Friday, 14 November 2014

Probiotics. Good and Bad.

Us folk with autoimmune disorder almost always have some kind of dysbiosis - an imbalance in the flora of our gut. For instance, just as an example of the gut-immune connection, gut disorders like Crohn's disease and Ulcerative Colitis are both associated with Ankylosing Spondylitis. Also, taking antibiotics can bring autoimmune symptoms into remission briefly.. although the flora adapt quite quickly, especially the pathogenic ones. 

We are certainly missing key flora necessary for good health (called commensal flora). People have been brought into remission for months at a time via Faecal Matter Transplants (FMT). And I myself experienced an amazing remission of my Ankylosing Spondylitis after my neighbours gave me their homemade Natto. 

But that doesn't mean Yoghurt will help you much. It is beneficial in that it crowds out pathogens and corrects pH (acid producing flora are beneficial). Unfortunately beyond this, the standard probiotics don't do much. They just don't correct the underlying gut disorder, leaky gut or missing commensal flora. 

Some of us have experimented with more exotic probiotics - those with 10 or more strains. I can't get these in Australia so I have to order them online. 

There are a few things to be wary of with probiotics

Our experience as a group (on with probiotics are hit and miss. Worthwhile experimenting with though..But be warned!.. Two members have actually had there AS become worse after taking probiotics. One had a stiff neck for the duration, and the other had his AS badly worsened for some weeks afterwards. Both these people were seasoned followers of the No Starch Diet, and knew to check for starch. 

Starchy additives are quite a common issue we face, as are other polysaccharides used as probiotics, namely inulin and FOS. So watch out for these. 

The other possibility is that the immune system is cross reacting with the flora (think "reactive arthritis" or "molecular mimicry"), especially when the gut lining integrity is poor (leaky gut). When flora get past the gut wall and into our blood stream out immune system will become highly irritated. 

More likely the new flora stimulated their immune system, thus causing the existing immune disorder to worsen. 
This immune stimulation with the flora is what I believe may have happened to the two seasoned NSD followers mentioned earlier. It is fairly rare for this to happen, but I just want people to be aware of this possibility.


- gut disease and yeast
Antibodies against S. cerevisiae are found in 60–70% of patients with Crohn's disease and 10–15% of patients with ulcerative colitis (and 8% of healthy controls).[2]

Anti-Saccharomyces cerevisiae antibodies (ASCAs) have been proposed as serological markers, which may differentiate Crohn's disease (CD) from ulcerative colitis (UC) and predict disease phenotype. Their importance in pathogenesis is unproven. We investigated the relationship between ASCAs, disease phenotype and NOD2/CARD15 genotype in CD and whether ASCAs were related to antibodies to other fungal proteins. Serum from 228 patients [143 CD, 75 UC, 10 with indeterminate colitis (IC)] and 78 healthy controls (HC) were assayed for ASCA. Antibodies (IgA, IgG) to other fungal proteins (Fusarium species ATC20334, Mycoprotein) were measured in the same samples using an in-house enzyme-linked immunosorbent assay (ELISA) assay. ASCAs were present in 57% of CD, 19% of UC, 30% of IC and 8% of HCs. ASCA-positive status was a predictor for CD with sensitivity of 57%, specificity of 87%, positive predictive value of 78% and negative predictive value of 68%. ASCA was associated with proximal (gastroduodenal and small bowel involvement) rather than purely colonic disease (P < 0·001) and with a more severe disease phenotype and requirement for surgery over a median follow-up time of 9 years (P < 0·0001). No associations with NOD2/CARD15 mutations were seen. There was no association between ASCA and antibodies to MP (IgA or IgG). These data implicate ASCA as a specific marker of disease location and progression in CD, emphasizing the heterogeneity within IBD.


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