The greatest hurdle in treating ME is trying to figure out exactly what it is and how it differs from other illnesses of chronic fatigue.

ME or myalgia encephalitis chronic fatigue syndrome in the US is a chronic disabling disease which affects an estimated 100,000 people in the UK, although new estimates are considerably higher. Yet it has only recently been recognized by the World Health Organization as a disease of the nervous system. While victims of the illness are slowly winning the battle for recognition of ME as a genuine illness (rather than a product of hysteria) against the near universal scepticism of the medical profession, there is still disagreement about the best way to treat it.The greatest hurdle in treating ME is trying to figure out exactly what it is and how it differs from the many other illnesses with which it is sometimes confused.

Research now supports the view that ME is probably a persistent viral infection causing an overactive immune system (Landay AL et al Lancet, 1991; 338: 707-712). There is inflammation throughout the central nervous system (Buchwald D et al, Annals of Internal Medicine, 1992; 116, 2: 103-13), and disturbance of hypothalamic function such as hormonal and nervous system changes (Bakheit AMO et al, BMJ, 1992; 304: 1010-2). Evidence of raised cytokines chemicals produced by the immune system, including interferon and interleukin 2 is clear in the symptoms: exhaustion, usually accompanied by myalgia (muscle pain), brought on and aggravated by relatively trivial exercise, flu like feelings and nausea. In one study, 80 per cent of biopsies showed evidence of damage to the mitochondria (which provide cells with energy) (Behan WMH et al Acta Neuropathologica, 1991; 83: 61-5). Sophisticated brain scans demonstrate disturbances of blood flow and other mid brain damage (Costa DC et al, European Journal of Nuclear Medicine, 1992; 19, 8: 733).

The depression experienced by patients with ME is different from that reported by psychiatric patients, and linked to the severity of the disease; the more severe the other symptoms, the greater the depression (Hickie I et al, Lancet, 1991; 337: 992). Other symptoms include digestive disorders similar to irritable bowel syndrome and bloating. Symptoms fluctuate, usually precipitated by either physical or mental overactivity.

Those who do take ME seriously divide into two camps: the virus hunters who blame a persistent virus and not the immune system which allowed the virus access, and those who see ME as activated by trigger factors, one of which may be a virus, but only as a co-factor with other triggers leading to weakened immunity.

Dr Betty Dowsett, Consultant Microbiologist to the Basildon and Thurrock Health Authority, Basildon Hospital, Essex, has suggested that viruses in the enterovirus group (polio, coxsackie, echo and other strains) are the most likely agents of infection in Britain (Journal of Hospital Infection, 1988;11:103). She argues that the reason why the virus is difficult to identify is that poorly replicated mutants fail to activate the immune system into mounting a defence. She also has found links between ME and polio ME was identified for the first time during an epidemic of polio in California in 1934.

The recent discovery of the post polio syndrome progressive muscular weakness and fatigue, and persistent viruses all occurring some 25 or 30 years after recovery from paralytic polio gives weight to the argument of a connection between polio and ME. Furthermore, from 1955, when general poliomyelitis immunization was introduced, the incidence of paralytic poliomyelitis fell but that of ME continued, in a changed form; it now rarely causes paralysis.

Trigger factors may play an important role (Komaroff in Bock and Whelan, Chronic Fatigue Syndrome, CIBA, Wylie, 1993). Viral and bacterial infections, injury, hormonal change and psychological stress are all possible triggers. Dr David Dowson of the Centre for the Study of Complementary Medicine in Southampton believes that the following factors may combine to trigger ME:

Persistent viral or bacterial infection. The latter can sometimes remain undetected for example infection in the teeth, tonsils or appendix.

Candidiasis, an over growth of yeast organisms in the intestines.

Magnesium, selenium and other mineral deficiencies.

Allergies and sensitivities to foods, pollutants, animal products, plant products and chemicals.

Depression as a result of the debilitating nature of the illness, not a direct cause of the condition.

A recent German study of 103 people with chronic fatigue dysfunction syndrome, the closest to ME of all the chronic fatigue syndromes, found that levels of vitamin B12 were low in 26 per cent of sufferers, and receptors for the immune system chemical interleukin 2 were significantly high in 21 per cent and raised in a further 29 per cent. Eighty five people were tested for candida overgrowth; 19 per cent were borderline, and a further 28 per cent had abnormally high levels (Zeitschrift Fur Klinische Medizine, 1992, vol 47).

Psychiatrists, neurologists and other specialists have devised programmes of graded activity and exercise for ME sufferers on the theory that they need to be gradually introduced to normal levels of activity. Their physical exhaustion is seen as caused by atrophy from disuse rather than disease.

A recent study has found that graded exercise plus cognitive therapy were no more helpful than placebo or other ineffective treatments (Lloyd, American Journal of Medicine, February 1993).

It set out to evaluate the potential benefit of immunological therapy with the immune system booster dialyzable leukocyte extract (DLE) and psychological treatment in the form of cognitive behavioural therapy (CBT) in patients with chronic fatigue syndrome. All patients received eight biweekly intramuscular injections containing either DLE or a placebo.

The CBT is built on the assumption that lack of activity is “maladaptive” behaviour which intensifies key symptoms, such as depression. It consisted of six sessions in which patients were encouraged to gradually increase physical activity and not to stop at the first sign of feeling tired. Patients were randomly allocated to one of four groups: those who received both therapies, those who received either and those who received none.

All four treatment groups had a very similar outcome, leading the researchers to conclude that both treatments “provided no clinically significant benefit”.

Action for ME’s advice, based on the experience of sufferers, is that programmes of gentle exercise can be helpful, but as an adjunct to other treatments and therapies, once the patient is well on the road to recovery.

Doctors may also suggest antidepressant drugs. Trials on Prozac suggest that if anti depressants work on the immune system, ME sufferers may feel better and less disabled.

It seems to be the general case that those with mainly brain symptoms and sleep problems gain the most benefit. However, the doses should be much lower than are normally prescribed for depression, otherwise the sufferer’s condition may be made worse. And Prozac is suspected of causing a range of serious side effects, including evoking murderous rages in patients (see WDDTY vol 4 no 2).

In those cases where depression is not predominant, it may be more beneficial to start by exploring the nutritional and dietary approach to ME, together with candida control. A survey of 695 patients carried out by Action for ME in 1991, to assess 34 different therapies, showed that of the 80 per cent who changed their diet, 73 per cent experienced improvement in their condition.

ME sufferers can end up barely able to tolerate any food because practitioners with a limited knowledge of allergies launch them on severe exclusion diets, permitting a very small number of foods, which very soon become badly tolerated as well. Instead, of allergy per se, the problem is often one of food intolerance and/or gut permeability. This can be tested to show whether there is abnormal absorption of molecules of different sizes. Treatment involves the use of anti fungals and supplements such as butyric acid, which heal the gut wall.

There is also evidence of a link between ME and low stomach acid (see WDDTY, vol 4 no 2) which leads to malabsorption of nutrients. The homeopath (and WDDTY Alternatives columnist) Harald Gaier reports that such patients often make a startling improvement when treated with pancreatin and or/betaine hydrochloride with pepsin.

Dietary manipulation must go hand in hand with correction of other imbalances, such as liver function, adrenal or thyroid exhaustion, malabsorption, and candida overgrowth.

A controlled scientific study conducted by Dr David Dowson indicated that many ME sufferers are deficient in magnesium (The Lancet, 30 March 1991). Treatment with a course of six weekly injections of magnesium sulphate benefited 80 per cent of the ME patients in the trial, and their red cell magnesium levels were significantly raised at the conclusion of treatment. (Serum levels can be normal even if there is an overall deficiency, so blood tests are not reliable indicators.)

Dr Dowson found that oral supplementation generally wasn’t sufficient to correct deficiency. Since this study, however, other studies have failed to replicate the results. The difference in results may have arisen, as Dr John McLaren Howard of London’s Biolab Medical Unit points out, because a deficiency can vary by very little from the normal range.

Dr McLaren Howard also stresses that magnesium injections won’t work without prior oral supplementation over several months. Since publication of his research, Dr Dowson has discovered that patients who take oral supplements of selenium at the same time as having their magnesium injections seem to do better.

Selenium is dangerous if taken in high doses not more than 200 microgrammes should be taken per day. A level which is normal for one may be low for another.

Some cases of magnesium loss occurs when cell membranes are subjected to free radical damage. This could be a result of essential fatty acid (EFA) deficiency. EFAs also kill enveloped viruses by destroying their fatty coats. At the same time, they are necessary for the normal function of interferon, the body’s own antiviral agent.

Professor PO Behan of the Institute of Neurological Sciences at Glasgow University carried out a placebo controlled study over three months, giving ME patients Efamol Marine, a particular brand of EFA, which contains gamma linoleic acid and fish oil. Eighty five per cent were judged to have improved in terms of fatigue, myalgia, dizziness, poor concentration and depression, (Behan, PO, and Behan WMH, Acta Neurol Scnd, 1990; 82: 209-19). Other possible factors in ME are severe zinc deficiency affecting the immune system, and low chromium levels (John McLaren Howard, InterAction, 12, Spring, 1993) .

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