One step closer in the fight against chronic pain

New research sheds light on chronic pain, a major concern in public health. About 20 per cent of the worldwide population is affected by acute and chronic pain.

Chronic pain depends on many different factors such as biology, psychology, and the environment, but the molecular mechanisms at the basis of it are not completely understood. A new study published in Nature Communications suggests a potential solution for chronic pain. The work done could also have an application for other complex diseases, such as schizophrenia and diabetes.

An international research group led by Jordana T. Bell of the department of twin research and genetics epidemiology at King’s College London discovered that a gene already known to have a role in pain sensitivity (TRPA1) also has an important role in sensitivity to heat. The gene is found to be active in pain receptors (a type of nerve cell) as well as some skin cells.

The study looked at 25 pairs of identical twins and 25 pairs of unrelated participants, and compared their tolerance for heat. Heat sensitivity is an environmentally influenced trait, as twin pairs exhibit differences in their tolerance to pain at high temperatures. However, there was a greater correlation of heat tolerance in twin pairs than in pairs of unrelated people, meaning that there is a genetic factor involved in pain sensitivity.

What this means is that pain sensitivity has an epigenetic basis. Epigenetics is the field of study that looks at how genetics works beyond just focusing on the genetic code. Even though the genes for pain tolerance are passed down genetically, the way the genes are turned on or off is influenced by the environment.

The results of the pain sensitivity study were measured via DNA methylation status. Changing the levels of DNA methylation (by adding or removing chemical signatures called methyl groups) is a method the genome uses to turn genes on or off at specific times in order to make protein. Where there is a lot of methylation, genes will be turned off, and where there is little or no methylation, genes will be turned on.

Levels of methylation can also be influenced by environmental factors.

Jeffrey Marcus, associate professor at the University of Manitoba in the department of biological sciences, shared his expert opinion on the implications of this research. Marcus told the Manitoban that the results of this study are “worth exploring for pharmaceutical applications related to treating chronic pain.”

He said the study “represents a very creative use of pairs of monozygotic [identical] twin volunteers to help find new gene targets for easing the suffering of patients who experience chronic pain.”

Marcus also said that having “knowledge of biological mechanisms can assist in developing pharmaceutical and other treatment options for patients with a particular condition by targeting the specific proteins responsible for causing the disease.”

The researchers hope that future epigenetic studies will provide significant insight into other complex diseases by using the results discovered in this study on chronic pain.

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