emirates7 - Researchers at the University of Edinburgh announced on Wednesday that they have identified DNA differences in individuals with chronic fatigue syndrome (CFS), offering fresh evidence that the condition is biologically rooted rather than psychological or a result of laziness.
Their study uncovered eight specific genetic regions that differ between people with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and healthy individuals.
According to the researchers, this discovery marks the first strong genetic evidence suggesting that a person’s risk of developing ME/CFS is influenced by their genes.
ME/CFS is characterized by extreme fatigue, pain, and cognitive issues such as brain fog, which worsen after minimal physical or mental exertion.
Until now, the causes of ME/CFS have remained largely unknown, and there are no established diagnostic tests or treatments. The condition is estimated to affect approximately 67 million people globally.
The findings come from the DecodeME project, which examined DNA samples from 15,579 people who reported having chronic fatigue and 259,909 individuals without symptoms, all of European ancestry.
The gene variants more frequently found in people with ME/CFS were linked to the immune and nervous systems. Two of the identified regions appear to play a role in the body’s response to infections, which supports previous observations that ME/CFS often begins after an illness.
Another gene region had already been associated with chronic pain, which is another frequent symptom of ME/CFS.
Researcher Andy Devereux-Cooke said the findings mirror the experiences that patients have shared for decades and could be transformative for ME/CFS research. However, he cautioned that while these results may not immediately lead to diagnostic tools or treatments, they do offer a path toward a better understanding of the disease.
Some scientists not involved in the study noted that relying on self-reported diagnoses rather than clinically confirmed cases could limit the study’s strength. They emphasized the need for larger, follow-up studies to validate the results.
Dr. Jackie Cliff of Brunel University London, who studies infection and immune response in ME/CFS, added that significant research and investment will still be required to convert these genetic findings into viable treatments.
Their study uncovered eight specific genetic regions that differ between people with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and healthy individuals.
According to the researchers, this discovery marks the first strong genetic evidence suggesting that a person’s risk of developing ME/CFS is influenced by their genes.
ME/CFS is characterized by extreme fatigue, pain, and cognitive issues such as brain fog, which worsen after minimal physical or mental exertion.
Until now, the causes of ME/CFS have remained largely unknown, and there are no established diagnostic tests or treatments. The condition is estimated to affect approximately 67 million people globally.
The findings come from the DecodeME project, which examined DNA samples from 15,579 people who reported having chronic fatigue and 259,909 individuals without symptoms, all of European ancestry.
The gene variants more frequently found in people with ME/CFS were linked to the immune and nervous systems. Two of the identified regions appear to play a role in the body’s response to infections, which supports previous observations that ME/CFS often begins after an illness.
Another gene region had already been associated with chronic pain, which is another frequent symptom of ME/CFS.
Researcher Andy Devereux-Cooke said the findings mirror the experiences that patients have shared for decades and could be transformative for ME/CFS research. However, he cautioned that while these results may not immediately lead to diagnostic tools or treatments, they do offer a path toward a better understanding of the disease.
Some scientists not involved in the study noted that relying on self-reported diagnoses rather than clinically confirmed cases could limit the study’s strength. They emphasized the need for larger, follow-up studies to validate the results.
Dr. Jackie Cliff of Brunel University London, who studies infection and immune response in ME/CFS, added that significant research and investment will still be required to convert these genetic findings into viable treatments.