Economist article on CFS (or ME)

[Guest guest]

Below is an article from the Economist. I follow ME very closely since there are

three female adult relatives in my children's family (one on their father's side

and two on mine) with this. I am very curious if there are any connections with

the genes in this study to CFS and autism.

http://www.economist.com/science/displaystory.cfm?story_id=11326174

ME is a puzzling illness, but it appears to have a biological basis and a test

for it could be developed

A DISEASE that carries with it a social stigma causes additional and

unnecessary suffering. This has often been so with myalgic encephalomyelitis

(ME), or chronic-fatigue syndrome, as it is also known. Despite debilitating

symptoms, patients have been accused of suffering from an imaginary illness:

“yuppie flu”. Doctors have struggled to distinguish the ailing from the

malingering. Nonetheless, evidence has grown in recent years that the syndrome

is real, and now there is news that it has its roots in genetics.

ME manifests as extreme exhaustion, something that may include a range of

other symptoms, such as disturbed sleep, difficulties in remembering and

concentrating, headaches, and painful muscles and joints. Psychological

symptoms, such as anxiety and irritability, can also be present. As the symptoms

can vary in severity, the syndrome can be hard to identify, and patients can

suffer for months before a diagnosis is made.

However, new hope for ME sufferers arrived this week at a conference in

Cambridge, in Britain. The event, organised by ME Research UK and the Irish ME

Trust, two charities that help to fund studies and assist sufferers, was

attended by researchers investigating what causes the illness and how it could

be treated.

Kerr of St 's University of London told the meeting that with

his colleagues they have identified 88 genes which are expressed differently in

the blood of patients who had been diagnosed with ME. Moreover, in studying the

records of 55 patients with ME, they found that they could divide them into

seven separate sub-types that consistently pair distinct genetic patterns with a

combination and severity of patients' symptoms. This, says Dr Kerr, points to a

biological basis for the illness and holds out hope that a blood test could be

developed to identify its different forms. His group are now trying to find the

biological markers that such a blood test would need to detect.

ME, myself, why?

One tactic for dealing with ME is to treat its symptoms with drugs that are

already used against other diseases. Patients with some of the severest symptoms

suffer from low blood pressure and have difficulty regulating their heartbeat.

Newton, of Newcastle University in Britain, says this is because of

problems with their autonomic nervous systems, which is responsible for

subconscious activities. In studies using a magnetic-resonance imaging scanner,

she found a build-up of acid in the muscles of ME patients when they took

exercise. This can cause muscle weakness and pain. Dr Newton believes the

build-up could be influenced entirely, or at least in part, by the degree to

which the autonomic nervous system fails to properly maintain blood flow. It

could also mean that drugs that already exist to help improve blood flow might

also help some ME patients.

But what triggers ME? Some estimates put its occurrence at around one in 200

people in America and Britain. Sufferers are often in their 20s and 30s, and

more women are affected than men. That it is so widespread suggests to some

researchers that there are many causes, including exposure to certain viruses

and other infectious diseases.

A long period of fatigue after suffering from an infectious disease is not

unusual. At the conference, a team of Australian researchers speculated that

many cases of ME are in fact cases of “post-infectious chronic fatigue”.

Graves, of the Australian Rickettsial Reference Laboratory, said they had found

a proportion of Australian ME sufferers may have a genetic predisposition to

developing ME as a result of exposure to Q Fever or Flinders Island Spotted

Fever. These are a pair of relatively uncommon diseases caused by two bacteria

which can pass between animals and humans. If their hypothesis is correct, Dr

Graves believes the incidence of ME in Australia may be reduced by greater

public-health measures.

Although the trigger for most cases of ME may remain a mystery, the discovery

of its biological roots and the promise of a test will bring hope of a diagnosis

to sufferers. And, perhaps, inspire a sudden recovery in the malingerers.

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