Lifestyle
and environmental factors can alter sensitivity to pain by switching certain
genes on or off, according to research from King's College London.
One in five people
suffers from chronic or acute pain, but its underlying molecular mechanisms are
not yet fully understood. The researchers hope that this study, which
highlights the epigenetics behind pain, will provide new drug targets for painkillers.
Dr Jordana
Bell, who led the study, said the results were 'very exciting and could lead to
a more effective pain relief treatment for patients suffering with chronic
pain'.
The study
looked at 25 sets of identical twins with a different pain tolerance, where one
twin had particularly low sensitivity. As identical twins share all their
genes, any differences would be due to environmental differences causing epigenetic
changes.
To determine
their pain threshold, each twin had a heat probe attached to their arm, which
became increasingly hot. When the heat became too painful, they pressed a
button. The DNA of each twin was then screened and differences between the
genes involved in pain sensitivity were examined.
Nine genes
were found to have epigenetic differences that meant they were expressed
differently when exposed to pain. The most significant chemical differences
were seen in a known pain sensitivity gene, TRPA1, which is currently a
therapeutic target in the development of some painkillers.
These
results were confirmed by examining, in the same way, a group of 50 unrelated
individuals.
Tim Spector,
professor of genetic epidemiology at King's College London, said that
epigenetic changes acted like a 'dimmer switch for gene expression'.
He added: 'This
landmark study shows how identical twins, when combined with the latest
technology to look at millions of epigenetic signals, can be used to find the
small chemical switches in our genes that make us all unique - and in this case
respond to pain differently'.
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