^ yes but at the concentrations that your building blocks exist in the brain, that won't happen. My biochemistry is weak, but I'm pretty sure that it won't work, unless the n-acetylethanol is a substrate for one of the enzymes that synthesize endocannabinoids. Then you've got to figure out it's bioavailability. DO check out that paper I uploaded, which shows the varied biosynthetic routes which produce anandamide. Perhaps with some luck, you can find a prodrug that is a substrate for one of those enzymes.
As for other possible dangers of inhibiting MAGL and FAAH on a regular basis, think about the dangers of the full agonists like the members of the JWH series. There are several case reports that I have read which states that ceasing administration precipitates severe withdrawl symptoms. Additionally, routine administration of full CB1 agonists produces marked cognitive and learning defects. The endogenous ligands are, by default, full agonists, no?
By endogenous ligands I presume you mean Anandamide and 2-AG. I don't have any articles on hand to prove this (sorry) but Anandamide was found to be a partial agonist at the CB1 and CB2 receptors and 2-AG was found to be a full agonist at the CB1 receptor.
EDIT:
Based on the PNAS paper and a few miscellaneous papers I have come across it is quite clear that both Anandamide and 2-AG affect both CB receptors. The above is just what I recall being mentioned in most papers. To my knowledge no one really knows exactly what these two compounds do and how they interact with each other. The PNAS paper "proves" that they are both important if you are after a THC-like effect without ingesting agonists.
PEA.pdf