It is with much sadness that the pioneering work by Dr Les Simpson and his assistant Dylan at the Red Blood Cell Research Limited in Dunedin, New Zealand, have ceased. After all avenues were explored this vital work received no further funding. 

This Red Blood Cell Research was set up in 1998 by Dr. Les Simpson so that he could continue his research into the the pathophysiology of chronic disorders.

The majority of his work relates to ME and this began in 1983 in conjunction with Professor Campbell Murdoch who had recently arrived from Scotland to take up the position of Head of the Department of General Practice. At that time the technique of blood filtration was used to assess the stiffness of red cells and in 1986 it was reported that ME blood did not filter as well as the blood of blood donors. 

Because people with multiple sclerosis also complained of tiredness a similar study was carried out with multiple sclerosis blood and in 1987 it was reported that multiple sclerosis blood also filtered poorly. These findings stimulated the thought that scanning electron microscopy of red blood cells might provide some explanation for the poor filtrability of ME and MS blood. A technique was developed by modifying the standard procedure for the electron microscopy of samples obtained at operation. 

This involved the blood sample (5 drops of venous blood) being mixed as soon as possible with 5 ml of a special fluid - a fixative. Immediately-fixed blood samples did not show the sorts of red cell changes which Dr.Tapen Mukherjee reported as a letter to Lancet, and now, after more than 13,000 samples no such cells have been observed. The important difference was that Dr. Mukherjee washed and centrifuged his samples before fixation so the observed changes were a consequence of his preparatory technique.

Early observations showed very quickly that the medical textbook claim that all red cells have the same shape was not sustainable. In an article published in the British Journal of Haematology in 1989 it was shown that the red cells of healthy humans and animals could be classified into six different shape classes. Subsequently it has been found that chronic disorders in general share the common feature of altered red cell shape populations. 

Late in 1989 it was shown that blood samples from ME people in New Zealand had increased proportions of cup-transformed red cells. But by mid-1992 it was noted that only about 5% of ME people had cup-transformed red cells and the most common change was an increase in flat cells. It is not known what factor or factors was responsible for this change.

In the 1990's Dr. Simpson visited ME support groups in Australia, South Africa, the United Kingdom and Canada. The blood samples obtained after those visits totalled more than 2100 and the most common change was an increase in flat cells. However, 11% who were well at the time of sample collection had normal results. This demonstrates very clearly the relationship between wellbeing and red cell shape changes. As a result, patients are advised not to have a blood sample taken when they are feeling well - because the result will be normal.

It seems not to matter exactly what type of red cell shape change is involved as the outcome is the same; the cells reduce the rate of blood flow in capillaries. So it has been proposed - first at the Cambridge Symposium on ME in 1990 and in another article in 1998, that ME is a dysfunctional state resulting from reduced rates of capillary blood flow due to the presence of shape-changed, poorly-deformable red cells. 

Any impairment of capillary blood flow will mean that tissues will not receive the oxygen and nutrient substrates needed at a rate sufficient to sustain normal tissue function. Obviously, the effects of this would be most serious in those tissues which normally have a high rate of utilisation of oxygen and nutrient substrates. As such tissues include the brain and nervous tissue, muscles and secreting glands it is not surprising that dysfunction of such tissues is indicated by the development of symptoms.

This demonstration of an abnormality in blood which has been declared to be normal on the basis of the usual laboratory tests, is important as it could provide a basis for treatment. Given that the change in red cell shape is accompanied by red cell stiffening with reduced deformability it has been proposed that treatment should be aimed at improving red cell deformability and thus increasing the rate of capillary blood flow. In 1974 it was reported that prostaglandin E! reduced the viscosity of the lipid bilayer of the red cell membrane and in the following year another group reported that prostaglandin E1 improved blood filtrability. 

The blood levels of prostaglandin E1 can be increased by dietary supplementation with 4000mg daily of evening primrose oil. For reasons not yet explained, not all ME people respond to primrose oil, so it should be noted that the omega-3 fatty acids in fish oil have been shown to have the same effect on the red cell membrane as prostaglandin E1. There are other agents which also have a beneficial effect on red cell stiffness.

It should be noted that there are many studies which have used SPECT scans or other techniques to show that in various chronic disorders there are reduced rates of cerebral blood flow. While the cause of the reduced rates of cerebral blood flow are never explained, it is an expected effect of poorly deformable red cells - and such cells have been shown to exist in conditions with reduced rates of cerebral blood flow.

Altered red cell shape populations have been found in ME, CFS, Down Syndrome, CFIDS, cerebral palsy, multiple chemical sensitivity, manic depression, multiple sclerosis, Gulf War Syndrome, Fibromyalgia, arachnoiditis and aging. This implies that all of these conditions might benefit from improved red cell deformability. However it should be noted that although Fibromyalgia has flat cells like those of ME, Fibromyalgia pain remains unexplained. Nor has an opportunity presented itself to explore how many of these chronic states would respond in placebo-controlled trials of agents which improved red cell flexibility.

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