Aromasin...

[atrollappears]

I was asked a few questions today:

i) What do I know about Aromasin:

From GH-15:

Aromasin is the new generation of AI its a suicidal inhibitor, the difference being with the other AI?s is Aromasin will permenantly bind the aromataze enzyme so by doing so it stops any estrogen conversion via aromatase enzyme. This means when you stop using aromasin you wont rebound at all like you would with a temporary binding AI?s and if anything you will have to wait for a while for your body to start producing more aromataze (very bad if you crashed your estro comparing to the other AI?s). Each person is different in the rate they create new aromataze for some it takes around 2 weeks for someone else it can take one or three weeks. Only way you can speed up the process is by using HGH, you can use all the dbol you want all the test suspension you want if you crashed your estro with aromasin and you don't have aromataze you wont even bloat from those compounds there wont be any estrogen conversion, also you will get 0 results from the dbol at least.

From Anthony Roberts: 

Difference Between Type-I and Type-II Aromatase Inhibitors

To understand why Aromasin may be useful in conjunction with Nolvadex while both Letro and A-dex suffer reduced effectiveness, we’ll need to first understand the differences between a Type-I and Type-II Aromatase Inhibitor. Type I inhibitors (like Aromasin) are actually steroidal compounds, while type II inhibitors (like Letro and A-dex) are non-steroidal drugs. Hence, androgenic side effects are very possible with Type-I AIs, and they should probably be avoided by women. Of course, there are some similarities between the two types of AIs…both type I & type II AIs mimic normal substrates (essentially androgens), allowing them to compete with the substrate for access to the binding site on the aromatase enzyme. After this binding, the next step is where things differ greatly for the two different types of AI’s. In the case of a type-I AI, the non-competitive inhibitor will bind, and the enzyme initiates a sequence of hydroxylation; this hydroxylation produces an unbreakable covalent bond between the inhibitor and the enzyme protein. Now, enzyme activity is permanently blocked; even if all unattached inhibitor is removed. Aromatase enzyme activity can only be restored by new enzyme synthesis. Now, on the other hand, competitive inhibitors, called type II AI’s, reversibly bind to the active enzyme site, and one of two things can happen:

1.) either no enzyme activity is triggered or
2.) the enzyme is somehow triggered without effect.

The type II inhibitor can now actually disassociate from the binding site, eventually allowing renewed competition between the inhibitor and the substrate for binding to the site. This means that the effectiveness of competitive aromatase inhibitors depends on the relative concentrations and affinities of both the inhibitor and the substrate, while this is not so for noncompetitive inhibitors. Aromasin is a type-I inhibitor, meaning that once it has done its job, and deactivated the aromatase enzyme, we don’t need it anymore. Letrozole and Arimidex actually need to remain present to continue their effects. This is possibly why Nolvadex does not alter the pharmacokinetics of Aromasin

[Realtalk]

Thanks mate, very helpful with my quest.

[atrollappears]

Thanks mate, very helpful with my quest.

Erm....... Kudos pls Thomas... *mosking*