One of the things which drives me on this idea is that guy on AskDocWeb claiming that research found his DHT receptors had been reduced in quantity.
Just to remark on a few of your points, I don’t think we can conclude that someone with super-high DHT and low T still won’t have impotence, ED, and all the other lovely perks of hypogonadism. DHT is not a substitute for T.
I think a more curious inquiry is, why is all that T being converted, leaving such little T? With all that DHT already circulating, the body should know DHT is awfully high and T is awfully low, and ease up on the conversion. (But does the body control the conversion amount, or is that predetermined by the amount of 5AR enzyme in the body?) So perhaps it is simply a response to DHT not registering, as what happens in cases of AR insensitivity, causing the body to respond with high amounts of the hormone (as you and a few others have suggested).
Also, I think it needs to be determined how DHT impedes Estrogen (ie if binding to DHT receptor is necessary for the inhibitory effect on E). Supposing high E is a result of DHT not doing it’s job makes sense (only reason I can think of too), and yes this will contribute to shutdown of T production. Many pitfalls in using fin.
Sleep has a lot to do with hormonal production, and there are GABA receptors in the pituitary gland (which for one, modulate the release of Growth Hormone). I’m very interested in the role of the GABA receptors relative to endocrine function, because there may be a significant interrelation. Also the important place Nitric Oxide - the very substance depleted by DHT reduction - has in allowing for sleep to occur.
What we need to focus on is getting examined for this possible insensitivity.