A new nationwide Danish population study that covers nearly 40 years has revealed that people with inflammatory bowel disease have a 22 percent higher risk of developing Parkinson’s disease than people without the long-term gut disorder.
The study supports the notion of a “gut-brain axis,” note the researchers in a paper on their work that is now published in the journal Gut.
The gut-brain axis theory proposes that what goes on in the gastrointestinal tract (GI) affects the central nervous system.
Publication of the Danish study comes hot on the heels of another report of an observational study conducted in the United States that found that having inflammatory bowel disease (IBD) was linked to a 28 percent higher risk of developing Parkinson’s disease.
IBD is a chronic condition that inflames the GI, or gut, because the immune system attacks healthy tissue cells in the intestines and the beneficial bacteria that live there.
Estimates suggest that around
Although IBS does damage the gut, the cause is not inflammation. And, while celiac disease does inflame the gut, the cause is a specific reaction to gluten, which is a protein found in wheat and other grains.
Parkinson’s disease is a gradually worsening movement disorder caused by death of brain cells. The most common symptoms include muscle rigidity, tremors, slowness of movement, and impaired coordination and balance.
Estimates suggest that more than 10 million people worldwide have Parkinson’s disease, around 1 million of whom live in the U.S.
Previous studies have proposed that gut inflammation influences the development of Parkinson’s disease and multiple system atrophy (MSA), which is a rare neurological disorder that has symptoms similar to Parkinson’s.
In their study paper, the researchers — including corresponding author Dr. Tomasz Brudek, of the Research Laboratory for Stereology and Neuroscience at Bispebjerg and Frederiksberg Hospital in Copenhagen — note that GI dysfunctions arise early in Parkinson’s and “add significantly” to disease-related complications.
Dr. Brudek and his colleagues decided to investigate whether there might a link between IBD and risk of developing Parkinson’s disease or MSA.
They identified all residents of Denmark who were diagnosed with IBD between 1977 and 2014 and matched each of them to “comparable” members of the population at large who did not have IBD. Altogether, the study followed 76,477 individuals with IBD and more than 7.5 million without IBD.
The 37 years of follow-up started from day of diagnosis to “occurrence” of Parkinson’s or MSA, which was determined from records in the Danish National Patient Register.
The analysis revealed that people diagnosed with IBD had a 22 percent higher risk of developing Parkinson’s compared with their non-IBD counterparts.
The higher risk of Parkinson’s was not affected by gender, the age at diagnosis of IBD, or follow-up length. The study authors note, however, that people with IBD with ulcerative colitis “had slightly higher risk than” those with Crohn’s disease.
The analysis also suggested that there might be a 41 percent higher risk of MSA in individuals with IBD compared with their non-IBD counterparts, but this was based on a very low incidence of MSA.
The researchers point out that, since theirs was an observational study, they cannot say for certain whether IBD raises the risk of Parkinson’s disease.
However, because they did find a link — and because their study is the first “epidemiological study investigating the risk of parkinsonism in an unselected, nationwide cohort of patients with IBD with long-term follow-up” — they urge that clinicians “should be aware of symptoms of parkinsonism in patients with IBD.” They also suggest that:
“The identification of risk factors associated with prodromal phases of Parkinson’s disease may allow for early intervention studies that could modify or slow down disease progress.”