A new study is proposing a compelling hypothesis to explain the biological genesis of chronic fatigue syndrome (CFS). The research suggests the still mysterious condition is initially triggered by an overactive immune system and may help identify those patients most at risk of developing the illness.
Myalgic encephalomyelitis (ME), as many sufferers prefer it called, has no known treatment or cure, is difficult to diagnose, and for much of the 20th century was not even recognized as a physical illness. Over the last few decades doctors have come to accept CFS/ME as a real and serious condition, however, we still don't really understand how the illness begins.
Many sufferers often note their condition originated with a viral illness that led into the persistent symptoms we characterize with CFS/ME. This suggested that the condition may be propagated by an overactive immune system, but many studies have delivered inconsistent results in looking at immune system dysfunction in CFS/ME patients.
A new study set out to examine whether an excessive immune system response could at least trigger the onset of CFS/ME, and to do this researchers looked at hepatitis-C patients undergoing treatment with interferon-alpha. This drug treatment battles the hepatitis virus by triggering a strong immune response and many patients report persistent fatigue and CFS/ME-like side effects following the treatment.
The study followed 55 patients before, during, and after the treatment, tracking CFS/ME-like symptoms and immune system markers. Eighteen patients developed persistent fatigue that continued six months past the acute treatment phase. Interestingly, those 18 patients displayed a stronger immune system response during treatment than the other subjects. This immune system response was measured by tracking levels of immune proteins called interleukin-10 and interleukin-6.
Even more importantly, the researchers discovered those patients most prone to fatigue symptoms lingering after the treatment displayed higher levels of interleukin-10 before starting the treatment. This suggests that their immune system was already primed to be triggered into generating CFS/ME symptoms, and this could help point to an interesting biomarker that clinicians may utilize to target those patients more at risk of developing the illness.
"For the first time, we have shown that people who are prone to develop a CFS-like illness have an overactive immune system, both before and during a challenge to the immune system," says lead researcher Alice Russell, from King's College London's Institute of Psychiatry, Psychology & Neuroscience (IoPPN). "Our findings suggest that people who have an exaggerated immune response to a trigger may be more at risk of developing CFS."
The other significant finding from the study was that by the time CFS/ME-like illness has developed there seem to be no excess immune activation markers present. The research compared 54 CFS/ME patients with 57 healthy controls and discovered no marked difference in immune protein markers such as interleukin-10 and interleukin-6. This suggests that although an overactive immune system may trigger the onset of the illness, it does not explain its persistent characteristic symptoms.
The research does not explicitly offer insights into how to better treat patients currently suffering from CFS/ME and it doesn't explain why symptoms of the illness persist after the immune system trigger disappears. What the study does promise, though, is a greater insight into the origins of CFS/ME, and perhaps a new pathway towards identifying patients most at risk of developing the illness.
"A better understanding of the biology underlying the development of CFS is needed to help patients suffering with this debilitating condition," says senior researcher from the IoPPN, Carmine Pariante. "Although screening tests are a long way off, our results are the first step in identifying those at risk and catching the illness in its crucial early stages."
The research is published in the journal Psychoneuroendocrinology.
Source: King's College London
