The following is an edited extract of a transcript of a talk given by Professor Peter Behan of the Institute of Neurological Sciences, University of Glasgow, to an audience of health professional at the Coventry and Warwickshire Post-Graduate Centre on the 23rd November 1995. Note should be taken of the implication of neuro-toxins in this report - also remembering that Mercury is a very potent neuro-toxin. I propose that in many cases of ME Mercury is the toxin that precipitates the disease.

Professor Behan started by confirming that M.E. is an organic disease. He also confirmed that M.E. is not a new illness: it was well described in 1750 by Manningham in a book called 'Febricula' (little fevers), and was equally well described in the 18th, 19th and early 20th centuries. Although it remains essentially a diagnosis of exclusion, there are now laboratory techniques which will confirm the diagnosis.

At first his team thought M.E. was precipitated by a virus, but there is now no question that some cases of the illness are precipitated by toxins. The challenge is to explain why minute doses of toxin re-exposure cause the illness, or why, if there is an acute precipitant such as a viral infection, the illness goes on for 20 years. The first exposure may have induced in the patient a lesion at the DNA level.

Professor Behan then compared a condition known as myeloadenamate deaminase deficiency, from which patients they had taken a piece of muscle and had stained for this enzyme and found it to be missing. It is known that the enzyme is missing after a viral attack. Similarly, in M.E., there is a defect in that the enzyme is not present in muscle, which shows that there must be some persistant abnormality.

He then went on to address the nature of the fatigue found in M.E.; he stated that it occurs acutely and is exactly the same fatigue which occurs in other conditions such as multiple sclerosis, even going so far as to state: "Patients with multiple sclerosis have chronic fatigue syndrome and the fatigue is exactly the same."

Some patients with endogenous depression have exactly the same fatigue, as do patients with Gilbert's syndrome (a familial condition due to an inherited deficiency of an enzyme in the liver cells causing a form of jaundice). It is well documented that patients develop M.E.-like fatigue after stress, or after viral infection, or after exposure to toxins. Why, asked Professor Behan, should that lesion in the liver give patients fatigue?

Post-polio syndrome is another condition in which fatigue is a prominent feature. In line with other recent research findings on the post-polio syndrome, Professor Behan stated catergorically that "PPS is identical in every way to chronic fatigue syndrome". Another condition in which fatigue occurs is idiopathic cyclic oedema, in which the woman is water-logged throughout the menstrual cycle due to hypothalamic disturbances. Also, there is classic fatigue in Parkinson's disease, a condition in which the fatigue is grossly incapacitating.

He and his team at Glagow have been carrying out tests on M.E patients, along with a group of controls, in which participants are exercised until they are tired. The next day the exercise tests are repeated. In well-defined cases of M.E., by using refined techniques for measuring gait disturbance, and using an ergometer for measuring muscle power, there is a phenomenal drop off in maximum oxygen consumption.

Professor Behan then mentioned single fibre EMG studies (1). In patients with M.E. there are gross abnormalities. About 80% suggest that something is wrong with the muscle. Professor Behan then observed that if the same thing that is demonstrably wrong with muscle may be wrong with other cells, it is necessary to come back to the concept of a primary stimulas. What might this be?

He turned next to NMR imaging (2). He said NMR studies showed that in M.E. there is very early excessive intrcellular lactic acidosis with exercise and that this tends to persist, suggesting that there is something wrong with the glycolytic pathway (3). During strenuous exercise, pyruvic acid (a compound derived from carbohydrates) is reduced to lactic acid, which then accumulates in the muscles and causes cramp.

In M.E., there are two indicators that there is undoubtably something wrong: one is nuclear magnetic resonance and nuclear imaging: the other is in the field of neuroendocrinology. Still on tests for muscle pathology, Professor Behan emphasised that when doing muscle biopsies on patients with M.E., it was necessary to look at them expertly. He showed a slide of a normal muscle biopsy in which the mitochondria (the sites of the cell's energy production) appeared as little red dots. Only careful and expert study revealed an increase in the mitochondria in M.E. The Glasgow team have now done about 400 such biopsies and they have found another abnormality in that cristae (the infoldings of the inner membrane of mitochondria) have gone, leaving honeycombed patterns. This honeycombing suggested to Professor Behan a toxic or a stress phenomenon in the mitochondria.

When cells of M.E. patients are looked at in tissue culture, the lactic/pyruvic ratio of patients falls into two groups: patients are either producing too little or too much. Recently, Professor Behan has been interested in Syndrome X where an individual presents with what seems to be a coronary thrombosis. They may have very severe angina, but all the usual test results are normal: treadmill tests are normal. There is however, an abnormality of the lactic/pyruvic ratio, together with conspicuous abnormalities of carbohydrate metabolism. This Syndrome X has been reported from the Hammersmith Hospital in London, and also from Sweden. Professor Behan's team have discovered that these Syndrome X cases have gone on to develop chronic fatigue syndrome. The team at Glasgow has done thalium scans on patients with chronic fatigue syndrome, and in 100% of cases the scans are abnormal, yet again suggesting a cellular abnormality (4). Professor Behan showed a thallium scan of a young girl of 21 with M.E. He said he currently has a paper in press about these cases, all of whom have gross abnormalities of the myocardium. Referring to Syndrome X, Pr fessor Behan said that other data using PET scans (positron emission tomography) which measured the flow showed no ischaemia and no impairment and this is a metabolic abnormality.

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