AI Help

[thewarrior23]

I got this from a guy...
What do we know about the mechanisms of aromatase inhibitor resistance?

But it also says that this happens with tumors no longer responding, in using gear we are not fighting tumors but estro sides, so would that profoundly effect things. Since were basically going up against are body and not a tumor, it says the tumor no longer responded to it not that the AI just stop working...so do you think AIs continue to work forever, its just you never here guys who have been on a long time say 'my AI no longer works"

So just looking to see if you think AIs lose total and complete effectiveness over time or maybe just a lil here and there??

 

[Macro]

I got this from a guy...
What do we know about the mechanisms of aromatase inhibitor resistance?

But it also says that this happens with tumors no longer responding, in using gear we are not fighting tumors but estro sides, so would that profoundly effect things. Since were basically going up against are body and not a tumor, it says the tumor no longer responded to it not that the AI just stop working...so do you think AIs continue to work forever, its just you never here guys who have been on a long time say 'my AI no longer works"

So just looking to see if you think AIs lose total and complete effectiveness over time or maybe just a lil here and there??

ai resistance is really only highly relevant in cancers, and not all that common there. and its usually not really resistance per se, but rather lessened response.... see below (relevant to instances where ai's may not SEEM to work as well...)



non or lessened response when it occurs is generally due to other factors... adaptive or secondary actors-- eg PGR, EGF, IGF, PROLACTIN (especially), etc....

some of these can be addressed moderately easily, maintaining low bodyfat, staying hydrated and doing cardiovascular exercise being among the non drug options... as well as avoiding massive insulin spikes and over eating... alcohol and others (especially cocaine and ecstacy, and to a mixed extent marijuana) can also be problem causers...

through drugs prolactin is easy to address, the others fairly so but with drugs as secondary moderators


basically it should work the same.. other factors may amplify existing (though unless drinking, or higher body fat, or overly aged/damaged liver will mean more aromatase production--- generally requiring increased dose) estrogen levels.. so dose might need to be increased.

most often if it seems to be not working the culprit is prolactin (which androgens, particularly DHT and most synthetics will increase--- due to effects on both PGR and dopamine levels/metabolism in the brain... intially this will lower prolactin generally.. just fyi).... though higher insulin levels and orals may also increase need as lowered SHBG will result in less consistent blood levels from ester based drugs as well as more free testosterone and estrogen (estrogen will not high in affinity still does bind to shbg)... though you will often seen people arguing for it, lowered SHBG while allowing more free steroid is not a free ticket and it can be very problematic with steroid esters that rely heavily on the shbg pool to achieve their technical half life).

orals will also increase liver synthesis of aromatase (generally)