If you’ve suffered from chronic pain following a traumatic injury, your genes might be to blame.
A new study has found that a DNA mutation is responsible for why people suffer more pain after experiencing trauma such as sexual assault or a car crash.
The mutation results in high levels of cortisol, known as the ‘stress hormone,’ being produced, which sensitizes nerves in the muscles and makes them more prone to injury.
Previous studies have shown people with variants of this specific gene are more likely to develop post-traumatic stress disorder (PTSD), depression or aggressive behavior following a traumatic event.
But scientists from the University of North Carolina School of Medicine say their study is the first to show that having a different version of this gene also inflicts more physical pain on the body.
A new study has found that having a mutation of the FKBP5 gene could be why you’re more likely to suffer chronic pain after a traumatic injury (file image)
According to the DNA Learning Center, the FKBP5 gene is part of the body’s hypothalamic-pituitary-adrenal (HPA) axis.
The HPA system intertwines our central nervous system with our endocrine system and controls our body’s reaction to stress.
Studies have suggested that having subtle variants of FKBP5 can change how that gene functions and can cause the HPA axis to become overactive, resulting in too much cortisol being produced.
In turn, people are more likely to suffer from conditions such as anxiety, depression and PTSD.
For the study, the team looked at more than 1,500 people who had experienced a traumatic injury following a car crash.
They then studies the participants who had an increased expression of the FKBP5 gene, which helps regulate stress.
Gene expression is the conversion of DNA from genes into messenger RNA, which produce proteins – meaning that this gene was more effective.
Lead author Dr Sarah Linnstaedt, an assistant professor of anesthesiology at UNC School of Medicine, said this is because the gene cannot be regulated by a microRNA.
MircroRNA are small RNA molecules that help regulate gene activity by binding to the genes so that they are not over-expressed or under-expressed.
The participants had alternative variants, or alleles, of the FKBP5 genes because of this over-expression.
‘In individuals with the minor/risk allele, the microRNA does not bind well to FKBP5 thus causing FKBP5 to be over-expressed,’ she said.
‘High levels of FKBP5 can be detrimental because it alters natural feedback mechanisms that control circulating cortisol levels.’
Studies have shown that cortisol has been shown to sensitize the peripheral nerves, located in places including shoulder muscles; the wrist; forearm and hand muscles; and the lower abdomen.
Therefore, people who had higher levels of cortisol had the risk variant, or allele, of the gene and were more to suffer from chronic musculoskeletal pain
A technique known as gene editing has been used in other experiments such as one by the Massachusetts Institute of Technology, where scientists converted defective gene variant APOE4 into the healthy APOE3 version in dementia patients.
Many biotechnology companies are now trying to achieve gene-editing technology, which Dr Linnstaedt could result in therapies ‘that changes the risk allele in FKBP5 to a protective allele.’