In light of aromatase upregulation, it seems to make sense to taper off AIs, rather than to discontinue their use abruptly. Theoretically, one should be able to taper off slowly enough to allow aromatase to downregulate back to "normal" and thus to avoid E spikes.
My question is, Can anyone offer an educated guess as to how long the tapering process should take? How long until aromatase enzyme levels return to normal after an extended period of time (e.g., a couple of years) on, for example, letrozole (e.g., 1.5 mg/day)?
Specifically, if one were to transition from extended super-physiological doses of AAS (e.g., 500 mg TC and 300 mg deca weekly) to HRT doses (e.g., 125 mg TC/wk,) how would one handle the letro taper to avoid E spike issues?
My (arbitrary) proposal would be to taper in weekly 0.25 mg increments, such that the tapering process would take about 5 weeks to zero. Too fast? Too slow? Not an important issue to begin with?
Any thoughtful comments welcome. Thanks to all.
I prefer use Exemestane and don't burn my head with these "theories"
Re: Aromatase upregulation and tapering off AIs
In light of aromatase upregulation, it seems to make sense to taper off AIs, rather than to discontinue their use abruptly. Theoretically, one should be able to taper off slowly enough to allow aromatase to downregulate back to "normal" and thus to avoid E spikes.My question is, Can anyone offer an educated guess as to how long the tapering process should take? How long until aromatase enzyme levels return to normal after an extended period of time (e.g., a couple of years) on, for example, letrozole (e.g., 1.5 mg/day)?
Specifically, if one were to transition from extended super-physiological doses of AAS (e.g., 500 mg TC and 300 mg Deca weekly) to HRT doses (e.g., 125 mg TC/wk,) how would one handle the letro taper to avoid E spike issues?
My (arbitrary) proposal would be to taper in weekly 0.25 mg increments, such that the tapering process would take about 5 weeks to zero. Too fast? Too slow? Not an important issue to begin with?
Any thoughtful comments welcome. Thanks to all.
If I were me, I would monitor it via blood work in order to check E2 levels while manipulating AI dosing. Just a thought.
"The medals don't mean anything and the glory doesn't last. It's all about your happiness. The rewards are going to come, but my happiness is just loving the sport and having fun performing" ~ Jackie Joyner Kersee.
Guijr, monitoring would certainly be the smart thing to do, and would answer my question empirically... but I won't, of course.
R2E, a nice, long Nolva/Clomid PCT protocol would render the issue moot as a practical matter, but I am not really planning PCT, since the goal is HRT doses in perpetuity (with occasional real cycles, I should imagine.) I do have a metric tonne of nolva on hand, just in case, should I guess wrong on the taper and run into problems, but I'd rather get it right from the start.
MRJP,aromasin doesn't lead to aromatase and ER upregulation, like the steroidal AIs? I thought that it still did, despite its different method of action / pathway.
R2E, a nice, long Nolva/Clomid PCT protocol would render the issue moot as a practical matter, but I am not really planning PCT, since the goal is HRT doses in perpetuity (with occasional real cycles, I should imagine.) I do have a metric tonne of Nolva on hand, just in case, should I guess wrong on the taper and run into problems, but I'd rather get it right from the start.
I see. Well, in that case, I need to do some searching for ya.
"In any contest between power and patience, bet on patience."
~W.B. Prescott
"Only two things are infinite, the universe and human stupidity, and I'm not sure about the former."
~Albert Einstein
Anastrozol and letrozol are reversible AI. During the use, the organism tend to produces more aromatase to achieve the homeostasis. After stopping the treatment the up-regulated enzimes (sub-physiological levels) and the enzimes reversible inhibited by AI (physiological levels) can lead high concentration (supra-physiological) of aromatase and this can cause estrogenic related side effects.
Exemestane is irreversible / suicide AI. After stopping the treatment only up-regulated (yes, this compound cause up-regulate too) enzimes will be functionaly, and these will be in sub-physiological levels.
The up-regulate of ER will be more linked with the estrogens levels.
Exemestane is irreversible / suicide AI. After stopping the treatment only up-regulated (yes, this compound cause up-regulate too) enzimes will be functionaly, and these will be in sub-physiological levels.
Thanks, MRJP. That makes sense. I've never tried Aromasin, but it sounds like I will, come time for next cycle.
interesting MRGP can anyone else comfirm this or anyone have any studies?