Interesting. Reminds me that I once used to inject pure AMP. I can't for the life of me remember why though. It was gifted to me by someone who wanted me to try it.What follows is far-fetched conjecture, just my own application of a bunch of different ideas and it may be way off:
Of course, we use adenosine to form adenosine triphosphate - ATP. We break down adenosine with an enzyme called adenosine deaminase. During the day, we are breaking down ATP and adenosine builds up in our tissues from the energy use. This makes it a perfect molecule for signaling a need for sleep. Once it builds to a high enough level in our brains, we get sleepy. Caffeine is an adenosine antagonist - it blocks the action of adenosine and thus keeps us awake.
Once we are asleep, adenosine deaminase starts clearing out the built up adenosine, and it falls throughout the night (relatively quickly actually) and this creates a better environment for wakefulness.
Adenosine has an effect on every tissue in the body, and often contradictory effects because there are 4 different receptors and these receptors have different affinities, different tissues have different densities and distributions of these receptors, etc. This means that while adenosine may make our brains sleepy in general, too much can also be excitory.
So, for instance, when you have a certain level of adenosine in a certain area of the brain it will activate the A2a receptors (going from memory, the sub receptor may be wrong) because these receptors are abundant and have a higher affinity for adenosine - but if adenosine becomes so elevated that all these receptors are full, you will start activating the A1 receptors in this section of the brain with the remaining adenosine and this will have the opposite effect.
So, too high or too low and you may have seemingly paradoxical effects.
There is a heart connection as well because A2a agonists induce sleep, but also have negative effects on heart tissue (which is why we don't use them for insomnia).
Adenosine is also, again obviously, a major component of Adenosine Monophosphate (AMP) which builds in cells during energy usage (exercise, dieting, etc.) and we eliminate this with AMPK. Just for the connection.
So, I'm not sure if there is actually any genetic "disease" or clinical situation where some people might have lower levels of adenosine from dieting, or higher levels of adenosine deaminase - but it may play a role.
I did find this: https://www.pnas.org/content/102/43/15676
Perhaps you run low on adenosine early in the night - either because you have low levels of adenosine or because you have high levels of adenosine deaminase that clear it out quickly?
Not really sure what to do to test it...as I'm just thinking out loud here...but maybe those ideas create more discussion? I could be wrong as well about some of it...
As far as the B12 - do you take methylated formulations? I was wondering if you might have issues utilizing some forms of B vitamins - which is why I suggested the P5P for the ZMA formulations....
I'm really not sure what this is, but you're not the only person who claims they get insomnia from caloric deficits and I think most people write it off as "hunger is waking you up" or discomfort - but I'm not sure there isn't a chemical pathway underlying it all.