Science Update

New study shows low commensal bacteria in multiple sclerosis patients

According to a new study published earlier this week in Scientific Reports researchers indicate that low amounts of beneficial bacteria or a dysbiosis in the gut microbiome may have a direct association with multiple sclerosis (MS). This is not a new revelation however it is good to see more of this information in the medical research.

There is a study from Plos One that I reference quite a bit in my presentations demonstrating this association. In this 2014 study researchers at Lund University published their findings on the role of the intestinal barrier in MS. Scientists had previously shown that probiotics could provide a certain amount of protection against MS. However they questioned whether the intestinal barrier was affected which led to their examination of inflammatory cells and processes in the intestine. As a result they saw structural changes in the gastrointestinal mucosa of the small intestine and an increase in inflammatory T-cells. In addition they saw a reduction in regulatory T-cells (immunosuppressive cells). These changes are often linked to inflammatory bowel diseases. They concluded that future drugs to treat MS should not only focus on the central nervous system but also on repairing and restoring the intestinal barrier.

The gastrointestinal tract is 80% of our immune system. Whenever inflammation is present the tight junctions and intestinal mucosa can become damaged compromising the lining of the GI tract. Then toxic byproducts in the digestive tract can be absorbed into the bloodstream forming immune complexes which eventually affect numerous systems throughout the body and cause inflammation food sensitivities and autoimmune disorders. 

According to this new study in Scientific Reports the research team confirmed that relapsing remitting multiple sclerosis (RRMS) patients do have a distinct microbiome different from healthy individuals with certain gut microbes showing decreased or increased abundance in RRMS patients compared to controls. The analysis of bacterial diversity showed no difference between total RRMS patients and healthy controls. With that being said RRMS patients with active disease showed decreased abundance compared to patients in remission and controls. This decreased abundance in RRMS patients with active disease suggests an important role of the gut microbiota in disease exacerbation. This study further supports previous research indicating that MS patients have dysbiosis of the gastrointestinal microbiome.

These two studies are perfect examples demonstrating the big disconnect between medical research and the practice of traditional medicine when it comes to the management of chronic disorders. 

Gut bacteria has been identified as an important environmental factor in overall health and all autoimmune disease. Patients may need antimicrobials botanicals enzymes prebiotics and probiotics to optimize the gastrointestinal environment. 

Any practitioner who is working with patients with autoimmune disorders should consider a comprehensive digestive stool analysis for these individuals a concept supported by modern research. There are several other factors that play a role in autoimmunity such as gluten intolerance food sensitivities gastrointestinal infections hormone imbalances heavy metal toxicity and nutrient deficiencies (i.e. vitamin D magnesium EFAs). These environmental influences filtered through genetic predisposition are fundamental components in the expression of disease and a successful treatment approach must include investigation into these factors.

 

By Michael Jurgelewicz DC DACBN DCBCN

 

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Source: Jun Chen Nicholas Chia Krishna R. Kalari Janet Z. Yao Martina Novotna M. Mateo Paz Soldan David H. Luckey Eric V. Marietta Patricio R. Jeraldo Xianfeng Chen Brian G. Weinshenker Moses Rodriguez Orhun H. Kantarci Heidi Nelson Joseph A. Murray Ashutosh K. Mangalam. Multiple sclerosis patients have a distinct gut microbiota compared to healthy controls. Scientific Reports 2016; 6: 28484 DOI: 10.1038/srep28484