• 29 آذار 2026
  • 09:05
Why do we lose our appetite when we are sick

Khaberni - Scientists have finally uncovered the reason behind the loss of appetite during infections. It turns out that the story begins with small cells in the intestines that communicate with the brain in a way that was previously unknown.
When a person suffers from a severe intestinal disease, the feeling of hunger disappears, and this decrease in appetite often continues even after the symptoms improve.
This scenario is also familiar to millions of people around the world who suffer from chronic parasitic worm infections. But until recently, scientists did not have a clear explanation for this phenomenon.

Now, a team from the University of California, San Francisco has successfully mapped the biological pathway that links the immune response in the intestines to the brain during infection. Their results demonstrated how the immune system systematically suppresses appetite.

David Julius, a Nobel Prize winner and participant in the study, said: "We asked not only how the immune system fights parasites, but also how it uses the nervous system to change human behavior. We found that there is a precise molecular logic behind this."
The study published in the journal Nature revealed a new form of communication between two rare types of cells in the intestines. This discovery could also aid in understanding conditions like food intolerance and irritable bowel syndrome.

The scientists focused on two types of rare cells in the intestines, the first are the tuft cells—a rare type of epithelial cells found in the mucous membranes of the digestive and respiratory system, which act as sensors detecting parasites and triggering the immune alarm. The second is enterochromaffin cells, which send chemical signals to nerves connected to the brain and produce sensations such as nausea and pain.

The perplexing question was: Do these two cells communicate with each other? The answer was yes, but the way it happens was surprising.

Researcher Koki Tohara designed a clever experiment where he placed glowing sensor cells next to the tuft cells under a microscope, and when he exposed the tuft cells to a chemical secreted by parasitic worms, the sensor cells lit up, indicating that the tuft cells released acetylcholine, a substance typically used by nerve cells for communication. When the scientists added this substance to intestinal tissues containing the second type of cells (enterochromaffin cells), those cells responded by releasing serotonin, which activated the vagus nerve that transmits signals from the intestines to the brain.
Tohara commented that the tuft cells function similarly to nerve cells but in a completely different way, using the same communication substance without the cellular tools typically relied on by nerve cells.

An important discovery is that the tuft cells send their signals in two stages, explaining why humans do not lose their appetite immediately upon infection.

In the early stage, the cells release a short burst of acetylcholine, then later, once the immune system is fully activated, the number of tuft cells increases, and they begin to issue strong, continuous signals capable of alerting the brain to reduce appetite.

Julius explained that this accounts for why a person feels fine initially and then starts to feel sick as the infection continues, because the intestines wait to ensure that the threat is real and persistent before asking the brain to change its behavior.
To confirm that this mechanism actually affects behavior, the researchers studied mice infected with parasitic worms, finding that mice with normal tuft cells ate less as the infection progressed, while genetically modified mice that could not produce acetylcholine in their tuft cells continued to eat normally, confirming that the discovered signaling pathway is directly responsible for appetite loss.

This discovery is not only relevant for explaining loss of appetite but also opens new avenues for treating symptoms of parasitic infections, especially since tuft cells are found not only in the intestines but also in the bronchial tubes, gallbladder, and reproductive system.

Therefore, this new neural pathway may play a role in other conditions such as irritable bowel syndrome, food intolerance, and chronic abdominal pain.

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