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. A friend 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 (1–4). 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 (5, 6). 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 (6, 7). 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

• Prevalence of Small Intestinal Bacterial Overgrowth in Multiple Sclerosis: a Case-Control Study from China[2016].
  • “SIBO is highly prevalent in Chinese patients with MS. Further analytical work is required to establish a causal association between SIBO and MS risk and progression.” 38% of MS vs 8% of control
• Multiple sclerosis patients have a distinct gut microbiota compared to healthy controls[2016].
  • “We observed an increased abundance of Psuedomonas, Mycoplana, Haemophilus, Blautia, and Dorea genera in MS patients, whereas control group showed increased abundance of Parabacteroides, Adlercreutzia and Prevotella genera. Thus our study is consistent with the hypothesis that MS patients have gut microbial dysbiosis “
• “While there was overlap of gut bacterial communities, the abundance of some operational taxonomic units, including Faecalibacterium, was lower in patients with multiple sclerosis. Glatiramer acetate-treated patients with multiple sclerosis showed differences in community composition compared with untreated subjects, including Bacteroidaceae, Faecalibacterium, Ruminococcus, Lactobacillaceae, Clostridium, and other Clostridiales. Compared with the other groups, untreated patients with multiple sclerosis had an increase in the Akkermansia, Faecalibacterium, and Coprococcus genera after vitamin D supplementation.” [2015]
• Dysbiosis in the Gut Microbiota of Patients with Multiple Sclerosis, with a Striking Depletion of Species Belonging to Clostridia XIVa and IV Clusters [2015].
• Environmental factors in multiple sclerosis[2015].
  • ” Previous Epstein-Barr virus infection, especially if this infection occurs in late childhood, and lack of vitamin D (VitD) currently appear to be the most robust environmental factors for the risk of MS, at least from an epidemiological standpoint. “
• Gut microbiota in early pediatric multiple sclerosis: a case-control study [2016].
  • ” However, relative to controls, MS cases had a significant enrichment in relative abundance for members of the Desulfovibrionaceae (Bilophila, Desulfovibrio and Christensenellaceae) and depletion in Lachnospiraceae and Ruminococcaceae (all P and q < 0.000005). Microbial genes predicted as enriched in MS versus controls included those involved in glutathione metabolism (Mann-Whitney, P = 0.017),”
• Gut microbiota composition and relapse risk in pediatric MS: A pilot study [2016].
  • “A shorter time to relapse was associated with Fusobacteria depletion (p=0.001 log-rank test), expansion of the Firmicutes , and presence of the Archaea Euryarchaeota . After covariate adjustments for age and immunomodulatory drug exposure, only absence (vs. presence) of Fusobacteria was associated with relapse risk. “
• High frequency of intestinal T_H17 cells correlates with microbiota alterations and disease activity in multiple sclerosis[2017].
  • ” MS patients with high disease activity and increased intestinal T_H17 cell frequency showed a higher Firmicutes/Bacteroidetes ratio, increased relative abundance of Streptococcus, and decreased Prevotella strains compared to healthy controls and MS patients with no disease activity. We demonstrated that the intestinal T_H17 cell frequency is inversely related to the relative abundance of Prevotella strains in the human small intestine. Our data demonstrate that brain autoimmunity is associated with specific microbiota modifications and excessive T_H17 cell expansion in the human intestine.”
• Gut microbiota from multiple sclerosis patients enables spontaneous autoimmune encephalomyelitis in mice [2017].
  • “The microbial profiles of the colonized mice showed a high intraindividual and remarkable temporal stability with several differences, including Sutterella, an organism shown to induce a protective immunoregulatory profile in vitro. “
• Gut bacteria from multiple sclerosis patients modulate human T cells and exacerbate symptoms in mouse models [2017].
  • ” we identified specific bacterial taxa that were significantly associated with MS. Akkermansia muciniphila and Acinetobacter calcoaceticus, both increased in MS patients, induced proinflammatory responses in human peripheral blood mononuclear cells and in monocolonized mice. In contrast, Parabacteroides distasonis, which was reduced in MS patients, stimulated antiinflammatory IL-10-expressing human CD4⁺CD25⁺ T cells and IL-10⁺FoxP3⁺Tregs in mice. “
• Oral Multiple Sclerosis Drugs Inhibit the In vitro Growth of Epsilon Toxin Producing Gut Bacterium, Clostridium perfringens [2017].

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.