For orally ingested substances such as vitamin D, salt, or dietary fats, the intestine plays a special role with its total length of over 5.5 meters, a surface area of approximately 35 m2, and its variety of microorganisms in the intestinal lumen (intestinal flora).
The germs in the intestine (collectively also referred to as the microbiome) are divided into germs that benefit humans (so-called symbionts, e.g. with beneficial effects on the immune system), germs without pathological significance (commensals) and germs that can potentially have pathological significance (pathobionts, which can contribute to inflammatory processes). In a situation of equilibrium, there is a balance between symbionts and pathobionts. A microbial imbalance in the intestine, with an excess of pathobionts and pro-inflammatory influences, is called dysbiosis. This dysbiosis can be caused by many factors – for example, medical influences like antibiotic use – but can ultimately also be influenced by the individual’s lifestyle (stress, dietary factors).
In the context of autoimmune diseases like MS, it is currently an attractive hypothesis that changes in the gut, with an imbalance of the immune system, play an important role in the development of autoimmunity. Therefore, the microbiome (and its possible influence by dietary factors) is of great importance. The basis for this is a study from the Max Planck Institute for Neurobiology in Munich from 2011, which clearly demonstrated using a genetically modified mouse model and completely germ-free mice that intestinal flora is an absolute prerequisite for the development of autoimmune demyelination in the CNS in the experimental model.
Despite this essential finding about the role of the intestine in autoimmunity, the question of a specific intestinal germ that could be partially responsible for MS remains open – and it is also uncertain whether this question can be answered at all.
It is noticeable that all previous studies have found different changes in the microbiome and no uniform pattern has been demonstrated between the different cohorts. Most studies do not go beyond a purely descriptive approach. Accordingly, it is completely erroneous and misguided when third parties promote stool transplantation for the treatment of MS. Such a measure lacks any rational basis at this point in time.
In view of the somewhat disappointing results so far in examining individual intestinal germs in MS, the concept seems attractive that not only the sheer number of individual germs for the intestinal microbiome, but rather their metabolic products play a role. Thus, the intake of fiber-rich food leads to the production of short-chain saturated fatty acids (such as acetate, butyrate, and propionate) in the intestine, which have beneficial effects on the intestinal epithelium and also directly on immune cells.
Functional studies showed that adding propionate to T cells in culture increased the frequency of regulatory T cells and at the same time reduced the frequency of pro-inflammatory cells. Similar observations were found in vivo after administration of propionate in the MS model with a milder course and a reduction of demyelination and axon damage.
Propionate is mainly found in crustaceans and was used as a preservative in bread products until the 1990s. Accordingly, the substance is approved as a dietary supplement in Germany and is also available for purchase online. After initial positive immunological studies in healthy people and also MS patients, the substance could be an interesting addition as an add-on therapy to the approved immunotherapies for MS.
Many MS patients are already implementing this concept, although there are not yet any definitive proofs for the usefulness of propionate. Since propinate is a harmless dietary supplement, it is probably similar to vitamin D – there is nothing to object to a pragmatic intake in view of the current scientific findings.
This was part 1/4. The other contributions around nutrition and Multiple Sclerosis (MS) can be found here:
