ME: 'Invisible disease' is now easier to read

A simple blood test may revolutionise the way we treat patients with ME, reports Bob Ward

British researchers are close to developing, for the first time, a blood test and potential drug treatments for myalgic encephalomyelitis (ME), also known as chronic fatigue syndrome (CFS), following groundbreaking work on its genetic origins.

A woman suffering from fatigue
'The stigma associated with the disease can sometimes be as much of a problem as the symptoms'

ME/CFS affects about one in 200 people, and women sufferers outnumber men by six to one. It causes a constant feeling of extreme exhaustion and malaise for more than six months, along with sleep abnormalities, memory and concentration difficulties and a great deal of pain.

In its most extreme form, the disease leaves sufferers bed-ridden and can even be fatal.

But patients now have new hope, thanks to research published in the Journal of Clinical Pathology by Dr Jonathan Kerr of St George's University of London and his colleagues.

They have identified 88 genes that produce different levels of proteins and other molecules in ME/CFS sufferers compared with the rest of the population.
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Dr Kerr's team carried out a complex analysis of the records of 55 patients and found that they could be divided into seven sub-types according to the specific gene combinations found in their white blood cells, and the severity of their symptoms.

The most acutely affected patients had 71 of the 88 gene abnormalities.

The results of this work should allow better understanding of the causes and development of the disease. Many of the genes are known to be affected when a person contracts a virus, a factor which is believed to trigger many cases of ME/CFS.

Importantly, the researchers also recognised that five of the 88 genes are targeted by drugs which are already used to treat other diseases.

The team is now investigating whether the faulty genes produce abnormal levels of proteins that can be detected as minute quantities of "biomarkers" in the blood of patients.

"If proven to be sensitive and specific indicators of the illness, the discovery of protein biomarkers could lead to the development of a diagnostic test for ME/CFS, which would revolutionise our approach to this disease," explains Dr Kerr.

He will present his results at a conference on ME/CFS biomedical research in Cambridge in May.

The research may even lead to a change in attitudes to the disease, often trivialised as "yuppie flu".

Sarah, 31, who was diagnosed with ME/CFS two years ago, says: "The stigma associated with the disease can sometimes be as much of a problem as the symptoms.

"Some think that it is 'all in the mind' and can be cured by a good night's sleep. It can be difficult to get friends and work colleagues to understand just how difficult it is to live with a disease that is so debilitating but virtually invisible."

Attitudes among funders of medical research also need to change, says Dr Neil Abbot, operations director at the charity ME Research UK. "Studies on the psychological aspects of ME/CFS seem to have vacuumed up attention and funding at the expense of hard-core biomedical studies," he says.

"Most of the £3 million spent by the Medical Research Council on the illness in the last six years has gone towards projects on the psychological management of the disease, while there is evidence that around 30 applications, some from established biomedical research groups, have not been funded."

The work carried out by Dr Kerr and his colleagues is funded by a small charity, the CFS Research Foundation, which was set up in 1993 by a group of doctors and scientists who were concerned about the direction and quality of work on the disease.

Its director, Anne Faulkner, is optimistic about the search for a cure: "We believe that this disease can and will be conquered, but it will need th