We have previously reported that wild type strains of Escherichia coli grow on the
***chitin disaccharide***
N,N′-diacetylchitobiose, ***(GlcNAc)2,*** as the sole source of carbon."
A disaccharide is the carbohydrate formed when two monosaccharides undergo a condensation reaction which involves the elimination of a small molecule, such as water, from the functional groups only.
They dissolve in water, taste sweet and are called sugars.
Chitin (C8H13O5N)n is a long-chain polymer of
a N-acetylglucosamine, a derivative of glucose,
and is found in many places throughout the natural world.
It is the main component of the cell walls of ***fungi***, the exoskeletons of arthropods such as crustaceans (e.g. crabs, lobsters and shrimps) and insects, the radulas of mollusks and the beaks of cephalopods, including squid and octopuses.
(Many definitions/explainations from Wikipedia)
Okay...GlcNAc...(2 of them = disaccharide)
N-Acetylglucosamine = (N-acetyl-D-glucosamine, or GlcNAc, or NAG) is a monosaccharide derivative of glucose.
It is an amide between glucosamine and acetic acid.
It has a molecular formula of C8H15NO6, and it is significant in several biological systems.
It is part of a biopolymer in the bacterial cell wall, built from alternating units of GlcNAc and N-acetylmuramic acid (MurNAc), cross-linked with oligopeptides at the lactic acid residue of MurNAc.
This layered structure is called peptidoglycan.
GlcNAc is the monomeric unit of the polymer chitin,
which forms the outer coverings of insects and crustaceans.
GlcNAc is also of note in neurotransmission, where it is thought to be an atypical neurotransmitter functioning in nocioceptive (pain) pathways."
Bb NEEDS GlcNAc.
Not surprising many of you "react" to ...
This may begin to explain some of the most common allergies (dust mites, mold spores - both
chitin covered)
and speak to the relationship between allergies and worm (helminth) infections, as part of one version of the hygiene hypothesis (worms have chitinous mouthparts to hold the intestinal wall)."
Problem:
T-Cell dependent antibody response to the dominant epitope of streptococcal polysaccharide, ***N-acetyl-glucosamine***, is crossreactive with cardiac myosin.
Bb is robbing the infected defense cells of glucose (it ferments it to make ATP) and this -> "mitochondrial dysfunction" (powerhouses of the infected defense cells don't work).
In a JAM, WE can use ketones instead of glucose to supply energy to the mitochondria in the defense cells to "rev them up" so they can finish the job they were supposed to do.
BHB is the ketone which comes FROM a KNOWN anti-bacterial, anti-viral, anti-***fungal*** caprylic acid.
Control the inflammation (bigtime) and resultant ROS/DNA damaging free radicals
AND
rev up the defense cells by using ONE ketone (BHB) instead of glucose (which Bb must have to make "his" ATP).
Macrophages...
Could GcMAF work? Maybe. It may activate the not- functioning macrophages (think of them as "pac men").
Serum Gc protein (known as vitamin D3-binding protein) is the precursor for the principal
macrophage activating factor (MAF).
But the Gc protein is ***deglycosylated*** by
a-N-acetylgalactosaminidase).
Deglycosylated = Removal of carbohydrates from glycoproteins.
SOMETIMES the removal of carbohydrates is done for PROTECTIVE reasons such as:
It appears the body is trying hard to remove carbohydrates so Bb can't use them.
Our body "knows" Bb is a sugar-lover.
Instead...why not substitute a ketone for the glucose so our infected defense cells can finish their intended job?
Posted by kday (Member # 22234) on :
Well, it looks like people this CFS forum are all over GcMAF, and some are using it themselves.
Trials are being done in Belgium, Netherlands, and the UK.
Is XMRV associated with chronic Lyme disease? From what I read, this looks like it could be the case for many.
Do we need to get rid of XMRV to get rid of Lyme and other infections? That's the question that I don't know the answer to.
I lived where the first major CFS outbreak was when I got sick (though not during that time frame), and I do fit the criteria very well. I do have positive antibodies and a positive western blot indicating an active infection for Lyme and have observed many different bacteria in my blood stream (my blood is much more clear now), but even so, could XMRV be the engine behind these chronic pathogens for many of us?
It would be interesting to see someone with Lyme/CFS enter these studies or even try treatment with their doctor.
If GcMAF could work, do you think it's possible that sepsis could occur from die-off? How about patients that are still sick but are no longer herxing? Perhaps they are better candidates.
I guess a safe approach would be to lower bacterial infection load a much as possible with traditional approaches and then try GcMAF?
Posted by Carol in PA (Member # 5338) on :
I read kday's info about GcMAF on his other thread, and got excited. Keep an eye on this technology!
![[Smile]](smile.gif)