Our bodies use pain to alert us to damage or infection and assist medical professionals in making a diagnosis. Since pain is unpleasant, we frequently attempt to block it with drugs.

However, a startling new study conducted by scientists at Harvard Medical School raises the possibility that suppressing acute pain can possibly make it worse.

That’s because a process that shields the stomach from harm may be heavily dependent on pain.

In the study, the protective mucus that lines the gut is regulated by pain neurons in mice, which release more mucus in reaction to inflammation.

According to study principal scientist Isaac Chiu, PhD, an associate professor of immunobiology at Harvard’s Blavatnik Institute, “These neurons signal to the goblet cells in the gut that generate mucus.” Mucus guards the gut barrier from potentially hazardous microorganisms and tissue damage, therefore this is very important.

According to Chiu, interfering with that process can cause dysbiosis, an imbalance in the gut that can lead to inflammation and increase the likelihood of uncomfortable gut disorders including inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS).

What the Scientists Did

In the experiment, scientists created mice devoid of pain neurons. According to Chiu, these mice produced less mucus to protect them, and “their gut flora became dysregulated.” Additionally, colitis became more likely to affect them (inflammation in the gut marked by belly pain and bowel issues).

The reason for this, which was discovered by the researchers, was that the mucus-producing goblet cells possess a receptor called RAMP1 that aids them in responding to pain. This receptor is triggered by a neuropeptide called CGRP, which is released by pain neurons in reaction to pain.

The gut won’t receive the signal to generate more mucus without that CGRP or those receptors, and mucus production decreases as a result.

According to Chiu, “We require this signal to keep a healthy gut.”

A class of migraine drugs that reduce CGRP are of particular concern, according to Chiu.

According to him, long-term CGRP targeting could lead to poor gut mucosal health, which would result in the loss of beneficial bacteria and increased sensitivity to inflammation.

Additionally, the researchers note that because painkillers are frequently prescribed to patients with colitis, it may be crucial to take into account any negative effects.

Why It’s Important

The discovery relies on a growing corpus of knowledge about “inter-organ communication,” or how molecules in the body communicate with one another among organs to support our continued health. It clarifies the signalling between the central nervous system and the GI tract, or gut-brain axis.

According to Chiu, since acute pain is intended to keep us from harm, it makes sense that it would be connected to mucus secretion. “We are more prone to have a damaged or irritated gut if we lose this signal.”

On the other hand, excessive pain signals is probably also counterproductive.

On the opposite side of the coin, according to Chiu, is chronic pain. “We need to figure out how to keep the positive components of pain signalling, like preserving gut homeostasis, and turn off the part of pain perception in the brain that causes people suffering.”

To “tune it down” without turning it off entirely, he says, we need to better understand the factors that regulate pain signalling in the stomach.

The findings in humans need to be confirmed by more study. According to Chiu, this could alter how we manage pain and pave the path for novel treatments for patients with gut disorders, depending on how the research proceeds.

In the interim, Chiu says that enhancing gut health might aid in controlling the pain-signaling process. In order to maintain mucus without causing gut pain, healthy microorganisms may just barely activate pain fibres. By eating more fibre and fermented foods while consuming less fried food and red meat, you can nourish healthy gut microorganisms. Getting outside, exercising, and managing your stress can all be beneficial.

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