Researchers at the University of Edinburgh said Wednesday they’ve identified DNA differences in people with chronic fatigue syndrome, offering new evidence that the debilitating illness is biological—not psychological or linked to laziness.
Their study found eight areas of genetic code that are different in people with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) than in healthy volunteers.
The finding provides "the first robust evidence that genes contribute to a person's chance of developing the disease,” the researchers said in a statement.
The key features of the condition include worsening of fatigue, pain and brain fog after even minor physical or mental activity.
Very little is known about the causes of ME/CFS, and there is no diagnostic test or cure. The condition is believed to affect around 67 million people worldwide, the researchers said.
The DecodeME study analyzed DNA samples from 15,579 people who reported having chronic fatigue on a questionnaire and 259,909 people without it, all of European descent.
Gene variants that were more common in people reporting ME/CFS were linked to the immune and nervous systems, according to a report of the study that has not yet been peer-reviewed.
At least two of the gene regions relate to how the body responds to infection, which aligns with reports that the symptoms often start after an infectious illness, the researchers said.
Another gene region has previously been identified in people with chronic pain, another common symptom of the condition.
The findings "align with decades of patients reporting on their experiences,” researcher Andy Devereux-Cooke said in a statement, adding that they "should prove game-changing in the ME/CFS research field.”
"These results will not mean that a test or cure will be developed straight away, but they will lead to a greater understanding," he said.
Scientists who were not involved in the study said using volunteers who self-reported chronic fatigue syndrome rather than restricting participation to those with a diagnosis from a medical professional somewhat weakened its conclusions. They called for larger studies to replicate the results.
Substantial work will be necessary "to translate these findings into new treatments," said Dr. Jackie Cliff, who studies infection and immunity in ME/CFS at Brunel University of London. "This will take considerable investment in academia and by industry.”
