A new study adds to the growing evidence that Parkinson’s disease, once believed to start in the brain, may begin in the gut.
The research points to a possible connection between gastrointestinal problems and the development of the disease, offering important insights for earlier diagnosis and treatment options.
Researchers, led by Subhash Kulkarni of Beth Israel Deaconess Medical Center, found that individuals with upper gastrointestinal conditions, such as ulcers or damage to the lining of the stomach and esophagus, had a significantly higher risk of developing Parkinson’s disease later in life.
Published in JAMA Network Open, the study reveals that people with mucosal damage were 76% more likely to develop the disease during a nearly 15-year follow-up period.
Parkinson’s disease, which affects the nervous system and impairs movement, has traditionally been viewed as a brain-first disorder.
However, the new research supports a “gut-first” hypothesis, first proposed by German anatomist Heiko Braak in 2003.
This theory suggests that the disease begins in the gastrointestinal tract, where misfolded proteins like alpha-synuclein spread to the brain via the vagus nerve.
“The evidence is accumulating,” says Ted M. Dawson, a professor of neurodegenerative diseases at Johns Hopkins University, “and this study is another step toward accepting that the gut may play a major role in Parkinson’s development.”
The analysis involved over 9,300 patients, most aged 50 to 64, with no previous history of Parkinson’s disease.
Mucosal damage, such as erosion or ulcers, was found to precede the onset of Parkinson’s motor symptoms by an average of 14 years, underscoring the importance of early detection and treatment for those with gastrointestinal problems.
Experts like Delaram Safarpour, an associate professor of neurology at Oregon Health & Science University, highlight the need for careful monitoring of patients with a history of gastrointestinal issues.
“Early detection could allow doctors to intervene before motor symptoms develop,” Safarpour explains, as neuroprotective treatments may be more effective in the early stages of the disease.
Parkinson’s disease has been on the rise globally, doubling in the past 25 years, and is now the fastest-growing neurological disorder.
While genetics account for only 10% of cases, the majority are sporadic, with environmental factors like gut health potentially playing a significant role.
The study’s findings suggest that preventing mucosal damage could reduce the risk of developing the disease, though more research is needed.
Kulkarni and his colleagues plan to explore the cellular changes associated with mucosal damage and its impact on alpha-synuclein.
For now, experts urge caution but highlight the importance of timely treatment for gastrointestinal conditions.
“There is no reason to panic,” Kulkarni says. “We’re not saying every person with mucosal damage will develop Parkinson’s, but there is an increased risk. We need to focus on how to reduce that risk.”