To facilitate diagnosis, ask early for routine laboratory tests.Play safe prior to official diagnosis. Many ME sufferers deteriorate through pushing themselves too hard.

If your doctor diagnoses “Chronic Fatigue Syndrome” ask if he will call it “CFS/ME” recommended by the National Task Force. CFS on its own covers numerous conditions.

Keep daily notes of symptoms for medical consultations and as evidence for insurance or benefit claims.

For pain or headache avoid non-steroidal anti-inflammatory drugs, eg aspirin or ibuprofen, especially in children.

Move carefully to avoid accidents due to lack of coordination.

Learn to manage so-called panic attacks. If panic begins, distract yourself. Phone someone, make a drink, talk.

Eat foods that won’t irritate the gut well cooked vegetables and easily absorbed protein, like white meat and fish. Carbohydrate is essential; potato is an excellent source. You may develop food sensitivities, especially to grains (often wheat) or dairy products. Avoid too much fibre or sugar.

Considering having your digestive ability tested. Alternatives columnist Harald Gaier finds that many ME victims have low or no stomach acid (possibly as an after-effect of a gut virus or vaccine). After testing for this and, when necessary, sorting out stomach acid problems, many patients improve.

Avoid alcohol. Smoking is particularly bad, affecting heart, respiratory and immune systems.

Don’t be persuaded into therapies your body protests against. Polio victims should have been rested and helped to pace their lives; ME sufferers need similar treatment to avoid further disability.

Be wary of regimes, whether orthodox or alternative, promising a cure. There is no proven cure for ME, just as there was none for polio. Nevertheless, certain treatments may help symptoms and aid recovery.

ME can be a relapsing condition. Avoid triggering factors, such as immunizations, or too much mental or physical activity.

Children with ME frequently need home tuition. Full-time schooling often provokes relapse. Part-time attendance helps; restrict exam subjects and avoid PE.

Never assume that your ME has totally gone, even if you are symptom free. Evidence shows that “Post-ME” occur many years after initial infection, like Post-Polio. Pace your life; don’t overwork a body that may have as yet unrecognized brain problems.

I have ME, and at one point I was seriously considering the purchase of a stair lift.

I had been using filtered water regularly for two years without any noticeable benefits, but I still felt that I was correct in trying to improve upon tap water. So, about four years ago I began to drink distilled water, which I am quite sure brought me back from the brink of disaster

Although it’s not possible to be completely precise, here are the symptoms I had and an approximate percentage improvement rate:

100 per cent improvement: Scalp irritation. Weight loss became normal to approximately one and a half stone. My bowel movements and faeces became normal, and anal itching and thin, brittle finger and toenails completely resolved.

95 per cent improvement: Early morning heart palpitations or pronounced heart beat. Aching leg muscles when at rest. Muscle twitching. Sharp, stabbing chest pains.

90 per cent improvement: Night time leg cramps, ‘drawing ‘ sensations and inner ‘crawling’ sensations. Profuse night sweats.

80 per cent improvement: Difficulty in waking (morning). General muscle weakness, which used to wake me at night as I was unable to turn over naturally.

70 per cent improvement: Amnesia.

50 per cent improvement: Muscle ‘pulls’, mainly in the lumber region, knees and thighs. Dilated blood vessels. Need to nap during the afternoon. Bloated stomach. Aching leg muscles when walking.

40 per cent improvement: Headaches and overall head pressure due to over concentration.

20 per cent improvement: Difficulty in waking after daytime nap. Constant background headache.

The only symptom I have that hasn’t resolved to some extent is constant tinnitus.

But long standing catarrh problem was normalised. S A L, Brentwood, Essex…..

CASE STUDY

Samantha is one of many children today in a no-win situation. Under the definition of this syndrome, by exercising her legal right to refuse treatment – even treatment that is unsuitable – she is considered mentally ill.

The consequences of disagreement between doctor, child and parents can be horrific. Samantha’s doctors had never encountered such a severe and long-lasting case of ME. They could not see how something often called ‘chronic fatigue syndrome’ could produce continual vomiting, even when being fed by tube. So this young girl ended up on the at-risk register.

Police and social workers swooped down on her home to take her back to hospital. It made no sense. She had stopped vomiting and was putting on weight. Then I read the advice to psychiatrists about this new psychiatric condition.

PRS is not an illness, but a collection of symptoms. Doctors are not encouraged to identify the cause, but to help recovery by forcing children back to normality.

The illness is supposedly most common in girls aged 9 to 14, and was first defined by Lask et al. (Arch Dis Child, 1991; 66: 866-9) as a ‘potentially life-threatening condition manifested by a profound and pervasive refusal to eat, drink, walk, talk or care for themselves in any way over a period of several months’. Confirmed or suspected sexual abuse and/or domestic violence may play a part. Treatment can involve tube-feeding to stop the child starving.

However, where severe physical illness shares the same symptoms, there is much potential for confusion and injustice. A child with severe ME can be physically unable to
speak, swallow, walk, move around or care for herself, and may find social contact too demanding, giving the impression of social withdrawal. Heart rhythm abnormalities, hypotension, failure to thrive or gastrointestinal abnormalities can result from malnutrition as well as from ME.

A child with ME may collapse, but so will a child who, as a psychiatrist sees it, resists efforts to make her perform. Physiotherapists assume that the muscles of such a child are capable of normal functioning once built up again, but abnormal lactic-acid levels and other physical abnormalities are common in ME-affected muscles. A misdiagnosis could therefore lead to more damage.

A diagnosis of PRS is not possible if organic illness can explain the symptoms. Where a previously normal child has a severe case of ME following a viral infection, it can reasonably be assumed that the illness is physical in origin. Even according to Lask et al., physical illnesses must be excluded before making the diagnosis of PRS.

But even then, there is a potential for error. As PRS is thought to reflect severe post-traumatic stress, any severe physical illness – such as severe ME, where a child may be unable to think clearly, recognise his parents or even breathe – may be a predisposing factor.

Clearly, a psychiatrically ill child who retreats from the world to the point of starvation desperately needs help. The team treating a child with supposed PRS is encouraged to stick together to avoid the family becoming too close to any one individual who may reinforce the family’s own views. But this could mean that a doctor or nurse who might come to understand that the child’s illness is physical will feel unable to develop this idea unless he is willing to go up against the majority view. How often have we heard of a tragedy resulting from a physician not making a stand against his peers?

Chillingly, the literature on PRS talks of ‘physical or chemical restraint’. The idea behind this is to protect the child and others from aggressive outbursts that might occur. Nevertheless, studies of PRS warn us that one of the main dangers of treatment in hospital is that the staff can become punitive towards the child. If your child were being punished for being ill, what would you do? Take her home? Think again.

In his report on PRS, Lask says: ‘If the child expresses a clear wish to return home and . . . the parents are able to accept and work on the fact that there is a psychological explanation for their child’s illness, then a gradual return to the family home is indicated.’

This sinister instruction allows for no possibility of a misdiagnosis. Another report on the management of PRS (Clin Child Psychol Psychiatry, 1998; 3: 229-49) states that removal of the child from therapy is a major problem and lists it as a ‘specific problem behaviour’ in the family. ‘This is often the result of a failure to fully accept the diagnosis plus the overprotective nature of the parents,’ say the authors.

So, if you dare to challenge the diagnosis, you are an overprotective, problem parent and you could lose your child. This is pure ‘witchhunt syndrome’. Admit you’re a witch and repent, and we’ll let you go; say you’re innocent and we’ll burn you. In the 21st century, we are telling people to deny that their children are physically ill just so they can get them out of hospital.

Jane Colby
Jane Colby is a medical educator and writer, and is currently also chief advisor to the Tymes Trust, a charity dedicated to The young ME sufferer (01245 263 482).

My case history of ankylosing spondylitis was of a calcified repetitive strain injury (RSI) of the spine. My condition may have been generated by RSI, but was sustained by a pharmaceutical drug that made it impossible for me to recover my health naturally.

Conventional, or allopathic, medicine must be the cause of the growth of chronic conditions such as multiple sclerosis and Parkinson’s disease throughout the 20th century.

This school of medicine has succeeded as a business because it relieves the early symptoms. However, in the long term, it produces a chronic spiralling exaggeration of the original symptoms, and then causes a biological addiction because the body’s natural reaction against drugs is to fight back with the opposite biological effects – which are, of course, the symptoms that the drugs are suppressing.

MS and Parkinson’s, as we know them, must be illnesses caused by allopathic addiction. Important aspects of this form of addiction are a susceptibility to the symptoms, a long-term reactive effect of the drugs and the autosuggestive effect of allopathic diagnosis.

The causes of the original problems in these conditions are quite easy to determine. In the case of MS, it appears to be stress shock or stress fatigue (to which those who get it are susceptible) and, in Parkinson’s, it is the other way around. This disease occurs in people who have adapted successfully to a high-stress situation over many years (for example, the former world-heavyweight boxing champion Muhammad Ali) and whose health has become dependent on it, and who then have this stimulus too-suddenly removed for their health to adapt successfully.

This explanation is supported by an experiment carried out in Honolulu, which found that drinking coffee prevented Parkinson’s. Naturally, such a mild stimulant could not prevent the chronic symptoms of the disease, but it would artificially sustain the stress stimulus that prevents them from occurring.

I think that the history of the NHS’ spiralling costs justifies an investigation into the cost of allopathic-medicine addiction. It seems to me that everyone would benefit from a full, public investigation into this subject. – David Dixon, Letchworth, Herts

It is generally accepted that when a disease such as influenza reaches 400 per 100,000, or 0.4 per cent of the population, it is then considered to be of epidemic proportions. In January 1997, the British Dental Association (BDA) issued a fact file on mercury, stating: “About 3 per cent of the population are estimated to suffer from mercury sensitivity. ”

Three per cent of the UK population alone would represent some 1.75 million people, of whom about one million would have mercury amalgam fillings.

Despite these potentially huge casualties, no action is taken on mercury toxicity and, unlike BSE and AIDS, it has atttracted relatively little media attention. No public money has been allocated for research.

Nevertheless, current research suggests that mercury vapour from fillings may be one of the predominant underlying causes of a broad spectrum of conditions, ranging from gum disease, migraine, headaches, poor memory, depression, anxiety, mental lethargy, chronic fatigue, growth, allergies such as eczema and asthma, and sensitivity reactions to food and inhalants, to rheumatism, arthritis, backache, kidney disease, Alzheimer’s disease, Parkinson’s disease, multiple sclerosis and other neurological disorders.

Hormonal imbalances

Some research has focused on particular problems among women exposed to mercury. One study showed that such women experienced disturbances in the menstrual cycle such as excessive blood flow, irregular periods, premenstrual tension (PMS) and painful menstruation (Pediatr Akush Ginekol, 1971; 33: 56-8). Another showed a higher than expected incidence of spontaneous abortion and premature labour (Gordon A, “Pregnancy in Female Dentists A Mercury Hazard”, presented at the International Conference of Mercury Hazards in Dental Practice, Glasgow, 1981) in women exposed to mercury compared with controls. Their rate of failure of ovulation was also nearly double that of the controls (Akush Ginekol, 1974; 13: 20).

Tests were carried out at the University of Heidelberg on women who had hormonal irregularities and amalgam fillings and who had difficulty in conceiving. At the same time, blood samples were investigated for levels of pesticide contamination. The women tested showed higher levels of urine mercury when given a test that measures the amount of mercury excreted through a chelating agent.

The most common problem by far was mercury contamination, which correlated with the number of amalgam fillings. After removing the fillings, nutritional support and treatment of other environmental contamination burdens, 70 per cent of the women became pregnant without the aid of hormonal therapy (Gynakologie, 1992; 14: 593-602).

Further tests carried out at the University of Heidelberg involved 132 women with amalgam fillings who had abnormal hair growth or hair loss. Nearly half 49 per cent of these women showed significantly elevated mercury levels. After removal of their fillings, the symptoms disappeared in 68 per cent of cases (Klin Labor, 1992; 38: 469-76).

But it is not only women who suffer infertility problems caused by mercury. It has been estimated that about 50 per cent of infertility problems are associated with defective male sperm motility (Pharmacol Toxicol, 1988; 69: 440-4). Research has directly pointed to mercury.

Workers who are occupationally exposed to mercury vapour have been found to have a significant reduction in fertility rate (Am J Industr Med, 1985; 7: 171-86).

Mercury and the heart

Heart attacks were practically unknown in the nineteenth century a time when the general diet was high in fat and dairy products.

There is no full explanation for the substantial increase in heart disease, but the suspect factors are mainly diet, stress, smoking and general lifestyle.

Increasing evidence points to amalgam fillings as one major contributory factor.

A series of studies carried out at Washington University (Proc Soc Exper Biol Med, 1965; 120: 805-8; Proc Soc Exper Biol Med, 1967; 124: 485-90; Am J Physiol, 1970; 219: 755-61; Am J Physiol, 1971; 220: 808-11) demonstrated that mercury causes hypertension by contracting smooth muscle in arterial walls. Inorganic mercury caused blood vessel constriction and subsequent hypertension within minutes of exposure organic mercury did not. The work was subsequently confirmed by researchers at Harvard Medical School (Am J Physiol, 1975; 229: 8-12).

In 1974, the National Institute of Health, part of the US Department of Health, Education and Welfare, published a 333 page account of research in the Soviet Union on the effects of chronic exposure to mercury and its compounds (Cardiotoxic Effects of Mercury, DHEW (NIH) Publication No 74-473, 1974, pp 109-34, 199-210). They reported that mercury affected the function of the heart in a variety of ways, including the ability of heart muscle to contract, and its electrical conductivity and regulation of cardiac activity.

The Soviet researchers also found that mercury produced functional changes in cardiac activity and in heart muscle, and that it accumulated in heart muscle and valves. The damage was evident from ECG changes and through histological studies. They found that heart function was influenced by the effect of mercury on hormones from the pituitary gland.

In 1983, work carried out at the medical school at Lodz in Poland (Thromb Res, 1983; 30: 579-85) found that various mercury compounds in low concentrations accelerated blood clotting.

In 1990, Siblerud (SRI Total Environ, 1990; 99: 23-35) compared subjects with and without amalgam. They found that those with amalgam had significantly higher blood pressure, lower heart rate and lower haemoglobin counts. They also had a greater incidence of chest pains, tachycardia, anaemia and fatigue, and became tired easily and awoke feeling tired. The researchers concluded that: “The data suggest that inorganic mercury poisoning from dental amalgam does affect the cardiovascular system”.

Mercury and the immune system

In 1984, David Eggleston, Associate Professor at the Department of Restorative Dentistry, published a preliminary report which demonstrated the ability of amalgam and nickel to affect the total percentages of T cells (J Prost Dent, 1984; 51: 617-23) those cells which help killer cells to recognise foreign invaders. Two cases involving dental amalgam, and one involving nickel, were presented. The results were similar in all cases. In one of Eggleston’s 21 year old patients who had six amalgam fillings, 47 per cent of lymphocytes were T lymphocytes with amalgam fillings. After removal of these fillings, 73 per cent of lymphocytes were T lymphocytesan increase of 55.3 per cent.

When four amalgam fillings were again placed in the patient, the T lymphocyte count dropped to 55 per cent a decrease of 24.7 per cent. When the patient’s amalgam fillings were replaced with gold, the T lymphocyte count rose from to 72 per cent an increase of 30.9 per cent.

The most recent research (Int J Occup Med Tox, 1995; 4) involving 34 patients with CNS disorders indicated intoxication from dental amalgam. Tests showed pathological findings in 88 per cent of these patients, of whom 60 per cent showed an immune reaction to mercuric chloride. These findings support the view that chronic low level exposure to mercury can compromise or weaken the immune system and adversely affect the defence mechanisms of the body.

ME and chronic fatigue

Mercury may contribute to chronic fatigue conditions and, in some cases, play a predominant role. Chronic fatigue is one of the main presenting symptoms of mercury toxicity, and practitioners expect the condition to improve when fillings are removed. Patients who are severely ill, and often bedridden and test positive to mercury find that symptoms improve to a varying degree when amalgam fillings are removed, but are not cured unless mercury is the predominant factor.

In one instance, a 42 year old GP had been housebound for four years with severe chronic fatigue syndrome (ME). She could only leave home for short journeys using a wheelchair, and had great difficulty in climbing stairs. She had 13 amalgam fillings and tested positive to mercury on a lymphocyte response test. Besides ME symptoms, she also complained of other symptoms such as burning mouth, blurred vision, nausea, constant low grade diarrhoea, muscle pain, depression, tension, irritability, poor memory, low blood pressure, asthma, sinus pain, aching joints and allergies to a range of chemicals.

The patient had all her amalgam fillings removed and, three months later, reported that her physical and mental energy had improved and that her nausea was completely cleared. She was also enjoying her food for the first time in years. The day after her final fillings were removed, her husband gave her some soup. She was amazed that it was the same soup her husband had given her the day before, which she had found tasteless. She also reported that her muddle headedness and lack of concentration had improved, and that she felt much more relaxed. Two years later, the patient confirmed that her improvement had continued.

Whether mercury was the initial cause of her chronic fatigue is a matter of conjecture. What this case illustrates is that even though, in some cases, mercury may not be the predominant causative factor, it can exacerbate an existing condition.

Bacterial resistance to antibiotics

A survey of 356 patients who had not recently been exposed to antibiotics showed a high prevalence of mercury resistant bacteria. They were also significantly more likely to concurrently have resistance to two or more antibiotics (Antimicrob Agents Chemother, 1988; 32: 1801-6).

These findings prompted a three university collaborative investigation in primates (Antimicrob Agents Chemother, 1993; 37: 825-34). This showed that a large proportion of common oral and intestinal bacteria became resistant to mercury two weeks after receiving amalgam fillings. Nearly all the mercury resistant bacteria were resistant to one or more antibiotics such as tetracycline, ampicillin, streptomycin and erythromycin. As in the human study, the monkeys had not had recent exposure to antibiotics, demonstrating that the bacteria had become antibiotic resistant due to exposure to mercury from dental amalgam.

In both studies, the proportion of mercury and antibiotic resistant bacteria declined markedly during the two months after amalgam removal.

These studies confirm earlier work carried out in Japan (Antimicrob Agents Chemother, 1997; 11: 999-1003; Appl Environ Microbiol, 1977; 33: 975- 6; Nature, 1977; 266: 165-7) which showed that the bacterial resistance to antibiotics and mercury can be transferred to other bacteria by strands of DNA. The mercury resistant bacteria constantly recirculate the mercury as vapour exacerbating the increase of antibiotic resistant bacteria. Thus, the situation cannot improve until the source of the mercury is removed.

In a recent paper (Sci Prog, 1997; 80: 103-6), a team from the Eastman Dental Institute pointed out: “It must be remembered that oral streptococci are a major cause of infective endocarditis with a high mortality”. The general systemic consequences of the inability of antibiotics to contain or eliminate these resistant bacteria, commonly called ‘superbugs’, is an escalating and serious problem. The role of mercury in their growth should not be ignored.

Research has shown that mercury from dental amalgam fillings:

Increases mercury resistant bacteria, resulting in the constant recycling of mercury in the body;

Increases antibiotic resistance in bacteria the superbugs with obviously more serious consequences;

That bacteria are capable, via DNA strands, of transferring their resistance to other neighbouring bacteria; and

Mercury in the body and antibiotic resistant bacteria markedly decline after removal of mercury amalgam fillings.

!ADr Jack Levenson

Dr Levenson is author of Menace in the Mouth, published by and available from WDDTY (£9.99 + p&p). He will be speaking on the latest dangers of mercury and fluoride on May 4 at Friends’ Meeting House in London. For tickets or his book, contact WDDTY at 020 8944 9555.

The fluoride issue, a perennial hot potato, is heating up once again. In Britain, the government has recently announced its intention to fluoridate the water of deprived inner city areas, supposedly to improve the dental health of children living there. Later, water fluoridation may be introduced nationwide. A White Paper outlining the government’s plans is scheduled for this spring.

The government and the dental profession have convinced the public that fluoridated water offers nothing but benefits that there is overwhelming evidence that it prevents tooth decay and contributes to the strength of bones. There is tacit admission in the pro fluoride camp that fluoride can also cause harm, but only at high levels: more than 2 ppm in water may cause mottled teeth and over 8 ppm may lead to bone disorders and degenerative changes in the vital organs.

A few lone voices have countered the prevailing view, with published evidence that fluoride can have devastating effects, causing mottled teeth and osteoporosis at very low levels. While much has been written about the effects of too much fluoride on teeth and bones, little is known about the effects of fluoride on the rest of the body.

But new evidence has emerged demonstrating that it can have devastating effects on just about every organ in the body, and may even be partly responsible for behavioural problems like hyperactivity and many puzzling illnesses like ME.

Like mercury, fluoride isn’t exactly an obvious choice for dental health as it is a poison more poisonous than lead and only slightly less poisonous than arsenic (Clin Toxicol Commerc Prod, 1984; 11: 4, 112, 129, 138). It’s been used as a pesticide, and it’s a component in fungicides, rodenticides, anaesthetics and many drugs. The fluoride used in toothpaste, mouth rinses and dental gels is usually sodium fluoride, a waste product from the aluminium industry. Fluoride added to our water supply is hydrofluorosilic acid or sometimes silicofluoride waste products of fertiliser and glass industries.

The late US fluoride critic George L Waldbott discovered that, besides teeth and bones, fluoride can damage soft tissue. According to his research, the small fluorine ion with a high charge density can penetrate every cell of the body and combine with other ions (GL Waldbott et al, Fluoride: The Great Dilemma, Lawrence, Kansas: Corenado Press, 1978: 148-74). It interferes with the metabolism of calcium and phosphorus and the function of the parathyroid glands.

It has a strong affinity to calcium, but will also readily combine with magnesium and manganese ions and so can interfere with many enzyme systems that require these minerals. The interruption of these enzyme systems, in turn, may disturb carbohydrate metabolism, bone formation and muscle function. Indeed, every vital function in the body depends on enzymes; because fluoride easily reaches every organ, many diverse toxic symptoms can result.

Fluoride and enzymes

Enzyme systems react to fluoride in different ways; some are activated, others are inhibited. Lipase (essential for the digestion of fat) and phosphatases (needed to breakdown phosphates) are very sensitive to fluoride. In patients with skeletal fluorosis, succinate dehydrogenase activity is inhibited. In chronic fluoride poisoning, this diminished enzyme activity accounts for muscular weakness and even muscle wasting. Human salivary acid phosphatase is diminished by half when exposed to 3.8 ppm of fluoride. The blood enzyme cholinesterase is inhibited by 61 per cent on exposure to 0.95 ppm fluoride an amount within recommended levels adversely affecting functions of the nervous system (PA Smith, ed, Handbook of Experimental Pharmacology, Berlin: Springer Verlag, 1970: 48-97).

Alkaline phosphatase, an enzyme involved in bone growth and liver function, may also be affected by low level fluoride intake.

According to scientists from the University of California at San Diego, fluoride switches off the enzyme cytochrome C oxidase, an oxygen carrying respiratory enzyme; deficiencies of this vital enzyme have been linked to cancer, severe diseases and even cot death (J Biol Chem, 1984; 259: 12984-88).

It’s also been shown by research at Kings College in London that fluoride forms very strong hydrogen bonds with amides, which are formed when amino acids join together to form a protein (J Am Chem Soc, 1981; 103: 24-8). This can cause chromosomal damage. If the protein is distorted, the body’s immune system no longer recognises it, treats it as a foreign protein and will try to destroy it, which in turn triggers allergic skin or gastrointestinal reactions (J Yiamou-yannis, Fluoride: The Aging Factor, Delaware, Ohio: Health Action Press, 1993: 94-9).

Stomach and bowel disorders are the main features of fluoride intolerance. Even small amounts of fluoride can form hydrofluoric acid in the stomach to produce gastric pains, nausea and vomiting. Young children are particularly at risk. Fluoride tablets can even cause gastric haemorrhages; in one instance, a 9 year old boy sustained such damage that large parts of his stomach had to be removed (Fluoride, 1977; 10: 149-51).

Links with thyroid disease

The most readily identifiable feature of soft tissue fluorosis is extraordinary general fatigue, which is frequently linked to thyroid deficiency. The thyroid gland requires iodine to produce the hormone thyroxine, which controls the rate of metabolism in the body. But when fluorine is present, iodine is displaced, which will cause a thyroid gland to stop working properly (K Roholm, Handbuch Experi-menteller Pharma-kologie, Ergaenzung-swerk, Vol 7, Berlin: Springer, 1938: 20).

The parathyroid gland, which regulates the distribution of calcium and phosphorus in the body, is extremely sensitive to excessive amounts of fluoride. Over 50 years ago, Indian doctors found a close relationship between skeletal fluorosis and hyperparathyroidism (J Hyg 1942; 42: 500-4).

Fluoride has even been shown to affect the pituitary gland, which controls growth rate by regulating the production of thyroid hormones (Seances Soc Biol Fil, 1930; 103: 981-2). In animals, less than normal amounts of thyroid hormones are produced when animals are given water containing a fluoride content equivalent to that of water fluoridation (Bull Schweiz Akad Med Wiss, 1954; 10: 211-20).

Professor A K Susheela of the Fluoride and Fluorosis Research Foundation of India, a consultant to the Indian government, has published over 100 scientific papers on the hazards of fluoride. Using scanning electron microscope photography, she has proved that when exposed to fluoride, red blood cells are killed prematurely, lowering haemoglobin and causing anaemia. She also showed that calcium levels diminish as fluoride levels in the body rise; the gastrointestinal tract mucosa is damaged, causing irritable bowel syndrome; and blood fluoride levels rise continuously with prolonged use of fluoridated toothpaste.

When people are bombarded with fluoride, in the form of fluoridated water, toothpaste and mouth rinses, muscles and elements of connective tissue, particularly collagen fibre and bone tissue, undergo degenerative changes, says Prof Susheela.

At the 1998 US Conference of the International Society for Fluoride Research in Bellingham, Washington, Dr Jennifer Luke from the University of Surrey, UK, presented evidence of the effects of fluoride on the pineal gland in gerbils. In both gerbils and humans this gland helps control the aging process and the production of melatonin, which regulates the sleep/wake cycle. Gerbils exposed to a high level of fluoride experienced a significant decrease in the production of melatonin and earlier genital maturation. While animal studies may not always be applicable to humans, Dr Luke theorised that mass fluoridation may be behind the general decline in the age of puberty in the West (Fluoride, 1998; 31: 175).

In areas where water is fluoridated, evidence shows that dangerously high fluoride concentrations accumulate in many soft tissues and organs of the population, including the heart, kidney and bladder. The highest level ever recorded 8400 ppm was found in the aortas of people living in Grand Rapids, Michigan, where fluoride was first introduced in America.

The heart and blood vessels are affected by fluoride. Cardiac irregularities and low blood pressure have been noted in experimental poisoning using large doses (Publ Health Report, 1956; 71: 459-67). In 1950, five years after experimental introduction of fluoride into drinking water in Grand Rapids, the number of deaths from heart disease nearly doubled. Death rates due to cancer, diabetes and arteriosclerosis were all markedly increased compared to death rates for the rest of the state (The Grand Rapid Herald, July 28, 1955).

By recording the heart’s activity, Japanese researcher Taka Mori showed a direct link between damage to the heart and dental fluorisis in children who drank water with a fluoride content of 0.5 to 6.2 ppm (R Ziegelbecker et al, Emu Verlags Gmbh, Austria: Lahnstein, 1995: 43).

Fluoride affects the brain and entire central nervous system. Neurological problems like headaches, vertigo, spasticity in extremities, visual disturbances and impaired mental acuity can all result. Tissue damage to anterior horn cells (cells in the forward facing section of the spinal cord) has been found (Fluoride, 1975; 8: 61-85).

Official annual statistics revealed that among malnourished children in the Chilean town of Curico, fluoridated since 1953, death rates were 104 per cent higher than in comparable, non fluoridated towns. The general mortality was higher in Curico by 113 per cent, compared with the average for the rest of the country (Emu Verlags: 47-8).

Fluoride and ME

Although few researchers have looked at the role of fluoride in the development of myalgic encephalomyelitis (ME), there are conspicuous similarities between key features of ME/chronic fatigue syndrome (CFS) and those seen in the very early stages of fluoride poisoning (Fluoride, 1998; 31: 13-20; see box, p 1).

Dr John McLaren Howard of Biolab in London offers a few important clues as to why this may be. He discovered that ME patients experience reduced movement of white blood cells when exposed to quite low levels of fluoride (InterAction 14, Autumn, 1994: 53-4). This effect on white blood cells might render patients less able to fight infections efficiently, or lead to an exacerbation of their health problems.

Fluoride also interferes with phagocytosis, as well as causing the release of superoxide free radicals in resting white blood cells. This means that fluoride slows down and weakens the very cells which serve as the body’s defence system. Bacteria, viruses, chemicals and the body’s own damaged or cancerous cells are then allowed to wreak havoc. Minor infections take longer to clear and can cause more serious illness (J Yiamouian-nis, The Aging Factor, Health Action Press, 1993: 32). This is precisely what appears to be happening in many cases of ME.

We do not know how many children or teenagers had topical dental treatment with high concentration fluoride, before succumbing to infections which led to ME/CFS. Tests done by the Japanese researchers at the Nippon Dental College, Tokyo on potential hazards on high doses of fluoride showed that levels as low as 57 ppm could induce genetic damage and irregular synthesis of DNA in mammalian cells. These tests were undertaken to assess the hazards of rub on fluoride products used to prevent tooth decay, at concentrations of 9000 ppm (paper presented at a meeting of The Japanese Society for Cancer Research, August 23, 1982, cited in The Ecologist, 1986; 16: 249-52). Varnishes containing 20,000 ppm fluoride, supposedly to strengthen teeth, may in future be applied.

My son had fluoride treatment to prevent tooth decay in the autumn of 1979, after which his health dramatically deteriorated, commencing with gastric problems, various minor infections and glandular fever, followed by atypical measles, more infections and eventually resulting in ME in 1980.

In the end, the fluoride treatment didn’t work in preventing tooth decay he’s needed 15 fillings over nine years.

The American pathologist Majid Ali of Columbia University, New York, explains that chronic fatigue results from an “accelerated oxidative molecular injury”. Only a well functioning enzyme system can protect us from such injury and maintain normal energy levels. In ME there is a high frequency of membrane deformities, due to increased oxidative stress on the cell membranes, which is why sufferers lack energy similar to what happens in fluoride poisoning (The Canary and Chronic Fatigue, New Jersey: Life Span Press, 1994).

Experienced researchers who have studied ME for decades maintain that, as with polio, it is brought on by damage to anterior horn cells caused by a gut virus, which explains why polio victims are paralysed or suffer from impaired motor function (B M Hyde et al, The Clinical and Scientific Basis of ME/CFS, Ottawa: Nightingale Research Foundation, 1992: 111-6). But fluoride has also been shown to damage anterior horn cells. Gastrointestinal disturbances, often referred to as IBS, are also known to play a significant part in ME, as they are in the chronic fluoride toxicity syndrome.

Severe sleep disturbances, or reversal of sleep rhythm, are a common feature in ME/CFS (Clin: 285-91). Deposits of large quantities of fluoride in the pineal gland of animals have caused similar problems (J Luke, Bellingham Conference, 1998).

At this point, no one knows just how much these syndromes overlap, or to what extent fluoride facilitates the development of ME by various biological agents. The indications are that fluoride may act as as a “facilitating co-factor” and exacerbate existing problems in such patients. Or it could be, as Dr H C Moolenburgh Dutch author and fluoride critic suggests, that ME is one of the end stages of a general chemical poisoning, with fluoride one of the worse offenders.

!ADoris Jones

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) .

I had been ill for the past 35 years of my life but, obviously, had no idea that I was slowly being poisoned

My symptoms up to this year included chronic short-term memory problems (such as walking into a room and forgetting what for, forgetting peoples names, losing the thread of my thought mid-sentence), slurred speech, blurred vision, a fuzzy head, swollen tongue and throat, a metallic taste in my mouth, asthma, IBS, pain in arms and legs (for 17 years), tingling and numbness all over, leg weakness (such that I had to give up driving), food allergies, chronic fatigue and collapsing after using an escalator. I couldn’t enter a shop because clothing and carpets made me feel ill.

For the last few years of my illness, my symptoms were made worse after I had a nickel-backed crown put in. Not only did I have to give up work, but I also couldn’t wear any jewellery, especially earrings, which would make my ears itch. This year, I’ve tried wearing earrings again, and I can leave them in for as long as I like without any ill effects at all.

People are driving with fuzzy, unclear heads and not thinking straight. This may be why cars shoot across in front of you at turnings, because the driver forgot he saw a car coming. I can now look back and see how my driving had deteriorated over the years. Now that I can drive safely again, it concerns me that there are others on the road affected by the mercury in their teeth, but completely oblivious to the fact. It took me three years of special detoxification to remove all the metal from my brain and body.

The majority of doctors don’t believe people who arrive at surgery with a long list of symptoms, and many are referred to psychiatrists. When patients manage to have a mercury test, this often comes up negative as the correct procedure for such a test hasn’t been followed. – Pam Clayton, Irthlingborough, Northants

The condition is identical to neurobehavioural abnormalities noticed since the early 1960s in farmworkers who had been working with sheep dips and insecticides.

These abnormalities, which have never been given a collective name, are identical in onset, symptoms and results of neuroendocrine studies to those suffered by patients with CFS.

To test the theory, Peter Behan of the Institute of Neurological Sciences in Glasgow studied 10 patients suffering from neurobehavioural symptoms for over a year and who had exposure to organophosphates through a sheep dip from between two and five years. Their symptoms included an acute influenza like condition followed by incapacitating fatigue. In all cases, there was a long delay between exposure to the pesticides and the onset of the condition (J Nutr Env Med, 1996; 6: 341-50).

Five years ago, I went to see a different cardiologist, who gave me an ECG and a stress test. He stopped the digoxin and put me on a prescription of flecainide acetate (Tambocor) – 50 mg in the morning and 100 mg at night – together with 3.5 mg/day of warfarin (a blood-thinner).

All my troubles seem to have started from then. My skin is very dry and inclined to break out in rashes. I had a dreadful fungal rash on my feet, which took a long time to clear up. My skin and nerves are very sensitive to heat or cold, and even touch.

I am also getting white rings around my irises; my hair is not in good condition, and my scalp is itchy.

All my joints and muscles are so painful that I find it difficult to walk even short distances. My weight has increased by four stones and it seems almost impossible to keep it under control, let alone lose any.

I am desperately tired all the time and keep having short naps during the day, yet I am not sleeping well at night.

All in all, I feel the quality of my life is not good. The phlebotomist whom I see regularly for blood checks will not admit that any of my problems are due to the drugs I’m taking, and tends to write me off as neurotic.

My doctor has also sent me to a rheumatologist for blood tests, X-rays and a bone-density scan, but nothing much has shown up. I just feel that nobody is listening to me. – DW, Ruislip, Middlesex