Multiple Sclerosis and microbiome

Prologue

This blog main theme is Chronic Fatigue Syndrome. I have diverged in a few posts into other autoimmune diseases. One reason is simple: once a microbiome dysfunction happens, the dysfunction may progress into other autoimmune diseases. My wife started with IBS, then went to CFS followed by remission to be followed over a decade later with atypical Crohn’s disease.

What conditions develop is like a combination of microbiome (which appears to be inherited) and DNA. Some people may ask … what microbiome and dna are both inherited? The answer is pretty simple to understand — like all complex environments — they interact.

A long winded summary from 2011
“The mutualistic relationship between the host and its intestinal microbiota (microbial community) plays a major role in mammalian immunomodulation and metabolism (14). Outstanding examples of this are Crohn’s disease (CD) and ulcerative colitis (UC), chronic human disorders that are collectively designated as inflammatory bowel diseases (IBDs). Growing evidence supports the hypothesis that these entities develop secondary to a genetic predisposition for an exaggerated mucosal immune response against components of the intestinal microbiota, and that this process is modulated by environmental factors (56). The microbiota and the host may simultaneously and/or interdependently respond to such factors. These responses are likely affected by the genetic composition of the host. With regard to this relationship, epigenetic mechanisms (molecular processes that can influence gene expression without a change in the genetic code) are environmentally responsive and have been implicated in the pathogenesis of IBDs (67). An increasing number of observations reveal associations not only between genetic and epigenetic variation (8), but also between intestinal pathogens and mucosal epigenetic changes (9). However, these interactions have rarely been addressed in regard to IBD susceptibility genes, bacteria, and host-specific epigenomic modification, such as DNA methylation (methylation of cytosines in CpG dinucleotides; ref. 8). Meanwhile, environmentally sensitive nongenomic alterations are likely significant in the development of these diseases (6), and relevant intestinal epithelial epigenetic modification can occur in response to bacterial components (10).”

“Furthermore, a growing body of evidence suggests that the gut microbiota plays a role in the development of a range of autoimmune diseases including inflammatory bowel disease, multiple sclerosis, type one diabetes and rheumatoid arthritis.” [2016]

Multiple Sclerosis and the Microbiome

Bottom Line

Many people with CFS had EBV and are low in Vitamin D – thus increase risk of evolving to MS.  Having SIBO may increase the risk of MS by a factor of 5.

While it is not possible to “unget” EBV, it is very possible to increase Vitamin D levels (IMHO at the top of the normal range is desired, not just inside of the bottom of the normal range).

Above there are many bacteria genus associated with MS — if you have had your uBiome done, you may wish to do comparisons and if heading towards the MS profile — you may wish to consider aggressive actions to alter you microbiome away from this profile.

As always, this is an educational post and not intended as medical advice.