OK, that's interesting. I am a bit confused now by the rules governing the sensitivity of AR's. After reading a study on rat penile tissue, which revealed that the higher the presence of DHT the more up-regulation of the AR occurred (which was opposite to the hypothosis the author was trying to prove!) I was under the impression that all receptors would up-regulate/sensitise is the presence of more of the androgen the particular AR is programmed to take- even though even to me this does seem counter intuitive.
If i recall correctly, CDSNUTS recovery by cycling pro hormones was based on this theory - though that was just one facet of his programme so no one can ever know whether that element was critical or not.
I'm open to using clomid in the future, but i just need to know for sure why i am doing something. Your explanation makes sense if it is correct for sure that the E receptor becomes more sensitive in the absence of E - this is certainly logical, but how do you know that? Is there a study or whatever demonstrating this?

What you are saying does also make logical sense when applied to a finasteride users issues. They take fin, their T rises (due to DHT being blocked), users often feel great for a while (i certainly did) then E rises. Meanwhile the AR's downregulate in the presence of additional T and E, causing ever more E to be produced (based on a desensitised Pituitary/hypothalmic E receptor action + no DHT present to reduce E), leading to very high SHBG and ultimate crash.

Almost all Fin users get high E symptoms at some point - Personally, i grew an enlarged left nipple! So it is fairly safe to say high E is the beginning of the issue.

So i do believe you are right, but like i say, i would love to know of any studies on this as i can only find the rat one which demonstrates the exact opposite (i appreciate rats aren't human!)

Finally, onto the long term use of AI resulting in low T and E - yeah i have read the results of the year long trials of an AI which resulted in T starting to fall around month 6 and continuing to do so until month 12 in all users. To be fair though end T levels were still at around 17 with a baseline of around 10/11 ish, so they were still way higher. This is why i think i can buck that trend:

1- I have noted that most AI users only need the higher doses for a short while - 8 weeks or so, then they can cut the dose to a fraction and maintain healthy E levels, which i plan to do.
2- The moment i have energy, i workout. The trials used obese and hypogonadal patients who were in that position for - most probably - reasons of diet and exercise, so it is no wonder their bodies couldn't persistently kick out higher T.
3- If you are correct regards the E receptor upregulating in the presence of less E, then i should be able wean off completely before the long term trend of lowering T kicks in - ie within a year.

I am looking for your comments on whether this all makes sense by the way! I am dangerous at the moment as i have a little knowledge!

If you tell me my plan makes sense, i will go for it for the next 12 months, and if i am still not where i need to be, then i will use clomid, provided you can point to some evidence that E receptors sensitise in the absence of E etc.

I really appreciate your help Jel. Having a plan is only any good for me when i both believe in it and understand why i am doing it, hence your explanations are very helpful.