Kickas.org Forums Treatments, Drugs and Alternatives NSD and diet-related; Does it work or does it not?

Hi Jake,
If you thought that was double dutch, cop this one, the association of AS with CMP2

Capillary Morphogenesis Protein 2 (CMP2) Chromsome 4q 21.21
CMP2 (also known as ANTXR2, Anthrax Toxin Receptor 2) is widely expressed in human tissue, indicating that this receptor is likely to be relevant for disease pathogenesis. It should be noted that for both axial and peripheral disease sites in SpA inflammation develops in close proximity to cartilage or fibro-cartilage enthesis and there is a very pronounced neo-vascularisation in all inflamed tissue.

Although the precise function of CMP2 is not yet known, it’s extracellular VWA/I domain (von Willebrand Factor type A domain also known as Integrin inserted domain) binds collagen type IV and laminin, suggesting that these are its natural ligands in vivo and that it may be involved in extracellular matrix adhesion.
There are three isoforms of CMP2. Isoform 1 is expressed on cell surfaces; isoform 2 is expressed predominantly within the endoplasmic reticulum, and isoform 3 is secreted.

ANTXR2 (CMP2) is sufficiently similar to ANTXR1 (ATR/TEM8) to function as an anthrax toxin receptor. Other than this similarity the two receptors are encoded by genes on two different chromosomes and their apparent functions in vivo are probably unrelated.

It is thought that CMP2 functions to promote endothelial (cells that line the blood vessels) proliferation and morphogenesis (beginning of the shaping of new capillaries) during sprouting angiogenesis (formation of new blood vessels), consistent with expression of CMP2 in several vascular beds. CMP2 may have a possible role in endothelial (and epithelial) basement membrane (the thin sheet of fibres that underlie the endothelium or epithelium) matrix synthesis and assembly.

It is well known that vascular endothelial growth factor (VEGF) is increased in active AS (as is IL-6). Also IL-23 is known to promote angiogenesis. In RA (and presumably in AS) VEGF is released in response to raised TNFa increasing endothelial permeability and swelling and stimulating angiogenesis (formation of new capillaries).

Note that recessive mutations of CMP2 (that is 2 non functioning genes) causes juvenile hyaline fibromatosis and infantile systemic hyalinosis, conditions characterised by multiple skin nodules and hyaline deposition (at or near the basement membrane?), osteolytic bone lesions, and joint contractures. In infantile systemic hyalinosis (at least) gastrointestinal dysfunction (diarrhoea) is a major symptom.

Cheers David

http://www.ncbi.nlm.nih.gov/pubmed/20392505

Without ERAP functions we have unregulated IL 23/ IL 17 inflammation that leads to the disease process.

It is complex reading this stuff and I hope I am getting it right. There are good reasons the researchers are driving in this direction. Hopefully it pays off in the long run and is not another dry hole so to speak.

According to my doctor, when a disease is still at the stage of being defined by a symptom or set of symptoms, subgroups of patients with different root causes often get lumped in together. AS is currently at that stage where there is not a deep understanding of the disease and it gets defined by a symptom, in this case the defining symptom being bone inflammation that tends to fuse SI joint and vertebrae.

It seems likely that Klebsiella triggers this symptom for at least some people with AS, but how could we know that it is the only thing? Any particular case of AS could easily be an exception to the rule -- Klebsiella leaking from the gut might be the most common trigger only because Klebsiella itself is so common. There could easily be something else living in your gut that doctors don't even know to look for yet.

BTW, I'm curious -- do you know if you have HLA-B27 gene or not? Wonder if people with a different gene defect might have different triggers although same resulting symptoms...

@SJLC

yes - i'm HLA B27 positive.

SJLC - i am HLA B27 negative ..... i totally agree with your thought.

Hello there,

Adding my 2 cents rather late... but I agree with a lot of the posts prior. I have been on diet for 8+ years now and do well. But I will still flare from time to time... this may be some reasons why.

- Cheat on diet (i.e. eat starch knowingly or unknowingly)
- Stress
- Over doing exercise

The last two are not related to diet... but 3rd I think is related to the existing mechanical damage I have. It is not much, but I think enough in my hips that I probably notice with overdoing.

Tim

Tim, I got curious here...

After 8 years on the diet, you still have problems with starch?

I mean, can't you tolerate some starch, or some starchy foods?

You do LSD or NSD?

nothing new or revolutionary or rocket science in here. just a few extra things that might help assuming that someone is already doing a LSD/NSD.

foods that could cause problems - dairy, nightshades (tomatoes, bell peppers, eggplant), chocolate, excess sugar.
beverages - cola drinks (anything with caffeine and sugar), coffee, alcohol.

things that could help - butyric acid producing foods like prunes, green tea (theanine content boots immunity), garlic, ginger (starchy but anti-inflammatory).

supplements that can help - glutamine (fuel for gut lining), olive leaf extract (antibacterial + antiviral immune support). boswellia extract - natural TNF-a inhibitor has been to shown to have similar efficacy to ibuprofen without the gut damaging side effects, omega 3's.

that's all i can think of for now - one thing for sure is that everybody responds different to everything and one persons poison may be anothers medicine.

Thanks jroc

I am very confused by garlic. I thought it was starch?

I will investigate the otherss.

john mentioned in a recent post that benefits of antimicrobial activity could outweigh the small amount of starch in it.