Trillions of microorganisms live inside the human digestive system, forming a complex ecosystem involved in digestion, metabolism and protection against disease-causing microbes. But what we eat can dramatically influence how this microbial community behaves.
Experimental research has revealed an intriguing mechanism: when certain gut bacteria do not receive enough dietary fiber, some of them begin using the mucus protecting the inner surface of the colon as an alternative source of nutrients.
This does not mean that bacteria literally begin eating the intestine itself. Instead, they break down carbohydrate-rich glycoproteins known as mucins, which form the protective mucus layer covering the intestinal epithelium.
This mucus performs an essential function. It creates a physical barrier between the enormous microbial population living inside the intestine and the body’s own cells.
Researchers investigated the process using mice whose intestines were colonized with a controlled community of human gut bacteria.
When the animals consumed a diet rich in plant fiber, the microorganisms primarily used complex plant carbohydrates as an energy source.
But when dietary fiber was removed, the situation changed.
Bacterial species capable of degrading mucins increased their activity and began making greater use of the carbohydrate structures contained in the protective mucus.
If degradation occurs faster than the body can replenish the mucus, the protective barrier can gradually become thinner.

This can have important consequences.
In the experiments, the pathogen Citrobacter rodentium gained easier access to the intestinal surface in animals consuming a fiber-deprived diet, resulting in more severe inflammation of the colon.
The study revealed another interesting finding. Even intermittent periods of fiber deprivation encouraged the microbial community to shift toward using mucus-derived nutrients.
This demonstrates how rapidly the gut microbiome can respond to changes in diet.
Dietary fiber also plays another important role. When certain intestinal bacteria ferment plant fibers, they produce short-chain fatty acids such as butyrate, acetate and propionate.
These compounds participate in maintaining the intestinal environment and interact with the body’s cells through numerous metabolic and immune pathways.
Research into the microbiome has increasingly demonstrated that different dietary fibers can influence different microbial populations and the substances they produce.
However, this does not mean that consuming as much fiber as possible will automatically make someone healthier.
The human gut microbiome is considerably more complicated than an experimental animal model. Different types of fiber are processed by different microorganisms, while their effects depend on a person’s overall diet, individual microbiome and health.
For some gastrointestinal conditions, even the amount and type of dietary fiber may need to be adjusted individually.
The main message of the research is therefore not simply that everyone should consume the maximum possible amount of fiber.
The more important discovery is that our food does not feed only us. It also feeds the enormous microbial ecosystem living inside our intestines.
When the preferred nutrients of some microorganisms disappear, they can switch to another available source of food – including molecules that form the protective mucus produced by our own bodies.
The relationship between nutrition and intestinal health may therefore be more direct than it initially appears. What we eat can influence not only which microorganisms live inside us, but also what those microorganisms do.
The original experiment was conducted in mice carrying a defined community of human gut bacteria, so its findings should not be interpreted as proof that a low-fiber diet will inevitably damage the intestinal lining in humans.
Instead, the research reveals an important biological mechanism that scientists are continuing to investigate as they try to understand the complex relationship between diet, the microbiome and human health.
Sources: Cell, PubMed, Nature Reviews Microbiology.
