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 β- 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:
The APOE gene provides instructions for making a protein called apolipoprotein E.
This protein combines with fats (lipids) in the body to form molecules called lipoproteins.
Lipoproteins are responsible for packaging cholesterol and other fats and carrying them through the bloodstream.
Apolipoprotein E is a major component of a specific type of lipoprotein called
very low-density lipoproteins (VLDLs).
But...
in lipoprotein (VLDL)-induced
foamy macrophages...
In TB infections and others:
The foamy macrophage appears to be a key player in both sustaining persistent bacteria and contributing to the tissue pathology that leads to cavitation and release of infectious bacilli.
PLEASE read my (new) Lyme Vaccine to OspB link.
Posts: 9424 | From Sunshine State | Registered: Mar 2001
| IP: Logged |
posted
reading!
Posts: 631 | From the south | Registered: Nov 2008
| IP: Logged |
Razzle
Frequent Contributor (1K+ posts)
Member # 30398
posted
Interesting! So the infections may make mutations in the methylation pathway more of an issue... Thanks for this - it fits with my own experience...
-------------------- -Razzle Lyme IgM IGeneX Pos. 18+++, 23-25+, 30++, 31+, 34++, 39 IND, 83-93 IND; IgG IGeneX Neg. 30+, 39 IND; Mayo/CDC Pos. IgM 23+, 39+; IgG Mayo/CDC Neg. band 41+; Bart. (clinical dx; Fry Labs neg. for all coinfections), sx >30 yrs. Posts: 4166 | From WA | Registered: Feb 2011
| IP: Logged |
The Lyme Disease Network is a non-profit organization funded by individual donations. If you would like to support the Network and the LymeNet system of Web services, please send your donations to:
The
Lyme Disease Network of New Jersey 907 Pebble Creek Court,
Pennington,
NJ08534USA http://www.lymenet.org/
UBBFriend: Email this page to someone!
Printer-friendly view of this topic