. Employing powerful endocrine disrupters is contraindicated to that end. |
You make some good points.. The cardiovascular risks with AI's especially are too often overlooked. Personally, I've had some of my best lipid profiles during the post cycle window while taking
Nolvadex. I'd never trade it for or even add in an AI myself.
I agree with your general line of thought here. The focus should be on returning endocrine balance post cycle. I could see how skewing this balance for the sake of increasing serum T a little more quickly might not be the best overall strategy for recovery. Perhaps it can just lead to more problems.
There are a number of people reporting delayed onset gyno after PCT had ended. The PCT programs invariably have a strong AI in them. It seems to be happening with enough frequency that I think "something" is definitely going on with AI's. Estrogen and LH do not seem to be the weak links post cycle anyway, so is there really any advantage to major E2 suppression here?