It is well-known that people who are more sensitive to pain are more likely to develop chronic pain later in life. Despite the fact that 20 percent of the population in Europe, for example, goes on to develop chronic pain during their lifetimes, treatments for the condition are generally for short-term use or carry a load of side effects. However, a new study published in PLoS One indicates that certain genes are responsible for the brunt of chronic pain issues, suggesting a better pathway for treatment.
The study was a collaborative effort among King's College London in the United Kingdom, drug manufacturer Pfizer based in the United States, and the Beijing Genomics Institute in China. It was conducted with 2,500 volunteers, who were tested for pain sensitivity using a heating probe. When the heat became painful for them, the volunteers were told to press a button, which indicated to the researchers their level of pain sensitivity. Then researchers analyzed the DNA of the 400 participants with the highest and lowest sensitivity to pain by using a technique called exome sequencing, which only analyzes the portion of the genome that is translated into protein.
Researchers did not find one gene that was culpable for increased pain sensitivity, but they did find a gene pathway, called the angiotensin pathway, that contained differences between individuals who were extremely sensitive to pain and those who were not. In addition, the pain-sensitive group had less variation in their genes than the pain-insensitive group.
Xin Jin, from the Beijing Genomics Institute, added in a statement, "More and more evidence supports our theory that rare variants, which were overlooked in genome-wide association study, play a very important role in complex diseases and traits. The next generation of sequencing will make it possible to explore these rare variants and will lead to a wave of new discoveries in biomedical research."