Chronic constipation, a common digestive issue, affects millions and is characterized by infrequent bowel movements or difficulty passing stool. Doctors typically explain this as a unhurried movement of food through the intestines.
While generally not a serious health risk beyond causing discomfort, constipation can significantly impact quality of life. Although, a standard medical explanation doesn’t apply to everyone. Some individuals experience chronic constipation without a clear cause, a condition known as chronic idiopathic constipation (CIC).
Now, researchers at the University of Nagoya in Japan have identified two gut bacteria that, when working together, may contribute to chronic constipation. According to a study published in Gut Microbes, Akkermansia muciniphila and Bacteroides thetaiotaomicron break down the intestinal mucus essential for lubricating the colon and keeping stool hydrated. This degradation can lead to dry, immobile stool, potentially explaining why standard treatments often fail for millions.
Link to Parkinson’s Disease
Patients with Parkinson’s disease also frequently experience severe, treatment-resistant constipation, though it’s clinically categorized separately from CIC. Many struggle with this issue for decades before developing tremors and movement problems, but the underlying cause remained unknown until now.
While constipation in Parkinson’s disease has traditionally been attributed to nerve degradation, this study suggests that these patients have higher levels of the mucus-degrading bacteria. These findings indicate that bacterial activity may also play a crucial role in the development of their symptoms.
The Role of Mucus Loss
Instead of focusing on nerve and muscle movement in the gut, the researchers examined the protective gelatinous layer called colonic mucin, a substance in the large intestine that coats the intestinal walls and is also found within stool. Colonic mucin keeps stool moist, aids smooth passage through the digestive tract, and protects the intestinal wall from bacteria.
The study found that two gut bacteria work sequentially to break down this mucin. B. Thetaiotaomicron uses enzymes to remove protective sulfate groups from the mucin, and then A. Muciniphila breaks down and consumes the exposed mucin.
Sulfate groups normally protect mucin molecules from bacterial degradation. When too much mucin is destroyed, stool loses moisture and becomes hard and dry, leading to constipation. Because the problem is mucus loss, rather than slow intestinal movement, standard laxatives and motility medications are often ineffective.
“We genetically modified B. Thetaiotaomicron so that it could no longer activate the sulfatase enzyme that removes sulfate groups from mucin,” explained Professor Tomonari Hamaguchi of the University of Nagoya, the study’s lead author. “We then introduced these modified bacteria into germ-free mice along with Akkermansia muciniphila, and surprisingly, the mice did not develop constipation; the mucin remained protected and intact.”
This experiment demonstrated that blocking the sulfatase enzyme prevents the bacteria from degrading mucin. Drugs that block sulfatase could potentially treat bacterial constipation in humans. This discovery offers hope for novel therapies targeting the underlying microbial causes of the condition for millions of patients with treatment-resistant constipation, including those with Parkinson’s disease.
