Study Finds Elusive Biological Evidence Of Chronic Fatigue Syndrome

Sarah Myles

The diagnosis of Chronic Fatigue Syndrome (CFS) - or Myalgic Encephalomyelitis (ME) - has long been problematic and controversial. With a diagnostic process reliant wholly on the patient's description of symptoms, there is a great deal of stigma attached to the condition, which has often been assumed by non-sufferers to be psychological in nature. The lack of biological evidence in the illness has also made it exceedingly difficult to determine effective drug therapies and treatments.

Now, however, research from Columbia University has identified for the first time a physical identifier for the condition. Director of translations research at the Center for Infection and Immunity at the university, Dr Mady Hornig, explained to The Telegraph the implications of the latest findings.

"We now have evidence confirming what millions of people with this disease already know, that ME/CFS isn't psychological. Our results should accelerate the process of establishing the diagnosis after individuals first fall ill, as well as discovery of new treatment strategies focusing on these early blood markers."

While it has long been theorised that Chronic Fatigue Syndrome occurs after an infection of some kind - implicating the involvement of the immune system - the new study findings indicate that an infection can cause the immune system to remain active, even after the infection has been neutralised - effectively becoming stuck in the 'on' position, as Dr Hornig explained to Science Codex.

"It appears that ME/CFS patients are flush with cytokines until around the three year mark, at which point the immune system shows evidence of exhaustion and cytokine levels drop. Early diagnosis may provide unique opportunities for treatment that likely differ from those that would be appropriate later in the disease."
"This study delivers what has eluded us for so long: unequivocal evidence of immunological dysfunction in ME/CFS, and diagnostic biomarkers for disease. The question are trying to address in a parallel microbiome project is what triggers the dysfunction."