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LONDON, Aug 6 – Researchers at the University of Edinburgh have uncovered key genetic differences in people with chronic fatigue syndrome (CFS), offering new biological insights into the often-misunderstood condition and countering claims that it is rooted solely in psychological or behavioral factors.
The study, part of the DecodeME research project, analyzed DNA from over 15,000 individuals who self-reported chronic fatigue, compared with nearly 260,000 healthy volunteers, all of European ancestry. Scientists identified eight regions in the genetic code that differ in people with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). The results provide, according to the research team, “the first robust evidence that genes contribute to a person’s chance of developing the disease.”
ME/CFS is a debilitating illness characterized by severe fatigue, pain, and cognitive issues—symptoms that often worsen after even mild physical or mental exertion. The cause of ME/CFS has long eluded the medical community, with no definitive diagnostic test or cure available. An estimated 67 million people worldwide are affected by the disease.
Genetic Roots
The study found gene variants more common in people with ME/CFS were linked to immune and nervous system processes. In particular, at least two of the identified genetic regions appear involved in how the body responds to infection—a finding that echoes many patients’ reports of symptoms beginning after an infectious illness. Another gene region had previously been implicated in chronic pain, another hallmark of ME/CFS.
“These findings align with decades of patients reporting on their experiences,” said researcher Andy Devereux-Cooke, who noted that the results “should prove game changing in the ME/CFS research field.” He cautioned, however, that the discovery will not immediately translate into clinical tests or treatments, “but they will lead to a greater understanding.”
Cautious Optimism
Scientists not involved in the study urged caution, citing the reliance on volunteers who self-reported their symptoms, rather than those recruited through formal medical diagnosis. They called for more extensive, independently replicated studies to confirm the results.
Dr. Jackie Cliff, a ME/CFS expert in infection and immunity at Brunel University London, emphasized that “substantial work will be necessary to translate these findings into new treatments. This will take considerable investment in academia and by industry.”
Disclaimer: The findings reported in this article are based on a study that has not yet been peer-reviewed. Caution should be exercised until further validation by the scientific community. The information contained herein is not a substitute for professional medical advice.
