I think this is the crux of the issue. If one ascribed to the prion hypothesis, than ketogenic metabolism would almost certainly have to be related to higher probability of prion formation, and more survivable conditions in vivo.
Another common way some AAs are metabolised is by hydrogenation is red blood cells. So I think this eats up a hydrogen ion at the very least, leading to greater intra-cellular oxidisation and a messed up blood plasma pH, increasing the occurrence of abnormal enzymatic reactions. The metabolites you mentioned are present in much larger quantities on low carbs, due to increased synthesis and use of proteins for energy, including for the brain...
Oh and at least a few of those metabolites sometimes ultimately metabolise to acetone, especially if normal metabolism disrupted by wonky pH balance.
Anion gap in soft tissue cells may also explain 'twitches': spontaneous muscular activation due to soft tissue cell hyper-natremia (unbalanced towards sodium).
Crazily, excess acetone restoration is one theory that explains spontaneous human combustion (acetone is quite volatile and flammable)...
Another common way some AAs are metabolised is by hydrogenation is red blood cells. So I think this eats up a hydrogen ion at the very least, leading to greater intra-cellular oxidisation and a messed up blood plasma pH, increasing the occurrence of abnormal enzymatic reactions. The metabolites you mentioned are present in much larger quantities on low carbs, due to increased synthesis and use of proteins for energy, including for the brain...
Oh and at least a few of those metabolites sometimes ultimately metabolise to acetone, especially if normal metabolism disrupted by wonky pH balance.
Anion gap in soft tissue cells may also explain 'twitches': spontaneous muscular activation due to soft tissue cell hyper-natremia (unbalanced towards sodium).
Crazily, excess acetone restoration is one theory that explains spontaneous human combustion (acetone is quite volatile and flammable)...