Poolesville, MD – Your genetics may have a big impact on how chronic pain affects you, a new study shows. According to the new study conducted by the UNC School of Medicine and published in the Journal of Neuroscience, a variation of chromosome 6 may be linked to the likelihood of developing post-traumatic chronic pain.
Studies conducted in the past have shown that the gene FKBP5 plays a major role in the body’s stress response, including the development of post-traumatic stress disorder, depression, and suicide risk.
In 2013, the UNC School of Medicine found a link between FKBP5 variations and post-traumatic chronic pain, not just post-traumatic stress disorder.
Patients with a variation of an allele on chromosome 6 known as rs3800373 are more likely to experience chronic pain after suffering from some form of trauma compared to those without the variation.
In the UNC School of Medicine’s most recent study, researchers confirmed the link between the gene variants and post-traumatic chronic pain. Researchers analyzed a group of 1,500 participants who had suffered from motor vehicle collision trauma. Researchers collected blood samples of the participants and assessed both their DNA and their pain levels up to six weeks after the car accident.
None of the patients suffered from bone or tissue damage after their accidents. Despite claims that chronic pain may be caused by weight, which is the number one insecurity among Americans, post-traumatic chronic pain occurs despite having minor injuries. This, the researchers found, is most likely caused by the body’s inability to control stress hormones.
“In our current study, we showed that the reason this variant affect chronic pain outcomes is because it alters the ability of FKBP5 to be regulated by a microRNA called miR-320a,” said Dr. Sarah Linnstaedt, the lead author of the study.
MicroRNA play a critical role in how a gene is expressed. In participants with variations in the allele on chromosome 6, the microRNA doesn’t bind well with FKBP5. What this means is that the microRNA is unable to regulate the gene, which causes the gene to become over-expressed.
An over-expressed FKBP5 gene can be bad for a person’s health because it changes the body’s feedback mechanisms when circulating the stress hormone known as cortisol. Those with higher levels of cortisol are more likely to experience more severe chronic pain compared to those who don’t.
By preventing the onset of chronic pain, we may be able to reduce the need for opioid medications to treat chronic pain.
Opioid medications such as Oxycodone are considered dangerous because of their addictive qualities. Four out of every five new heroin users first began suffering from addiction when they started to misuse prescription painkillers. And, globally, 1.5 billion people suffer from chronic pain.
Linnstaedt says the findings of their study are important because it suggests there’s a way humans develop chronic pain after suffering from trauma exposure without suffering from any bone or tissue injury.
Linnstaedt says the study also highlights the gene involved in the development of chronic pain, which may be a promising target for future drug therapies. By looking at the way the FKBP5 gene regulates cortisol, she says, we may be able to mimic its actions to treat pain.