Biological Underpinnings Of Chronic Fatigue Syndrome Begin To Emerge

 

Ron Davis

 

By Amy Maxmen in Nature International Weekly Journal of Science.

 

Before his 33-year-old son became bedridden with chronic fatigue syndrome, biochemist Ronald Davis created technologies to analyse genes and proteins faster, better and more cheaply. Now he aims his inventions at a different target: the elusive inner workings of his son’s malady.

In his office at the Stanford Genome Technology Center in Palo Alto, California, Davis holds a nanofabricated cube the size of a gaming die. It contains 2,500 electrodes that measure electrical resistance to evaluate the properties of human cells. When Davis exposed immune cells from six people with chronic fatigue syndrome to a stressor — a splash of common salt — the cube revealed that they couldn’t recover as well as cells from healthy people could. Now his team is fabricating 100 more devices to repeat the experiment, and testing a cheaper alternative — a paper-thin nanoparticle circuit that costs less than a penny to make on an inkjet printer.

Davis’s findings, although preliminary, are helping to propel research on chronic fatigue syndrome, also called myalgic encephalomyelitis (ME/CFS), into the scientific mainstream. Physicians used to dismiss the disease as psychosomatic, but studies now suggest that it involves problems in the chemical reactions, or pathways, within cells. “We now have a great deal of evidence to support that this is not only real, but a complex set of disorders,” says Ian Lipkin, an epidemiologist at Columbia University in New York City. “We are gathering clues that will lead to controlled clinical trials.”

 

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