Fair reply. I now did read the whole thread. I agree that very comprehensive set of tests are the only thing that will give some hints as to what is going on. Experimenting based on "feeling" alone is going to be counterproductive.
(However, I've also dealt with (am still dealing with) health issues for which I could not for the longest time find any obvious contributors since most biomarkers on test were "normal". Doctors were unfortunately of zero help and attributed all of my issues to depression and to "it's gonna pass eventually". Turns out that one needs to be quite open-minded and proactive to find creative solutions to confusing health issues. I sympathize with OP because it's extremely infuriating and demeaning to keep hearing from certain others that what you're basically dealing with it is your mind messing with you.)
Regarding the issue of the lack of documented evidence. AI use in men is not as studied as AI use in women. Of course, there are some studies showing that AI use in women upregulates ER in certain tissues (breast tissues, for example), potentially accelerating cancer cells growth after discontinuation. The logic behind this (upregulation of certain ER to compensate for lack of E2) can be applied to men as well (since the general mechanism behind up/downregulation of whichever receptor is the same).
However, we cannot extrapolate without consideration from studies on women to men. Primary sex hormones, for example, do in general serve opposing functions in terms of immune system regulation (in men, test/dht suppress cortisol (the "anti-inflammatory" hormone) which increases IFN-gamma activity whereas estradiol provides opposing anti-inflammatory activity; vice versa for women).
The idea in this thread is that aromasin actually permanently disables aromatase enzymes which only exist in limited quantity. This is likely to be false. Enzyme resynthesis or enzyme turnover would eventually take place. Thought, the story might not be so simple in cases like this where OP used aromasin for years and years. I also think that the use of nonsteroidal AIs such as arimidex is not risk-free. In fact, this is a good thread to read for this:
Can estrogen crash cause desensitization/knock out of the estrogen receptor - lets discuss!
I wonder if nonsteroidal AIs affect receptor expression and function more severely (due to the infamous "rebound effect") than steroidal AIs...
There might be some inhibiton of aromatase activity at play. But I also think that what OP is dealing with can be more readily explained when one considers the pressure excessive test/dht levels in absence of adequate e2 levels (due to AIs) put on (mucosal) tissues in the form of oxidative stress/damage. IFN-gamma activity gets upregulated/increased in the presence of high test/dht levels which becomes problematic if the oxidative damage exceeds the tissue regenerative capacity. This leads to the membrane integrity/barrier function becoming heavily impaired over time which is exacerbated possibly by mucosal infections (maybe in the gut); what follows are innate immune responses due to toxins and different metabolites getting absorbed into bloodstream (aka leaky gut or leaky "whatever-mucosal-tissue-is-sufficiently-damaged"). The innate immune response alters a number of key energy pathways towards immune activity and leads to various (nutrient) deficiencies which further unable the body to fix the damaged tissues but at least further prevents as much damage as possible (*as long as the body doesnt get further blasted with test and AI's that just potentiate the damage)... I wager that OP's issues started or got worse either after covid or after the vaccine. Both heavily disturb the immune system and prepare terrain for pathogens to party on.
I think that OP is dealing with chronic inflammation along with heavily impaired barrier function, exacerbated possibly by mucosal infections (maybe in the gut), from which follow innate immune response, malnutrition due to impaired nutrient (vitamins, minerals...) absorption and due to shifted energy pathways and cascade of other compensations (that the body uses to help itself - compensations which are basically overrided when using AAS; compensations which also include receptor expression changes with regards to glutamate, gaba, nmda, serotonin, dopamine ...). The story gets very complicated.
Why does E2 work for OP? I think that this is partly due to actually being moderately aromatase deficient as a result of long term steroidal AI usage or, in my opinion, especially due to the fact that in males E2 is a potent anti-inflammatory and basically silences the immune system and it also upregulates certain serotonin and dopamine receptors, gaba receptors ....... Ah. It's wild. I don't even understand it that well.
@Jin23 has put forth some great leads - I would definitely like to hear more from him.
OP - do some blood tests. Along with the classic hormone panel (including also thyroid) - cholesterols, CBC, CMP, vitamin D, b12, folate, ferritin, LDH isoforms. I would also either stop TRT or at least drastically reduce the dose so that test levels (along with e2 levels) will be within "normal reference range". I would also make a note of all the meds you take (and have ever taken; 5aris, SSRIs, antibiotics etc.) and of all the supplements you take.
I believe that this condition is very real but very treatable. The recovery might be painful and long, though. Good luck.
(Sorry for this long ass reply. Looking forward to what others think about this.)