Autoimmune and Gut Health Part 2, The Gut-Brain Axis Series, The Microbiome-Autoimmune Connection

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Last week in Autoimmunity & the Gut Part 1, we introduced what is autoimmunity (AI) and discussed some gut issues that can contribute to autoimmunity; such as leaky gut and dysbiosis. This week we look at specific microbiome issues in common AI diseases and we will give you ways to manage and address an autoimmune condition.

As we saw last week in Part 1, certain pathological bacterial strains are found in dysbiosis and with certain AI conditions.

FURTHERMORE, THERE IS EVIDENCE OF MICROBIOME DISRUPTIONS IN COMMON AI DISEASES:

  • RHEUMATOID ARTHRITIS (RA): As we saw last week, patients with new-onset RA have higher levels of a pathological bacterial strain called Prevotella copri (Bo Li, 2018). A study comparing RA patients and healthy controls confirmed a disturbed microbiome i.e. dysbiosis, which was partially resolved after RA treatment (Bo Li, 2018). Other studies have distinguished patients with RA from healthy controls as having dysbiosis (Thomas S, 2017). Current treatments for rheumatoid arthritis target symptoms. However, by focusing on the role played by gut bacteria, new treatment options looking at reducing the spread of P. copri in the gut could delay or prevent the onset of this disease (Scher JU, 2013).
  • TYPE 1 DIABETES (T1D): Multiple studies have shown dysbiosis in individuals with preclinical T1D (Bo Li, 2018). Issues include a sharp decrease in microbiome diversity, low community stability, an abundance of the Bacteroides strain of bacteria, fewer Bifidobacterium species and a lack of butyrate-producing and lactate-producing species (Bo Li, 2018).
  • MULTIPLE SCLEROSIS (MS): Studies suggest a distinct alteration in the MS gut microbiome compared with healthy controls (Bo Li, 2018). A study of 60 MS cases has reported an increased abundance of Methanobrevibacter (Archaea) and Akkermansia and a reduction in Butyricimonas (Bo Li, 2018). These MS-associated bacteria in the gut predispose the body towards a pro-inflammatory profile (Bo Li, 2018). To continue reading CLICK HERE.

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