We usually experience pain and health problems following periods of acute stress, a phenomenon that doctors have noted, but the biological explanation for it remains unclear, leading some to consider stress personal or merely an “illusion.”
A new study published in the journal “Brain, Behavior and Immunity” contributes to changing this concept.
Researchers from the University of Illinois have discovered a biological pathway through which social stress can increase colitis, linking psychological experiences to significant bowel damage.
The results show that stress stimulates beta-adrenergic receptor signaling in the intestine, leading to oxidative stress that weakens the intestinal lining and increases inflammation.
Jacob Allen, associate professor in the Department of Health and Kinesiology at the College of Applied Health Sciences, and one of the authors of the study, said:
* Doctors have long noted that high-stress events, such as the death of a family member, major life events, or chronic stress, often precede worsening symptoms and flare-ups in patients with IBD.
*Our findings reveal potential physiological mechanisms for how stress transforms into gut changes that exacerbate intestinal inflammation.
Increased hormones in the stomach
Stress is known to activate the sympathetic nervous system, which is responsible for the body’s fight-or-flight response, leading to the release of catecholamines such as adrenaline and noradrenaline. These hormones prepare the heart, lungs and muscles for a rapid response, but their effect on the digestive system has not been completely clear.
Researchers have found that during social stress, levels of these stress hormones rise not only in the bloodstream, but also in the intestinal tissues themselves.
Allen said:
* We found that in response to social stress, levels of these hormones increase locally in the intestine.
* These stress signals can directly affect the intestinal lining, leading to increased production of reactive oxygen species, also known as free radicals.
Reactive oxygen species are chemically active molecules that can damage cells if not carefully regulated.
In this case, the study identified a specific pathway for producing reactive oxygen species, involving a protein called DUOX2.
Overproduction of reactive oxygen species weakened the intestinal epithelial barrier – the protective membrane that prevents the leakage of bacteria and toxins into internal tissues, making the intestine more inflamed and fragile.
“Overall, our data suggest that stress increases inflammation in the intestine and makes it more fragile,” Allen explained, adding that reactive oxygen species signaling may be “a direct trigger for increased risk of exacerbation of stress-induced intestinal inflammation.” Importantly, the study suggests that stress not only exacerbates existing inflammation, but may also predispose the gut to future disease activity.
