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The roots of chronic fatigue

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See the following new report regarding chronic fatigue. This kind of stuff

just infuriates me! They go thru and acknowledge that Chronic Fatigue is

real, then they end their " scientific findings " with, " And, perhaps, inspire a

sudden recovery in the malingerers. "

Sharon Kramer

Myalgic encephalomyelitis

The roots of chronic fatigue

May 8th 2008

From The Economist print edition

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

test for it could be developed

Eyevine

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

fluâ€. 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 fatigueâ€.

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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