That route makes more sense to me, too.
Maybe when the bacteria guy checks in he'll have some extra input, too.
I think most of this is, at the root, is an energy thing, including MK4 and Vitamin D biosynthesis versus a direct consequence of the bacterial organisms, but if Trevor Marshal has evidence of this, o.k. Of course I don't know exactly what is meant by "infected," I guess I just see this to be more likely an indirect consequence involving many other factors. In the bacterial world, some organisms, including some Bifidobacterial and Bacillus species biosynthesize K, and some use it for their growth. I'm not sure how important a microbial source may be to humans, but given that this synthesizing capability should be acquired at birth via innoculation Bifidobacterial organisms from the mother, it may be of consequence.
Hydrolysis of MK4 like Vitamin D would inhibited by free radicals. Really, I think we need to look at this situation more molecularly, so to speak. What is necessary for many of these hydrolase enzymes to function is Biopterin, aka BH4, but it is not really a biopterin problem, you have to go down further, looking at the nucleotides that make up DNA, purines and pyrimidine, which include guanosine and adenosine among others. This is part of the one carbon cycle, which cannot function without tetrahydrofolate, so there is a folate connection for you. Actually, by fake folates, I'm assuming she is referring to folic acid. There are a number of problems here that relates to what I was describing before, but I will spare you the details.
Purines are themselves aromatic compounds that are built around a nitrogen molecule. It so happens that there are some compounds that have a special affinity for LPS, and this includes nitrogenous heterocyclic compounds, amines including histamine and tetrahydropyrrole, as in HPU, KPU, Pyroluria. This is a well documented abnormality in ME/CFS, which may relate to the biological mess I have been describing. Seems that were LPS goes, these things follow.
Now this brings me to the catabolism of substances that seems to be relevant. From basic to more acid: amides are converted to more alkaloid carboxylic acid->amines->ammonia. Recall what I said about what can happen in the colon:
"The second, method whereby the Bifidum will decrease plasma ammonia is through it's ability to alter pH. Lower pH reduces the production of ammonia by intestinal organisms. What I think is more consequential though is that a lower, and more acidic pH will enhance hydrolysis. In the lower pH of the large intestine ammonia (NH3) can more readily bond with Hydrogen, creating ammonium (NH4). The importance of this reaction is that ammonium cannot pass through the bowel wall into the blood. Reducing pH in the colon thus allows for ammonia to be converted to a less toxic form, and one that does not diffuse into the blood."
You really need that hydrogen bonding and conversion to NH4 (Nitrogen + 4 Hydrogen Molecules). NH3 (ammonia) is, through the process of hydrolysis, combined with a water molecule to form NH4 and one of those OH groups again; the hydrogen molecule from H2O hops onto the ammonia and renders it much less toxic. You don't want that extra hydrogen molecule hanging around because your mitochondria are not going to like that nor is your cell lining, but lots of bad bacterial don't mind, in fact they prefer it.
So I started off talking about K & D, but maybe some of the food sensitivities are starting to make sense. Amines which includes purine rich plant alkaloids, phenols, which include salicylates, they cannot be efficiently metabolized if there is a hydrogen bottleneck. It's a hydroxyl radical problem, at least that's what it looks like to me, but I'm sure as heck not a chemist, microbiologist, immunologist, etc. We do know that bifidobacterial organisms enhance the metabolism of these substances, and I doubt this is coincidence even though we should have he inherent capacity to take care of this without the bacterial contribution. Of course you can see some real problems when you lose commensal clostridial species to produce butyrate and maintain the intestinal lining yet these are dependent upon the Bifidus species for acetate and for keeping the other pathogens in check. The high colonic pH maintains the problem of intestinal permeability, impairs the metabolism of amines, sustains the dysbiosis and simultaneously crushes the energy metabolism and the immune response.