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Califamily

Has anyone tried GlcNac?

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I started this thread -- and originally had wondered if glcnac were like ivig -- you were pushing out the bad igg with new igg. so if you supplemented with glcnac == were you trying to push out the bad glcnac. However, I still don't understand it and the mechanism. I wonder what the NIH thinks about this? or if any other doctors or researchers has a pov?

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califamily,

 

so if you supplemented with glcnac == were you trying to push out the bad glcnac.

 

Here is something that explains it much better than what has already been posted. I couldn't find it before, as the old link didn't work anymore. It has a diagram that is very helpful.

 

http://www.newscientist.com/data/pdf/press/2607/260720.pdf

 

forgt to post the link!

Edited by kim

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Just doing more reading on GlcNAc today and came across this article about Alzheimers and O-linked GlcNAc, Jan 2014 http://pubs.rsc.org/en/content/articlelanding/2014/cs/c4cs00038b#!divAbstract. Forgive me if it's been posted before. I don't have access to the full article though it might be interesting to read if anyone does have such access. Abstract:

 

Within the brains of AD patients O-GlcNAc levels have been found to be decreased and aggregates of tau appear to lack O-GlcNAc entirely. Accordingly, glucose hypometabolism within the brain may result in disruption of the normal functions of O-GlcNAc within the brain and thereby contribute to downstream neurodegeneration. While this hypothesis remains largely speculative, recent studies using different mouse models of AD have demonstrated the protective benefit of pharmacologically increased brain O-GlcNAc levels. In this review we summarize the state of knowledge in the area of O-GlcNAc as it pertains to AD while also addressing some of the basic biochemical roles of O-GlcNAc and how these might contribute to protecting against AD and other neurodegenerative diseases.

 

If anyone can explain this to me, a simpleton, I'd much appreciate it. I'm not sure whether these questions even make sense: (1) if there are antibodies in PANDAS that attack GlcNAc, would there necessarily be a "deficiency" of GlcNAc in the brain (that perhaps contributes to symptoms), and (2) if it were possible to raise levels of GlcNAc in the brain via oral supplementation, would the raised levels stimulate yet more unhelpful antibodies, or would the antibodies that were present become "deactivated" by binding with the new available GlcNAc? or both?

Edited by jan251

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Regarding the Yasko sulphating of the gags discussed upthread, just updating with this little tidbit that I hadn't noticed before, that the old study about IBD in a pediatric population found an increase in sulphated GAGs following supplementing with glcnac:

 

Taking together, all cases where pre- and post-treatment biopsies were available (i.e. rectal and/or oral), there was significant increase in matrix sulphated GAGs (mean OD post treatment 171.8 ± s.e. 19.6 units vs. pre-treatment 98.6 ± 13.1, P < 0.01), and epithelial GAGs (142.8 ± 20.4 vs. 79.7 ± 9.9 units,P < 0.05).

 

Edited by jan251

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from that same study

 

If primary repair is not then possible, fibroblasts alter their matrix secretion pattern in response to macrophage cytokines to produce collagens, resulting in scarring.1, 13, 17

 

Is that not thought to be what occurs in heart valve damage in Rheum fever?

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Patents

http://www.google.com/patents/WO1993014766A1?cl=en

Use of n-acetyl glucosamine for the treatment of food allergy

 

This is a great find, just for the discussion alone! I don't know about their overall hypothesis (and method patents have fallen out of favor since then, or at least that's my understanding), but the discussion of how things work is fantastic.

 

Adding on here in case someone's reading this: apparently glucosamine, and specifically n-acetyl glucosamine, is contraindicated in case of Lyme.

Edited by jan251

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