At the same time, after the 10 days, participants’ guts had shifted toward greater numbers of bacteria thought to produce helpful short-chain fatty acids (SCFAs), which are normally low in people with Parkinson’s. SCFAs support communication between the gut and brain and may help control brain inflammation.
A protein called zonulin, a sign of leaky gut, also decreased. Leaky gut, or gut barrier dysfunction, can allow harmful substances to escape from the gut and enter the bloodstream, where they can cause inflammation and other damage throughout the body and in the brain. The prebiotic bars may help shore up the lining of the gut, Hamaker says.
The researchers saw slight improvements in motor and non-motor symptoms too. Neurologists scored the study participants’ movement using the Unified Parkinson’s Disease Rating Scale — a composite score that factors in tremor, rigidity, slowness, balance, gait and speech — before and after the 10 days of bars.
“The change was modest but significant — the same kind of change that happens even with pharmacological treatment,” says Dr. Ali Keshavarzian, the study’s lead author and director of Rush University’s Center for Integrated Microbiome and Chronobiology Research.
But the study was not designed to measure improvements in motor skills. There was no placebo group, and the study lasted only 10 days, so the long-term effects of the prebiotic bars are still unknown.
“What needs to be done is a longer-term randomized controlled trial,” Hamaker says, which his collaborators in Chicago are planning.
Why target the gut?
The concept of targeting the gut in Parkinson’s research is based on three major lines of evidence demonstrating the gut’s role in this disease. First, says Dr. Rachel Dolhun, principal medical adviser at the Michael J. Fox Foundation for Parkinson’s Research, is constipation.
“Constipation, in some people, happens decades before the diagnosis of Parkinson’s disease,” she says. This common GI symptom of Parkinson’s, she adds, is a key indication that the gut is involved in the disease.
Second, the gut’s ecosystem just looks different in people who have Parkinson’s. Pro-inflammatory microbes tend to be more prevalent. Specific Parkinson’s symptoms, in fact, might be linked to specific types of bacteria, Dolhun says.
“We are starting to see some differences in people who have different symptoms of Parkinson’s,” she says. “People who have more tremor-predominant Parkinson’s might have a different microbiome than people who have more gait-, walking- and balance-predominant Parkinson’s.”
Third, research suggests that alpha-synuclein — the protein that accumulates in clumps in the brains of people with Parkinson’s — may be present in their guts long before the disease is diagnosed.
So it’s logical to explore whether improving the gut could help prevent, slow or stop Parkinson’s disease. But Dolhun stresses that scientists don’t yet know whether gut changes are a cause of Parkinson’s, a consequence or both.
“Is it that the microbiome is changing and that’s contributing to Parkinson’s? Or is it that you have Parkinson’s, you take medicines for Parkinson’s, maybe your diet changes, and that’s impacting your microbiome?” she asks.
That uncertainty is key context for interpreting the fiber bar study: Changing the microbiome may reduce markers of inflammation, which looks promising, but we still don’t know if that will meaningfully change daily life with Parkinson’s and its course over the years.
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