I was considering this as well but I'm not sure if this is the case for arimidex, it being a nonsteroidal inhibitor which is known for its rebound effect.
So after inhibiting aromatase this would prompt the body to upregulate ER, aromatase and decrease SHBG to free up some testosterone that could further convert to E2. But upon arimidex clearing from the body you'd have more test to convert - and with upregulated aromatase the conversion would be high, and the surge of E2 would hit sensitive ER. This would likely downregulate the receptors.
Maybe your comment might make sense for folks, like me, crashing with aromasin. Not sure. Still trying to figure it out. I don't see many PFS cases talk about joint clicking and dry mouth which I deal with, for example. Other symptoms do overlap with PFS, though (shrinkage, low libido, low EQ, fatigue, anxiety, depression, low motivation, gut issues ...).
To get back to this and your comment about ER overexpression. It could very well be so - upregulated ER but the transcription (binding of ER to ERE) can't happen properly. Just like when Helen talked about binding AR to ARE. Now the question is what to do about this if it is the case.
When you block your androgen receptor the body tries the hardest to upregulate ARs and transcription. IN your case transcription is not possible to upregulate, since you don't get to cysteine. So the body tried to keep ARs highly overexpressed, and here you come trying to upregulate that overexpression even further.
IT IS AT THE MAXIMUM ALREADY, man. I don't know why you don't get that.
all you can do is upregulate your AR density, which is already extremely high and you simply can't increase it beyond a certain a mount, but without cysteine, you simply still wont bind all those ARs to the ARE
Nothing gets upregulated. When you take fin you simply have more NAD. and NAD is what is needed to put cysteine into the cell. the minute cysteine is in the cell
then body can use zinc , and this is your ZINC FINGER which makes your AR work. That is all.
You have more chance cycling CORTISOL supplements,
since cortisol will get rid of CALCIUM and will get rid of copper. and permanently increase NAD levels.
and your cysteine will be more available and everything will be working. this is why cortisol induces Metalothionine enzymes which are ZINC FINGER enzymes.
And cortisol will downregulate your AR protein levels and expression, and then AR will block VDR and your will have less calcium.
Post AI Syndrome
@jaydoe is the only one on this forum who shared his story about perma AI crash (tons of others on excelmale forum, however). He reports to be severely estrogen insensitive (I suppose it would make more sense to say severely estrogen sensitive) and to have reacted very poorly to any increase in E2, listing phytoestrogens, endogenous E2 increase and SERMs as examples. That's interesting. SERMs are notoriously potent in PFS but he said that he got much worse permanently by just 1 pill of tamoxifen and 1 pill of clomid. Though, I don't think it makes sense to lump SERMs and phytoestrogens and E2 together in terms of their mechanism of action and with regards to how they affect ER. I wonder how he would respond to exogenous E2. Or resveratrol, for example.
The issue with ERs is, imo, also in part due to the fact that they are of 2 main types - ERa and ERb. This complicates things further but I don't think it's productive to try to focus too much on how they differ. I suppose the body would automatically try to find a balance between their expression in different tissues if it had the means and motive to do so.
On excelmale forum there's a very similar case to jay (both got done in by arimidex specifically) that worsened on DHEA after 1-2 month of ED application (idk if it's topical or oral). I wonder why. It has a strong binding affinity for ERb, not so much to ERa. Does this have any role here? Then there's some cases of aromasin crashers. One reports that his symptoms worsen (and his E2 levels in blood decrease) on all of these: progesterone, pregnenolone, dhea, and even HCG. Any ideas as to why? For some reason either aromatase activity decreases or estrogen metabolism increases (maybe they would present with high E2 levels in urine?). Is this because of ER overexpression and resulting compensatory mechanism of excessive lowering of E2 in blood?
Certainly there has to be a logic behind all these cases. I've read their reports and talked to some of them and despite there being some notable variance in symptoms (some have 0 gyno, some very sensitive nipples; some numb dick, some very sensitive; some ok libido, some nonexistent; some deal with gut issues, some have none ...) there's way too much commonality to think that underlying issues are not very similar (most other symptoms overlap, like low motivation, issues with joints, fatigue etc.). Years of this shit, where some improve and some see 0 progress in recovery. How can this be - is there actually some kind of permanent damage at play? Overall, it seems quite similar to PFS - but I feel that most of these PAIS cases have not yet tried to experiment much/have not yet tried to follow any consistent protocol. And there's not much blood tests to go off. In the coming months/year I'll try to do HTMA (maybe even TEI), OAT and some extensive blood work (DHT, E2, TT, progesterone, prolactin, cortisol, electrolytes, thyroid, ferritin, ceruloplasmin etc.) if my wallet will allow it. I'll make my own thread later on.
Sorry for rambling, haha.
