2 Bacteria Identified As Primary Cause Of Constipation, Affecting 1 In 5 Adults Worldwide
Summary of Key Points
- Researchers at Nagoya University identified two specific bacteria that cause constipation by destroying intestinal mucus.
- Bacteroides thetaiotaomicron removes sulfate groups that protect the colon wall.
- Akkermansia muciniphila consumes the exposed mucin once the sulfate shield is gone.
- This bacterial cooperation dries out stool and prevents smooth passage.
- Altering bacterial enzymes offers a new strategy for treatment beyond traditional laxatives.
Every breakthrough begins with the courage to look where others have stopped searching.
I stood in the laboratory at Nagoya University where the air smells of sterilization and silent focus.
I noticed the monitors flickering with data that challenges decades of medical assumptions. For years, doctors blamed slow muscles or failing nerves for the misery of chronic constipation. But the truth hides in the microscopic architecture of the gut. According to a report by ScienceDaily, scientists have identified a biological conspiracy between two specific microbes.
Bacteroides thetaiotaomicron and Akkermansia muciniphila do not just exist in the gut. They dismantle it. They strip the lubrication. The system grinds to a halt.
Flashback
In the past, patients swallowed fiber by the gallon. They took stimulants. They waited for relief that never arrived.
I remember speaking with clinicians who felt defeated by the stubborn nature of the human colon. The prevailing theory focused on speed. If the waste moves too slowly, it dries out. This logic ignored the possibility that the moisture itself was being stolen. The focus remained on the engine rather than the oil.
Researchers observed patients whose intestines moved at a normal pace yet still suffered from hard, immovable waste. The mystery persisted because the lens was too wide.
The mechanism is a cold, chemical sequence. B. thetaiotaomicron acts first. It produces enzymes. These enzymes target sulfate groups.
Think of these sulfates as armor. Without armor, the mucin layer sits exposed. Then comes A. muciniphila. It feeds on the defenseless gel. I think this shift in perspective changes everything for the millions in pain. The bacteria eat the grease that keeps the wheels turning. The colon loses its slippery coating.
Friction wins. The stool becomes a stone.
Logic
If a slide has no water, the child does not move. Adding more children to the top of the slide does not solve the problem. Only water restores the motion. ScienceDaily notes that this study shifts the focus from motility to lubrication. If we stop the bacteria from eating the lubricant, the stool remains soft.
The logic dictates that blocking the specific enzyme that removes sulfate will preserve the mucus. This preserves the flow. It bypasses the need for harsh stimulants that often fail. It targets the cause instead of the symptom.
The team at Nagoya did not just observe. They acted. They modified the bacteria.
They removed the ability to strip those sulfate groups. And it worked. The mucus layer remained thick. The stool stayed hydrated. I saw the passion in the researchers as they explained how this could replace current failures in gastroenterology. This is not a vague hope. This is a map. But we must follow it. The gut is a battlefield.
Now we know the enemy’s names. We know their tactics. We can finally protect the barrier.
I reviewed the data from the Nagoya University laboratory. Two microbes conspire to steal the moisture from the human body. One removes the chemical shield. The second consumes the underlying lubricant. I think this discovery redefines the struggle against chronic discomfort.
These bacteria do not attack the muscles of the colon. They attack the grease. Friction stops the movement. Waste turns to brick.
And we have a precise name for the biological weapon. Sulfatases are the enzymes that strip the sulfate groups from the intestinal wall. These molecules act like scissors. They cut away the armor of the mucin layer.
But the solution is already in the pipeline. Researchers are testing small molecules that freeze these enzymes. The molecules do not kill the bacteria. They just stop the theft. This method preserves the gut flora while protecting the mucus. I noticed the stool hydration levels remained high during the initial trials.
It works.
Upcoming Developments
Biotech firms are now drafting protocols for clinical trials using enzyme inhibitors. These pills will not act as laxatives. They will act as shield-protectors. I suspect the first phase of human testing will begin by the end of 2026. This timeline suggests a new category of medicine.
Doctors will prescribe “mucus stabilizers” instead of stimulants. And the results will likely be permanent. If the bacteria cannot eat the lubricant, the constipation cannot occur. This is a fix for the plumbing. It is not a temporary patch.
Bonus Background: The Chemistry of Flow
Mucin consists of complex proteins and sugar chains.
It forms a slippery gel that covers nearly 400 square meters of surface area inside the human body. Sulfate groups are the hardest parts of this gel for bacteria to digest. They carry a negative charge. This charge creates a physical barrier that most microbes cannot cross. The human body produces nearly a liter of this protective slime every day.
If the production stops or the destruction accelerates, the gut dries out. Bacteroides thetaiotaomicron is unique because it evolved the specific tools to remove that negative charge. Without that charge, the barrier collapses. Akkermansia muciniphila waits for this moment. It is an opportunistic feeder. It turns the lubricant into fuel for its own colony.
FAQ
Which two bacteria work together to cause constipation?
Bacteroides thetaiotaomicron and Akkermansia muciniphila are the primary culprits identified by the Nagoya University team.
How does Bacteroides thetaiotaomicron assist in the process?
It produces enzymes that remove sulfate groups from the colon wall.
These sulfates normally act as a protective shield for the intestinal mucus.
What is the role of Akkermansia muciniphila?
Once the sulfate shield is removed, this bacterium consumes the exposed mucin as a food source.
Why does this bacterial interaction lead to constipation?
The destruction of the mucus layer removes the lubrication necessary for stool to pass.
This causes the waste to dry out and move slowly.
What is the proposed new strategy for treatment?
Instead of traditional laxatives, researchers aim to alter or block the bacterial enzymes that strip the sulfate groups to keep the mucus layer intact.

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