Researchers at Mc Gill University have reported that treating pain with anti-inflammatory medication may be counterproductive. By using medication like ibuprofen or aspirin to treat pain, we may be promoting pain in the long term.

A paper published in Science Translational Medicine suggests that inflammation prevents acute pain from becoming chronic. By blocking the inflammation, we may be interfering with the inflammation process and leading to harder-to-treat pain.

Senior study author Jeffrey Mogil, a professor in the psychology department at Mc Gill believes that we should allow the inflammation to happen in order to stop chronic pain.

To understand why pain goes away for some but continues on for others, researchers looked at pain mechanisms in mice and humans. These results indicated that a type of white blood cell called neutrophil seemed to play a key role.

Luda Diantchenko, a professor in the faculty of medicine and Canada excellence research chair in human pain genetics at Mc Gill, said that by analyzing genes of people suffering from lower back pain, they were able to observe active changes in the genes over time. For some people, their pain went away and the changes in the blood cells and activity appeared to be the most important factor. Particularly, it played an important factor in neutrophils.

Researchers tested the link by blocking neutrophils in mice and found that the pain lasted 2 to 10 times longer than normal. This supports a separate analysis conducted on 500,000 people in the UK which showed that those taking anti-inflammatory drugs were more likely to experience pain 2 to 10 years later.

This research suggests we may need to rethink how we treat pain. While more clinical trials are needed, the research may lay the groundwork for new drug development for chronic patients.