Resuming his review of tests which are abnormal in M.E., Professor Behan said that one of his lecturers had a special interest in liver function abnormalities, and had noted that patients with M.E. had raised cholesterol levels, so they did a study of 30 well-defined cases, looking not only at cholesterol levels but also doing a full lipid profile. Of the 30 patients in the study, 27 showed not only gross but grotesque abnormalities. These same abnormalities have also been observed by Professor Anthony Komaroff at Harvard Medical School. Professor Behan said that in M.E. there is not only abnor,al carnitine metabolism, but abnormal lipid metabolism as well and that this has not so far been looked for in these cases.

He then mentioned briefly that there is abnormal immune function in M.E. and that there is non-specific impairment of NK cells especially (natural killer cells are able to kill certain types of cancer cells), and this is another abnormality in which there are gross differences between these patients and normal controls.

Professor Behan then moved on the SPECT scans, which his team have been doing for some years. They use serial SPECT scans to see if the abnormality which was present on one scan would have disappeared the next time. Patients with M.E. demonstrate that there are metabolic deficits in the temporal, occipital and fronto-parietal areas, all amounting to gross lesions within these patients. Another test used by the Glasgow team in M.E. patients is the water-loading test, which is given in the morning; the urinary output is measured over the next three hours, and in M.E. patients the results were grossly abnormal.

This study done by the Glasgow team was to measure the serum osmolarity and the urine osmolarity and also to measure the pruduct of the posterior pituitary, argenine vasopressin (AGP) (5). The stimulus for AGP comes from the paraventricular nucleus of the hypothalamus, and when patients were given the water deprivation and water loading tests, there was an erratic, crazy production in these cases. At this point, Prfessor Behan stated that in his opinion, these test results bring home the fallacy of simply examining someone in a clinic with a tendon hammer and a stethoscope and pronouncing the patient to be normal. He then showed a slide of the paraventricular nuclei of a perfectly healthy ratt which was stained to look for activated receptors on neuroendoctrine cells, and also to measure a hormone, the presence of which is an index of the activity of that part of the gland. He told us that Professor Christiansen of Sweden had injected these normal rats with trypanosomes (mycroscopic parasites) and that the trypanosome does not get into the hypothalamus, but does get into other parts of the brain stem where the blood-brain-barrier is broken down (6). Having got into parts of the brain stem, an immune reaction is elicited. The activated T-cells produce cytokines (chemical messengers) and once these cytokines are produced, an enormous turn-on of the hypothalamus occurs; this is a selective turn-on of the paraventricular nuclei.

Professor Behan then showed a slide of the brain stem demonstrating the reticular formation and various nuclei in the hypothalamus to which he had been referring, stating that these nuclei are the ones involved in viral infections, particularly polio infections. He said it is known that in the post-polio syndrome (PPS), if patients with severe fatigue have their growth hormone measured, it is low. Growth hormone has rapid daily fluctuations, but it is carried by a protein which does not fluctuate. The Glasgow team decided to measure growth hormone levels in patients with M.E., in patients with depression and in controls. They found that in M.E, at base line, the growth hormone levels are very low. Moreover, if patients are then stimulated by being given steroids (which should result in a massive up-swing), ther is no question that compared with controls, M.E. patients have no response. This work has been repeated in five different laboratories and the growth hormone abnormality in M.E has been absolutely confirmed. (Among other things, growth hormone increases protein synthesis.)

To tie the whole thing up, Professor Behan explained that 5 H-T is particularly interesting. It is produced in the median eminance of the midbrain and sends fibres directly to the paraventricular nucleus and from there to the median eminance controlling the release of steroids. Thus if you give a 5 H-T agonist, there would be a rise in cortisol, so with this in mind, the team did an experiment with a pure 5 H-T agonist and found that in patients with M.E. there is a very blunted response. This demonstrates that there is something wrong between the 5 H-T axis and the production of cortisol (the hormone required for normal response to any stress). This test has also been done with prolactin; again, there is a conspicuous difference between patients with M.E., with depressives and with controls. The depressives react entirely differently from patients with this syndrome. Professor Behan noted that with any adrenal damage, there is supersensitivity to 5 H-T receptors. So what causes this illness? Is it a defect of carbohydrate metabolism? Is it a muscle abnormality? The illness cannot be due to all of these but if you have a central cellular deficit which was giving rise to a number of other abnormalities, that might explain the whole picture.

The thinking at the moment is that in patients who are perhaps susceptiple, and depending on the stimulus and upon the time the stimulus is given, whether this is a virus or a toxin, damage occurs. This damage has to be fundamental because of the number of tissues involved, and is almost certainly at an enzyme level. this affects the subtle metabolism of the cell, probably in relation to potassium channels.

At present, professional departments in Sweden, London, Harvard, and of course Glasgow are looking carefully to see if they can dissect out of this abnormality in very subtle ways, to see what the lesion is. This lesion will have enormous importance, not only for M.E., but particularly in multiple sclerosis and all those other diseases where fatigue is a feature. Until this particular lesion is understood, a rational mode of therapy cannot be brought about.

Professor Behan concluded that in his own time of looking at M.E., he has seen far too many people who have been told that it's all in their head and that they are crazy. The end result has been that several committed suicide and others have been caused the most terrible distress.

1.Electromyogram, is a continuous recording of the electrical activity of a muscle by means of electrodes inserted into muscle fibres.

2.Nuclear magnetic resonance is a technique of chemical analysis used in the diagnosis of brain abnormalities based on the absorption of specific radio frequencies by atomic nuclei, enabling imaging of soft tissues anywhere in the body in any plane.

3.Glycolysis is the conversion of glucose to lactic acid, which process involves the production of energy.

4.Thallium scans are a method of studying blood flow theough the heart muscle using an injection of the radioosotope thallium-201.

5.Argenine is an amino acid which plays an important role in the formation of urea (the main breakdown product of protein metabolism by the liver, and vasopressin is the anti-diuretic hormone, or ADH.

6.Blood-brain-barrier (BBB) is the mechanism whereby circulating blood is kept separate from the tissue fluids surrounding the brain cells and which excludes solid particles and large molecules; this can break down after injuries such as whiplash.

Also make sure to read these books: Poison in Your Teeth: Mercury Amalgam (Silver) Fillings...Hazardous to Your Health! and Mercury Detoxification by Tom McGuire