I just first want to make clear that estrogen isn't bad, so when you hear that "aromasin blocks estrogen formation better", that's not really important to us. We only use AIs to slightly reduce estrogen levels to prevent excessive bloat and hypertension, so we use the appropriate doses to accomplish this. If we wanted to eliminate estrogen altogether, then it would make more of a difference which Aromatase inhibitor (AI) we used.
Lowering the ligand (estrogen) concentration will downregulate estrogen receptor concentrations, but there is no diract way to do so w/o lowering estrogen levels.
We want estrogen, because it's very anabolic......we are trying to grow, right? We use an Aromatase inhibitor (AI) to slightly reduce systemic estrogen levels......we use nolva to block estrogenic activity at the breast, and we also reap its benefits on lipid profiles as well. using nolva with a low dose Aromatase inhibitor (AI) allows us to have high estrogen levels but still not see any estrogenic sides....other than growth.
A suicidal inhibitor like aromasin (a Type I AI) just binds aromatase irreversibly....it has nothing to do with the estrogen receptor. Each aromatase enzyme bound by aromasin will never again convert a substrate to estrogen.
The class II AIs, letro and adex, work by competitive inhibition of aromatase......they are in a constant state of bind and release from aromatase....this means that when not bound to aromatase, a substrate (we'll assume testosterone here) can bind the enzyme and be converted to an estrogen. AIs are dose-dependent.....the more aromasin you have, the more potential for aromatase enzymes to be bound.....and the same holds true for the class II AIs.
I guess my point is......take advantage of estrogen....don't try to get rid of it....just redirect its focus