One more thing. For sleep acetylcholine transmission wants to exist in certain bounds: not too much, not too little -- just like the brain itself, with its cycles of greater and lesser awareness during sleep. Like shutting off too much for too long is bad and not shutting off is also bad.
With physostigimine memory consolidation that would occur in sleep gets abolished in rats. Certainly insomnia can result from acetylcholinesterase inhibitors and acetylcholine precursors taken at too high doses. There are studies showing that citicoline does not impair sleep over time in human study subjects -- but perhaps taking larger doses could do so. People's reported experiences on forums like these would support that. We also should consider here that an acetylcholinesterase inhibitor, preventing acetylcholine's breakdown, is intuitively and definitively more disordering to normal function than providing precursors, whose further use would be regulated by any number of secondary systems. There would be an especially marked difference with a very powerful acetylcholinesterase inhibitor like physostigmine -- perhaps as well with an irreversible one, like many organophosphate pesticides and nerve gases.
For practical use this is mainly meant to say that for this purpose, I wouldn't try and overdo the doses, nor would I be too forceful and combine it with one of the plants/supplements that among their effects inhibit acetylcholinesterase, e.g. bacopa monnieri, ginkgo biloba, and coffee.
Edited by graatch, 08 September 2019 - 04:13 PM.