Last month, in his excellent blog, ME/CFS Research Review, Simon McGrath summarised some of the fascinating developments in the work of Stanford researcher, Dr Ron Davis.
Dr Davis’s central hypothesis is that there is some factor in the blood plasma of ME/CFS patients that is driving their illness. Plasma is the liquid component of blood in which the blood cells and platelets are carried, but it carries many other components – such as antibodies and other proteins – which are important for health.
In previous experiments, the electrical impedance of a sample of white cells in plasma from ME/CFS patients increased when stimulated with salt, while there were no electrical changes in samples from healthy volunteers.
However, these changes in impedance disappeared when the ME/CFS cells were placed in plasma from healthy people, suggesting that something in the ME/CFS plasma is making the cells act abnormally.
The dramatic difference between ME/CFS and healthy plasma suggests this test might be useful as a biomarker, but the results may also lead to discoveries about the pathology of the illness.
Dr Davis has also seen that deformability of red blood cells (their ability to squeeze through the smallest capillaries) is reduced in samples from ME/CFS patients, but only when the cells are tested in patients’ own plasma (as opposed to the stabilising fluid commonly used in these kinds of experiments). This also implicates some factor in the plasma.
More recently, he has found that the rise in impedance in ME/CFS white cells seen in the salt tests can be prevented by adding the mitochondrial antioxidant SS-31 or the multiple sclerosis drug copaxone.
Furthermore, ongoing experiments in Dr Davis’s laboratory are looking at whether the offending factor in the plasma of ME/CFS patients is some form of microorganism such as a virus, bacteria or parasite.