A common gene variant has been linked to differences in pain sensitivity, according to a new study by scientists based at Cambridge University. The finding could help to explain why people have different pain thresholds and might help in the search for effective pain killers with tolerable side effects.
'Because current therapies have limited efficacy, with up to 50 per cent of treated subjects receiving inadequate pain relief , there exists a significant need to develop better therapies', said Dr Geoffrey Woods of Cambridge University, lead author of the study published online in the journal Proceedings of the National Academy of Sciences
The discovery could be one part of the genetic puzzle explaining why patients respond differently to different classes of painkillers. Dr Woods emphasised the urgent need for better treatments, particularly with regard to people suffering from persistent pain: '[T]he development of maladaptive persistent pain states in response to tissue injury is common, with one in six adults suffering from a chronic pain condition.'
The genetic variant was found within the DNA sequence of a gene previously linked to pain. Four years ago, Dr Woods and his colleagues discovered a mutation in a gene known as SCN9A, which leads to the rare condition of being unable to feel pain. In their most recent study, the researchers compared the DNA sequence of the SCN9A gene in 578 people with osteoarthritis, the most common form of arthritis. They found that patients who reported the most severe pain in realtion to their condition all shared a particular mutation in the SNC9A gene. The same mutation was found in patients with sciatica (caused by compression of the sciatic nerve), phantom limb syndrome (pain in an amputated limb) and who had undergone a lumbar discectomy (a spinal operation to relieve pain caused by compression).
The SCN9A gene is known to produce a protein found in nerve cells, which controls the flow of sodium into the cells in response to painful stimuli. This sodium influx stimulates the nerve cell, thereby triggering a signal which the brain interprets as pain. Differences in pain sensitivity may be due to variations in the gene that cause the sodium channels to open too easily or stay open longer, according to the researchers.
Dr Woods identified drugs targeting the SCN9A gene as a possible avenue for future research. 'As individuals appear to have differing genetic susceptibilities to pain, future studies should be directed toward understanding whether responsiveness to different classes of analgesics is also genetically determined,' he told the Daily Telegraph.