Chronic fatigue syndrome (CFS) or myalgic encephalomyelitis (ME) is a condition that manifests as fatigue that refuses to go away that makes people unable to perform their daily activities. Patients spend their time sleeping or laying bed. The condition affects around 17 to 24 million individuals worldwide who are often not diagnosed and seldom treated. A new study has shown that overactive immune systems may be the trigger that gives rise to CFS. The study results were published in the latest issue of the journal Psychoneuroendocrinology. The team of researchers from the King’s College London looked at the connection between sensitive immune system and CFS. Chronic fatigue syndrome is associated with long term fatigue that refuses to go away even after the infection is controlled. Alice Russell, a psychiatrist at the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) who works with CFS says: “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. Our findings suggest that people who have an exaggerated immune response to a trigger may be more at risk of developing CFS”.
Research in this area is fairly recent they explain. The team now finds that the immune system has a lot to do with the condition and it is not a psychological condition as believed earlier. The researchers looked at a model that can mimic the symptoms of CFS to understand its cause. They included 55 patients with Hepatitis C and these patients were given Interferon alfa as part of their treatment. Interferon-alfa is the standard treatment for Hepatitis C and mimics the effects of the immune system when it goes into an overdrive to fight an infection. Interferon alfa can cause fatigue as a side effect and even after the therapy is completed, the drug can cause long lasting fatigue that is similar to CFS. The team noted that 18 of the patients did not recover from the symptoms of fatigue long after the treatment. These patients had similar levels of fatigue as other patients before their treatment started. However their fatigue symptoms worsened and lasted longer than others once the treatment began and then was completed. They found that the fatigue in these patients was linked to a greater immune response compared to the other patients. This means that in some individuals the immune systems are “primed” so that they give an exaggerated response to infections and this can lead to long lasting fatigue.
Six months after the treatment was completed, these patients still complained of fatigue. The researchers were surprised to note that the immune systems of the 54 patients with CFS were similar to 57 individuals who were healthy controls. This means that once the condition develops, the differences in the immune system are no longer detectable. And this could be the reason why CFS is difficult to diagnose. There was no evidence of an association between persistent fatigue and peripheral inflammation six-months post-treatment, nor did we observe peripheral inflammation in the CFS cohort. With regards to IL-10 and IL-6, there were significant differences in the levels of these cytokines between the four groups. With regards to levels of IL-2, IL-8, IL-17 A and TNF-α (the cytokines that were regulated by IFN-α), for IL-2 there were no significant differences between groups. While there were changes in kynurenine metabolites (from tryptophan catabolism) in response to IFN-α, there was no association with persistent fatigue. CFS patients had lower levels of kynurenine / tryptophan ratio and 3-hydroxykynurenine than controls.
Co-author Carmine Pariante, an expert in biological psychiatry at King’s College explained: “CFS is a serious condition and its underpinning biology is poorly understood. A better understanding of the biology underlying the development of CFS is needed to help patients suffering with this debilitating condition. 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. In conclusion, our findings support the hypothesis that abnormal immune mechanisms are important in CFS, but only early in the course of the illness, around the time of the trigger, rather than when the syndrome is established…Moreover, our study confirms the importance of the acute fatigue response to the trigger, rather than of the recovery period preceding the illness. Encouragingly, this work sheds light on potential mechanisms of immune dysregulation underlying early stages of chronic fatigue syndrome”.
- Edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.
Russell A et al., Pariante CM. Psychoneuroendocrinology 2018 Dec 14.
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