Amid all the health crises facing Canadians, one particular disease tends to be left out of the normal conversation. It's known as irritable bowel syndrome, or IBS, and as the name implies, the symptoms are rather troublesome for anyone who suffers. Hundreds of thousands of Canadians are left with a variety of symptoms ranging from bloating to diarrhea. But the one common trait to this disease is abdominal pain, which can in some cases be overwhelming.
Figuring out why IBS causes pain has been a major focus of research for over four decades. At first, the most common denominator was stress. As the years went on, other options came to light such as genetics and the nature of the gut microbiota. Yet, these options did not take into consideration one aspect of pain — namely, how the signals end up in the brain.
Then, in 2008, an answer was at hand. A group of British researchers identified a massive increase in a particular molecule on the surface of rectal cells capable of transmitting pain to the brain. That molecule was transient receptor potential vanilloid type-1, but most neuroscientists refer to it simply as TRPV1.
This discovery may be considered somewhat odd because TRPV1, as one might infer from the name, is usually thought to be on the tongue. It's partly responsible for identifying the taste of salt. But it's best known as the molecule that causes your tongue to burn like fire when you have a chili pepper. When the active ingredient in any hot pepper — capsaicin — meets up with TRPV1, you instantly feel pain in the brain. The same occurs with the hot ingredient in black pepper, piperine, although to a much lesser extent.
At the time, the identification of TRPV1 in the rectum suggested that, much like the tongue, the bowels could be sensitive to a variety of different "taste molecules." But determining which suspects were to blame would be almost impossible, considering the diversity of possible chemicals in the bowels.
There was a surprise in store that changed the way they viewed IBS.
A group of European researchers had a different approach. Instead of looking at individual molecules from food and bacteria, they chose to look at human factors involved in forcing TRPV1 to send signals of pain to the brain. They used a 20-year-old description of IBS as their guide. Back then, the disease was considered to be a hypersensitivity reaction, essentially an allergy. The team hoped they could find the same molecule involved in allergies — histamine — as the reason for the pain.
When they tested this theory in humans they were pleased to find the link existed. Adding histamine before adding capsaicin led to more pain. But there was a surprise in store that changed the way they viewed IBS.
The researchers found they could change the way TRPV1 sent signals to the brain. If they left the molecule in the presence of histamine for a long period of time, the molecule would be more sensitive to capsaicin. This phenomenon, known as sensitization, was fascinating and suggested those with IBS may be more sensitized to pain.
As to how that might have happened, the team figured they knew the answer. Many people suffering with IBS note they endured a gastrointestinal infection sometime before the symptoms started. Pathogens such as norovirus, salmonella, and especially campylobacter jejuni all seemed to be at fault. If the team was on the right track, people who had suffered from one of these infections may have sensitized their TRPV1 leading to the pain.
Last week, the team revealed they were correct. As expected, they found highly sensitized TRPV1 molecules in those people with IBS following a gastrointestinal infection. However, there was a rather unwelcome realization accompanying this discovery.
The team began with the theory there was some type of long-term hypersensitivity occurring in the gut. Yet, when they looked for an increase in immune molecules — including histamine — involved in allergies, they were disappointeded. There was no allergy. A normal level of histamine in the gut was all it took to cause pain.
This meant even the slightest hint of a problem would cause pain signals in the brain.
Taking a closer look at the TRPV1 molecule, the team realized it had been trained to become more sensitive to low levels of histamine. Somehow, during the infection, the micro-environment of the bowels and rectum had become more cautious of any chemical coming into the area. This meant even the slightest hint of a problem would cause pain signals in the brain.
Because of this reality, the team felt there may be a way to block the pain. They tested their theory using two anti-allergy medications known as pyrilamine and ebastine, which already had proven to be effective in IBS patients. As expected, these molecules blocked the response to histamine and turned off the pain trigger.
The results offer some indication of how pain gets sent from the bowel to the brain. Yet the information also offers a possible direction forward for treatment by targeting the immune system. Granted, it will be years before histamine blocking medications are tested for IBS treatments in humans. Even so, thanks to this research, those who suffer from IBS may breathe a little easier knowing a way to stop one of the routes to pain may be coming sooner rather than later.
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