Very good grasshoppa, you have come far quickly.
If you are taking methylfolate it will become simply tetrshydrofolate (THF) once it donates its methyl group to cobalamin 1 in the MTRR catalyzed reaction. THF is then turned back into 5 10 methylene tetrahydrofolate in a SHMT catalyzed reaction. There has to be balance of b12 and folate in the cell, if there is an imbalance either way, it can cause methyl trap. I cant imagine what it would take to methyl trap from taking too much b12, Ben is basically saying make sure that the body is not short on methylfolate so it can “catch” cobalamin after the MTR reaction, when cobalamin is unbound and reactive. You are supplementing methylfolate and you are using very little methylcobalamin, so it is not a worry in your case, your body is basically creating cobalaimin 1 at a rate limited by methylfolate. You are taking plenty of b12. So no worries.
Yep, creatine places the largest on SAMe in the body. In a backwords sort of way supplementing boosts your bodies methylation status. Same with anything that is on a feedback cycle that uses SAMe or anything that is a net methyl donor.
Thats why so many doctors recommend protocols that boost NAD. Ive been studying that a bit more and I think Radio has the best idea on it, I still think tryptophan is a great idea to try. You have to think of your net antioxidant status as well and focus on that too, thats basically the link in the chain that broke that put you into the condition you are in. Anything you can do to create and reduce glutathione without harming any other part of your condition is huge plus.
That link I posted to the blog about thrombosis recommended enzymes, that was the best I could find on that in the limited time I spent looking. I’ll look some more. I think you should try that before you try something like VIP.
From my earlier comment on niacinamide. It looks like a super CFS sup, prolly why Ive seen quite a few cfs patients put on it by their docs.
“Niacinamide acts as an antioxidant by preventing NAD depletion during DNA repair by inhibiting poly (ADP-ribose) polymerase (PARP), which also modulates major histocompatibility complex (MHC) class II expression. Niacinamide inhibits free radical formation and facilitates beta-cell regeneration in vivo and in vitro.7,8 Additional protection from macrophage toxins may be involved in prevention of type 1 diabetes.9 Specifically, niacinamide has been shown, via PARP inhibition, to protect pancreatic islet-cell lysis after exposure to oxygen free radicals10 and nitric oxide.”