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January 2020 (Vol. 11 Issue 4)

New hope for spinal injury victims—it’s all in the gut
About the author: 
Bryan Hubbard

New hope for spinal injury victims—it’s all in the gut image

There’s been a major discovery about spinal cord injury—often seen as a life sentence—that opens up the possibility of a full recovery.

Researchers have discovered that spinal injuries cause a fundamental change to the type of bacteria living in the gut, and it is this that affects nerve signalling, which is the most significant symptom and the major block to a full recovery.

Eating probiotics helps re-establish the gut’s ‘good’ bacteria, and this could help kick-start communication between the nerves and reverse neurological damage.

Researchers from Ohio State University have discovered that the trillions of bacteria in the gastro-intestinal tract—collectively known as the gut microbiome—are overwhelmed by inflammatory bacteria when the spinal cord is damaged. This dysbiosis, or gut bacteria imbalance, could happen when someone with spinal injuries loses bowel control, the researchers think.

The biggest changes to the gut bacteria also resulted in the poorest recovery from the injuries, say the researchers in experiments with laboratory mice.

Probiotics, containing lactic acid-producing bacteria, activate regulatory T-cells, the gut’s equivalent of immune cells, which suppress inflammation. In turn, this repairs spinal cord injury and helps improve neuronal growth and function.

Specialists need to stop focusing only on the spine, but instead start looking at the health of the gut as well, says lead researcher Phillip Popovich.

This latest discovery adds to the evidence about the vital function our gut microbiome plays. Autoimmune diseases, such as multiple sclerosis (MS), type 1 diabetes and rheumatoid arthritis, have been linked to gut dysbiosis, and it’s also been associated with the progression of neurological disorders such as autism, pain, depression, anxiety and stroke.


(Source: Journal of Experimental Medicine, 2016; jem.20151345)

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