B12 is needed in the folate cycle which is part of the *remethylation* cycle (= recycle homocysteine back to methionine). (Not good...so long SAM = depressed.)
ALTHOUGH, to compensate - to lower very dangerous levels of homocysteine - the body may then be
forced to use an alternate pathway:
the transsulfuration pathway may kick in to lower homocysteine which requires B6 (PLP/P5P) and an enzyme called CBS to lower homocysteine...
resulting in the production of taurine (which lowers cholesterol!!!)+ GSH = glutathione + sulfate.
Bb wouldn't like to see cholesterol lowered - esp. the bad forms of cholesterol (!), so theoretically a fish tapeworm infection might be beneficial from that aspect...forcing the transsulfuration pathway -> taurine (lowers LDL), GSH and sulfate.
Bb needs cholesterol(esp. LDL it appears) and D-galactose:
Recent studies by other groups have demonstrated that
Borrelia burgdorferi, B. garinii, and B. afzelii attach a D-galactose molecule to a cholesterol molecule
via Î²- galactosidic linkage in place of a D-glucose molecule
Put simply, the O-glycoside bond between sugar molecule and sterol molecule in H. pylori differs from the O-glycoside bond between the same two molecules in other organisms.
It appears Bartonella (to clear) needs a Th2 immune response and since it appears in Lyme disease, a Th1 response BECOMES prominent - after an initial Th2 response, it is not surprising other infections (that require a Th2 immune response) can perhaps
more easily take hold.
OR...does the body make use of Bartonella to alter/shift the immune response back towards a Th2 response?
Interesting shifts in immune responses also happen during preganancy: