By the way ... At last, a clue to cause of chronic fatigue

I WAS beginning to despair whether science would ever reveal any breakthrough on the subject of chronic fatigue syndrome, a condition in which I have had a particular interest throughout my career.

But, at last, there is evidence that this is, as long suspected, an inflammatory disease.

One theory has been that this debilitating disorder is due to a dysfunction of the response of the body to infection — but this has never been established.

The latest research, published a few weeks ago by Georgetown University in the U.S., uncovered molecular changes in the brain that are specific to chronic fatigue syndrome. In particular, levels of certain microRNA — responsible for regulating protein production (proteins tell our cells what to do) — diminished after exercise in chronic fatigue patients, compared with healthy people, which could provide a basis for better diagnosis.

These findings add to research carried out earlier this year by Stanford University in California.

This showed that patients with chronic fatigue — those with a history of at least six months of unexplained physical and mental fatigue, malaise after exertion, sleep dysfunction, pain, neurological and cognitive symptoms — had raised levels of 17 cytokines, proteins that are the fingerprints of inflammatory processes. And the higher their level of cytokines, the more severe the illness.

This has established a strong immune component of the disease, the evidence that we have long awaited.

There is still a way to go, and this is by no means a complete answer, as, in some medical circles, the very existence of this disease remains controversial.

But I believe this is proof of chemical and inflammatory involvement, which points the way to new avenues of research: light, at last, at the end of a long tunnel, hopefully offering the prospect of future treatment — and prevention.