Steroid Forum: This is a discussion on Rationale for the Use of Aromasin with Tamoxifen During PCT within the Anabolic Steroids forums, part of the extensive steroid information at MESO-Rx; Rationale for the Use of Aromasin with Tamoxifen During Post Cycle Therapy
Aromasin (Exemestane) is one of those weird compounds ...
Aromasin (Exemestane) is one of those weird compounds that nobody really knows what to do with. What we generally hear about it makes it very uninteresting…It’s a third generation Aromatase Inhibitor (AI) just like Arimidex (Anastrozole) and Femera (Letrozole). Both of those two drugs are very efficient at stopping the conversion of androgens into estrogen, and since we have them, why bother with Aromasin? It’s a little harder to get than the other two commonly used aromatase inhibitors, because it’s not in high demand, and there’s never been a readily apparent advantage to using it. So, why would we need another AI and how can it be useful?
Make sure to go over to the other Forum here, and read my comments, before following any of the advice Mr. Anthony Roberts gives. The simple fact is that none of it stands up to any true scientific evaluation. I am concerned guys will make things worse, not better, if they listen to someone who has no idea what he is talking about.
Although the data on males is lacking (understandably so given the target market), there is some evidence that estrogen suppression with aromatase inhibitors causes the body to respond/adapt with an increase in sensitivity to estrogens, both by upregulating estrogen receptor levels and increasing E2 signaling via other pathways. This would not favor recovery. A lot of talk as of late on gyno caused AFTER PCT ended, when the PCT included an aromatase inhbitior. I am not knocking AR for coming up with this theory. Theories are good. But it is still a theory, and like all theories it will not be fact until it is proven and accepted. I am not so sure this one ultimately will be.
AI induced "estrogen hypersensitivty" aside, I am still inclined to think that AIs are an unnecessary addition given an environment that already favors lower E2 stimualtion and higher LH output.
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.
Another point which needs to be made is the failure of many (I have not read where Roberts has recomended this) to properly taper their SERM's at the end of PCT.
As Dr. Shippen and I have each discovered independently, and discussed in a private conversation at an A4M conference in Las Vegas over two years ago, just 25mg of Clomid is indeed a whalloping dose with respect to HPTA-stimulation. I therefore would want to see dosage decreases in 5 day increments, with the last step at 12.5mg QD.
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?
Rationale for the Use of Aromasin with Tamoxifen During PCT 
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