According to a study by researchers at King’s College, London, when a certain individual’s immune system is attacked by an infection it may cause long-lasting fatigue when that immune system over-reacts and that fatigue may continue long after the infection is eradicated.
This mysterious illness referred to as CFS and sometimes called myalgic encephalomyelitis (ME) is a debilitating illness that can become so severe it results in unrelenting fatigue where patients spend most of their time sleeping and often to the point some can’t even get out of bed.
Up to 17 million people are affected worldwide today by CFS and most of the time it’s improperly diagnosed and treated nor does it seem to have a cure. Unfortunately, some consider it to be a psychological malady rather than physical.
There’s hope though with the rise in research efforts in the last few years. And while it seems difficult to pinpoint the exact part the immune systems have in the development of CFS, the newest findings are showing that an overactive immune system may be the culprit.
Researches turned to people with an illness of Hepatitis C (HCV). 55 patients were treated with a drug called interferon alpha which is a common treatment for HCV and which causes the immune system to go into overdrive. It’s also known to cause acute fatigue similar to CFS which can last for many months after treatment.
As researchers chronicled each patient before, during and after treatment 18 out of the 55 exhibited fatigue that lasted beyond the normal time of recovery even persisting for months after.
They found a similarity between these 18 HCV patients and 54 CFS patients — both groups had no obvious differences in their immune systems when they compared them to 57 healthy people.
So according to the results, there are no detectable differences in a person’s immune system by the time they are consumed by CFS which then makes it difficult to diagnose because the period of an over-active immune system to an infection which triggered it has passed.
“In conclusion, findings from this study 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,” the authors conclude.
“A better understanding of the biology underlying the development of CFS is needed to help patients suffering with this debilitating condition,” says co-author Carmine Pariante, an expert in biological psychiatry at King’s College.
It may be a long time before accurate screening tests will be available, but at least the study brings the medical community closer to helping catch the illness at the beginning of its development and identifying people who may be at risk.