As you know, I’ve been closely following developments in the field of Parkinson’s disease (PD) research as I already have multiple friends diagnosed, and that, in their 40s and 50s. (Here are just a couple of the many, many posts I’ve written over the years, on this subject: here and here.)
Research out of Australia was presented at a conference for the American Academy of Neurology Science, describing findings from a multi-center study of 167 patients with PD, compared to 100 controls.[i] All individuals in the study completed a rating scale of 15 gastrointestinal symptoms, and donated stool samples for analysis. Compared to the controls, those with PD reported significantly more GI symptoms including heartburn, acid reflux, nausea/vomiting, rumbling/gurgling ( which is called borborygmus), increased flatulence, decreased passing of stool/constipation, feeling of incomplete evacuation, hard stools. Constipation is the GI symptom that appears most in the medical literature, often preceding the actual symptoms of PD by many years. To date, other GI symptoms have not really been explored much.
The microbial analysis showed markedly reduced microbial diversity overall in those with PD. It also showed increased Firmicutes and Proteobacteria, with somewhat increased Verrucomicrobia. Proteobacteria and Verrrucomicrobia are pro-inflammatory families of bacteria. Other kinds of bacteria that were found at low levels in the PD patients are known to produce the short chain fatty acid, butyrate, which – as you’ve read many times before on this blog – is a known anti-inflammatory and improves the integrity of the gut epithelial barrier.
To boot, this research showed that as PD and GI symptoms increase in severity, microbiota diversity decreases. Says the presenter of this data: “As reduced diversity is associated with increased intestinal inflammation, this indicates that the altered microbiome we saw in [individuals with Parkinson’s disease] may be instigating the increase in incidence and severity of GI symptoms.”
Another paper on this very subject was published a few months back. This looked at association between gut microbiota and the inflammatory bacterial metabolite, lipopolysaccharide (LPS), which is often used to induce inflammation in laboratory experiments. Like the Australian study above, an increase in Verrocomicrobiae was also found in those with PD, as well as LPS-producing Gammaproteobacteria. In a mouse model of PD, exposure to LPS resulted in the development of PD symptoms by 10 weeks, as opposed to untreated mice who, after 10 weeks, were still asymptomatic. They conclude that, “This study reaffirms that an altered microbiome exists in patients with PD, and supports the notion of a proinflammatory gut microbiome environment as a trigger for PD pathogenesis.”[ii]
By the way, just a week ago, a paper came out providing more support for PD as an autoimmune disease: “The team discovered that a protein called alpha-synuclein acts like a beacon for the immune system’s T cells, causing them to attack brain cells, and thus contributing to the progression of Parkinson’s.”[iii] This autoimmune activity can be seen at least 10 years before the actual development of any PD symptoms – I’m sure not coincidentally, at the same time that early GI symptoms are often experienced, like the constipation mentioned above.
It’s fascinating, having watched this space for several years now, to watch the evidence continue to mount for the gut origins of Parkinson’s disease. And it’s exciting to contemplate the possibilities for the not-very-distant future. By the time symptoms are seen, it’s likely too late to reverse things as the dopamine-producing cells are already lost. But hopefully soon, we’ll be able to stop the symptoms of PD from developing in the first place and, at the very least, stop the progression for those already affected.
[ii] Gorecki AM, Preskey L, Bakeberg MC, et al. Altered Gut Microbiome in Parkinson’s Disease and the Influence of Lipopolysaccharide in a Human α-Synuclein Over-Expressing Mouse Model. Front Neurosci. 2019;13:839. Published 2019 Aug 7. doi:10.3389/fnins.2019.00839