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Tim Newman recently composed an article that was fact-checked by Jasmin Collier on chronic fatigue syndrome. There is new evidence of the immune system’s role in chronic fatigue syndrome in unprecedented depth. This could help to design future treatments for the condition.
Chronic fatigue syndrome (CFS) is also called myalgic encephalomyelitis (ME) and is a mysterious condition. The main symptom of CFS is extreme and unrelenting fatigue, muscle and joint pain, sleep issues and flu-like symptoms. The reason for CFS is unknown by researchers. There are some suggestions, such as viral or bacterial infection, changes in the immune system, hormone imbalance and mental health conditions. They have not yet been able to design a test that can diagnose CFS, so treatment currently only relieves symptoms. However, an interest in the role that the immune system might play in CFS has grown.
Many with CFS report their symptoms began after an infection or another insult to the immune system. These are common reports, but it is impossible to assess how the body was behaving before they arrived once the symptoms have appeared.
People who were taking treatment for hepatitis C called interferon-alpha were investigated by researchers. It works by triggering the immune system in the same way a significant infection would. Those taking this course of medication often report CFS-like symptoms during the treatment. Others experience a CFS-like condition that can last 6 months after the end of treatment. This includes fatigue, cognitive impairment, and joint and muscle aches.
For those experiencing CFS-like symptoms, the researchers observed greater immune responses to the interferon-alpha treatment. This group did produce around twice as much interleukin-10 and interleukin-6, both that are important immune system messengers. Higher levels of fatigue during treatment were reported but not higher levels of fatigue before treatment.
Scientists saw that levels of interleukin-10 were elevated before interferon-alpha treatment began on these people. An exaggerated response to interleukin-10 and interleukin-6 was also shown early on in the treatment. They think this might mean the immune system was already primed to over-respond. They have shown that people who are prone to develop a CFS-like illness have an overactive immune system, before and during a challenge to the immune system. They also believe it suggests those who have an exaggerated immune response to a trigger may be more at risk of developing CFS.
They compared the immune systems of 54 people with CFS with 57 people without CFS and found no significant differences in interleukin levels. They hope these findings might open the future possibility of screening for those who might be most at risk of developing CFS. They want to progress with future research to examine the molecular mechanisms that underlie an exaggerated immune response and that are involved in the conversion from acute to persistent fatigue symptoms.
Dr Fredda Branyon