Well, it's difficult to say, but it may be somewhat similar to that seen with monoamines, where just adding SE doesn't result in MDMA or psychedelic effects, adding DA doesn't result in amphetamine or cocaine like effects (though there is some very minimal evidence that l-dopa can be somewhat recreational, though we are talking pretty minimal, at least so far).
Or does it have to do with the nature of the conformational change that endocannabinoids produce at the CB1 receptor?
I assume that it is related to this, though in animal models, they seem to produce changes somewhat related to that seen with exogenous cannabinoids. Perhaps there are other endogenous cannabinoids that could do this, I'm not really sure.
Is FAAH's catabolic activity comparable to MAO's?
I'd have to look into this more, but there are some pretty major differences between these. It seems that all of the MAOIs are either irreversible (or they're reversible, but the concentrations required to reverse aren't clinically relevant for most part, though I'm sure that this is not entirely true, but seems to be for the most commonly used RIMAs, at least those I'm familiar with). From what I know of FAAH inhibitors, they don't inhibit FAAH to nearly the extent that MAOIs do MAO. It seems more comparable to other enzyme inhibitors like those used with opioid enhancement.
This might be entirely wrong, I've read very little on the subject and this is mostly the impression I've gotten.
But really, one trial isn't worth much and probably shouldn't be used for any sort of generalization. There'll be people given fair doses of morphine who don't notice an effect either, and I tend to always expect nothing to happen with new new things. All of this said, I have heard another report that had the same results (without the headache).
Ham
I'm still talking about positive modulation of the CB1 receptors. Benzodiazepines are somewhat more relevant to that discussion.
Ah, I see. I don't know. I'm not even aware of any, honestly.