A bit of hopeful news for you today[i]. I don’t know about you all, but lately, I really feel like I need WAY more good news.
Researchers at the University of Illinois, Chicago, have published research which shows that there appears to be a link between intestinal inflammation and the microbiome in both the development of, and the progression of, ALS (amyotrophic lateral sclerosis). Apparently, the lead researcher, Dr. Jun Sun’s, interest in ALS was sparked by the upsetting recognition that many soldiers who suffer from GI issues go on to develop ALS, and subsequent research has shown that veterans have an elevated risk of developing the disease. According to the opening paragraph of their paper, these early GI symptoms (also apparent in other chronic illnesses like Parkinson’s disease, by the way) have been ignored for too long: “Thus, the current evidence indicates that intestinal dysfunction and dysbiosis may actively contribute to ALS pathogenesis.”[ii]
The scientists focused their attention on the interactions between the enteric nervous system (ENS), which is the nervous system of the gut directing its functioning and the microbiome. For their study they used mice which had been genetically engineered to carry the SOD1 gene (mutated superoxide dismutase 1, which is known as a cause of ASL). The mice were given the short-chain fatty acid butyrate, which is known to have a protective effect (as I’ve written about many times: see here and here as just two examples) or antibiotics. They then tracked intestinal motility, microbiome alterations and protein markers of the ENS prior to the onset of ALS. And what did they find?
The mice had significant microbiome alterations, decreased intestinal motility, and loss of physical stamina before the onset of the disease. BUT – in the good news – in the mice that were treated with butyrate or antibiotics, these changes took way longer to appear. SOD mice showed dysbiosis (for example, increased Clostridium sp. ASF502) by 1 month of age, before the dysfunction of the ENS. By 2 months of age, still before the onset of ALS, they had significantly lower intestinal mobility, decreased grip strength, etc.: “These changes correlated with consistent dysbiosis and increased aggregation of mutated SOD1G93A in the colon and small intestine.” ALS had set in by 3 months of age, and by then, showed significant changes in gut motility and an altered microbiome.
The scientist though found, “…that butyrate treatment and antibiotic treatment restored intestinal mucosal function and corrected dysbiosis in the ALS mice. Manipulating the microbiome improves the muscle performance of SOD1G93A mice. Our study provides insights into the fundamentals of intestinal neuromuscular structure/function and the microbiome in ALS.”
The conclusion of the study states that there is a link between early microbiome changes, the ENS (which regulates motility) and the onset of ALS. However, by inducing changes in the microbiome, via antibiotics or the protective short-chain fatty acid, butyrate, they were able to improve neuromuscular function in ALS in the animals, suggesting “…the potential to use microbial biomarkers for the diagnosis and to manipulate the intestinal microbiome for the treatment.”
They are not claiming that this is a cure for ALS but – they already they can make these animals live markedly longer. Dr. Sun states, “One mouse year equals about 30 human years. The treated mice lived an average of 38 days longer, which if you promote that to human life, it will be years of longer lifespan compared to the current drugs available to treat ALS.” And that is some good news at least.
[ii] Sarah Martin et al, A Gut Feeling in Amyotrophic Lateral Sclerosis: Microbiome of Mice and Men, Frontiers in Cellular and Infection Microbiology (2022). DOI: 10.3389/fcimb.2022.839526