Aromatase Inhibitors Tolerance

I’d like to collect some information from users consciously using and dosing aromatase inhibitors in their TRT/cycle protocols. There’s no official data available to state any of these drugs induces aromatase gene expression in chronic therapy (indirectly through a lowered level of available aromatase or directly). This is a drug group of non-receptor mechanism of action, so tolerance was not expected.

Commonly used 3rd generation selective AI’s: anastrozole, letrozole, exemestane (irreversible). I’d focus on anastrozole and letrozole here - exemestane’s mechanism of action and dosing excludes its convenient use.

To the point. Over the years of cycling and using different AAS coupled with anastrozole to control aromatization I’ve collected over 60 E2 results from bloodworks. Each time I go down with high doses of variable AAS and I’m set on TRT dosage of testosterone - my anastrozole dose rises slightly when the goal is to keep my E2 narrow range (25-35 pg/mL). Now I need double the dose of the AI than just 3 years ago with the same testosterone amount used. There are no other variables (diet, health condition, lifestyle are “constant”).

Understanding endocrinology, it’s possible that if your aromatase enzyme is inactive due to chronic AI use - aromatase gene expression is induced to restore its active level, but still, it’s just my hypothesis. A possible restoration to original condition could be a complete withdrawal of anastrozole and single application of exemestane to “kill” almost all produced aromatase proteins, to start with, let’s hope so, lower aromatase dosage again few weeks later (or stop using an AI at all with proper TRT regimen).

Can’t collect much from me, but I’ll chime in. I don’t Use aromatase inhibitors, serms/ any method of aromatase control as I’ve never had a reason to. Water retention, fatigue, blood pressure etc have never been an issue for me in the slightest. Furthermore the issue regarding aromatase inhibition and impact on cholesterol management concerns me (as someone who is genetically prone to not having the best HDL/LDL ratio), thus I prefer to keep my androgen/aromatisation ratio within homeostasis (whatever ratio my body would convert T/E regardless of dose implemented)

Then there’s the issues regarding glucose tolerance, not gonna say BMD as androgens themselves also stimulate an increase in BMD hence the approval for use as adjunct therapy for treating frailty relating to osteoporosis.

Furthermore, I don’t believe there any reputable data stipulating there is an optimal range for E2 to reside at. Should also say, after years as a teenager on 7mg anastrazole/wk, on trt I tend to stay within ref ranges regarding aromatisation even on higher dosages (say 200mg/wk). So you’re hypothesis to inactive and/chronically desensitised aromatase enzyme may have some plausibility

I recall older blood tests about 6 months after ceasing anastrazole usage (around the time my testosterone concentrations started to dip rapidly), E2 was damn near undetectable at 400ng/dl if I remember correctly that is (this was before I dipped down serrrrioouusslly low)

@chemania I have a question for you. What induces “pumps” from C17AA AAS or even high dosages of DHT derivitaves (drostanolone, methenolone etc). I doubt it’s due to RBC synthesis, as the amt RBC/HCT will be driven up from 4-6wks or use is like at max (according to literature) 4-5%, and that’s a MAXIMUM, probably closer to 2-3 percent if that. Furthermore the ability to deliver more oxygenated blood to a muscle wouldn’t equate to a muscle cramping up and swelling up with absurd amounts of blood and/or cramping up when making movements such as brushing ones teeth.

I apologise if my grammar is atrocious. I’m using an old phone of which freezes constantly, autocorrects at random times and sometimes outright changes words and sentences entirely. I try to proofread but with the incredibly slow nature of said phone it’s difficult.

I’d send you my bloods but I’m super uncomfortable with people having my data. Only like two people on this forum know my name. One of which is gone