These findings are consistent with a 2017 study by Dr. William Pridgen that suggested taking the anti-EBV medications Famvir and Celebrex for six months can help a subset of people with CFS and fibromyalgia. I’ve also seen this in thousands of people that I’ve treated.

Meanwhile, another recent study shows that an old diuretic called spironolactone (Aldactone) is also active against Epstein-Barr syndrome. Combining it with other antiviral treatments may enhance their effectiveness, although this must be done cautiously, as the diuretic can lower both testosterone and blood volume. And both of these are already low in people with fibromyalgia.

The price of spironolactone treatment is only $0.20 a day. For most healthy people, it’s also quite safe. However, there are concerns using it to treat CFS/FMS:

• Because it’s a diuretic, spironolactone can dehydrate people. But people with chronic fatigue syndrome and fibromyalgia already tend to be chronically dehydrated. This is because having CFS/FMS lowers your antidiuretic hormone, which leaves you “drinking like a fish and peeing like a racehorse.” Some people I’ve treated have improved with prescription antidiuretic hormone pills (DDAVP or vasopressin, the same medication used for bed wetting). In those needing spironolactone who have low blood pressure or orthostatic intolerance, it can be combined with the DDAVP.
• Spironolactone lowers testosterone levels, which are already in the lowest 30% of the population in 70% of men and women with CFS and fibromyalgia. Research by Prof. Hillary White of Dartmouth showed that treating women who had fibromyalgia with testosterone, despite normal blood levels, decreased their pain. So testosterone levels need to be monitored and optimized when using this treatment.
• Anything that kills off a chronic infection can trigger a “Herxheimer reaction,” which is a severe flare up in symptoms. Years ago, a young woman I was treating was put on spironolactone for high testosterone (called polycystic ovarian syndrome). The first dose put her in the emergency room. I assumed it was because of the diuretic effect and her orthostatic intolerance. But now I suspect it was a Herxheimer reaction. So when adding spironolactone, especially combined with other antivirals, it’s important to start with a very low dose.

Bottom Line?

Spironolactone offers another potential tool for treating people whose CFS and fibromyalgia began with an acute viral infection, have the severe form that leaves them housebound, or who have chronic flu-like symptoms. However, it needs to be used cautiously for the reasons noted above. Fortunately, simple measures can prevent these problems.

Despite the World Health Organization’s listing of this condition as a neurological illness, many doctors and others have for years believed that it was ‘all in the mind’. Such doctors have held sway over the provision of benefits and wheelchairs, and home tuition and distance learning for children. Such help has been routinely refused, leading exhausted patients and parents into legal struggles and appeals to tribunals.

The government’s groundbreaking statement clearly contradicts this view. ‘The Department of Health endorses the view of the CFS/ME Working Group report that there should be no doubt this is a chronic illness and that health and social care professionals should recognise it as such,’ it says.

Benefits, wheelchairs and other equipment are, for the first time, recognised as aiding people with CFS/ME towards independence and enabling them to lead more socially normal lives.

Many mainstream doctors were involved in this report. Decades ago, clinicians knew that this was a disease of physical origin and that their patients were genuinely disabled. Then, two psychiatrists suggested that the 1955 ME epidemic among nurses at the Royal Free Hospital was mass hysteria. One of them had also labelled an epidemic of winter vomiting disease (due to the Norwalk virus) as mass hysteria, a blunder that was forgotten in the rush to include CFS/ME under a psychiatric label.

Since that time, patients have been caught in the middle of a war between factions of the medical profession which still rages with the resignation of several psychiatrists from the Chief Medical Officer’s Working Group in protest at the swinging of the pendulum back to the centre and away from their more extremist view of things.

The myth that psychiatrists can cure CFS/ME is exploded by the report’s admission that, as yet, no one has a cure. ‘Although there is no cure for CFS/ ME, the condition has been found to improve in most patients both with and without treatment; it is good practice to encourage patients to become experts in self-management and to choose between treatment options.’

This is a huge step for patients’ independence. They can now quote this report when choosing whatever treatment they wish – or none.

The government is now developing the concept of the ‘expert patient’, patients who have become experts in self-management. This encompasses the right to decide what is and what isn’t right for them, including alternative therapies.

The report also confirms that, contrary to what many believed, children do suffer from CFS/ME, citing the Dowsett/Colby study involving 333,000 schoolchildren (J CFS, 1997; 3: 29-42). The study found that the illness was causing over half of all long-term sickness absences, more than any other condition. The report acknowledges that CFS/ME is a relatively common condition in both adults and children.

Early recognition with an authoritative, positive diagnosis is cited as key to improving outcomes. This is perhaps the biggest victory of all for patients. It overturns the psychiatric view that, if you give patients a CFS/ME diagnosis, they will develop ‘illness beliefs’ about their condition that will stop them from getting better. In what other disease does the doctor refuse to diagnose the patient?

Some doctors themselves have developed ‘treatment beliefs’ about CFS/ME, believing that graded exercise therapy and cognitive behavioural therapy are, in fact, cures. These therapies involve setting targets for patients to achieve. Many patients feel this is inappropriate. Aiming at targets means failure for many, and an increase in symptoms.

The new report gives ‘pacing’ equal weight. Pacing – promoting healing by living within one’s limits and not provoking symptoms – is the safest management option, according to patient groups, 60 per cent of whose members report becoming worse or receiving no benefit from other treatments. The report admits that all interventional approaches may cause harm in some patients and states that, where adverse effects occur, these could be due to either the therapist’s approach or the fact that the therapy itself is not appropriate.

It is made clear that the trials of graded exercise and cognitive behavioural therapies only covered those patients who were fit enough to attend clinics regularly and were able to cope. The oft-quoted research by K.Y. Fulcher and P.D. White (BMJ, 1997; 314: 1647-52), which claimed success for graded exercise therapy, excluded any patients with known psychiatric illness or sleep disturbances, despite the fact that sleep disturbance is a key symptom of CFS/ME.

This new report is a victory for common sense and the real world and, above all, for the individual patient. It offers clear warnings that evidence of child abuse must be obtained before invoking child protection procedures.

This dictum at last absolves those families who have found themselves the subject of investigation, when their only ‘crime’ was that their child was too ill to go to school and that they didn’t believe that the illness was all in the head.

Jane Colby

Jane Colby is a member of the Chief Medical Officer’s Working Group and Chief Adviser to the Tymes Trust (tel: 01245 401 080), a charity dedicated to the young ME sufferer. Also, see http://www.youngactiononline.com for more information on CFS/ME.

That’s the conclusion of the first randomized placebo controlled, double blind trial (ie, one the medical community approves of) carried out at the University of Southampton medical school, which tested injected magnesium therapy against a placebo, both given to ME patients.

The study found that two thirds of the patients with ME had lower red cell magnesium concentrations than did healthy counterparts.

Of the 15 patients given intramuscular magnesium sulphate for six weeks, 12 reported improved energy levels, better emotional states and less pain compared to only 3 of the 17 controls.

Furthermore, the red blood cell magnesium of all the patients on magnesium returned to normal, compared to only one of the controls.

Just a few decades ago, hospital wards were full of children in iron lungs as a result of polio. No longer. The horrific spectacle appeared to abate with the advent of vaccination, but nothing is without its price.

The public breathed a sigh of relief and even the medical profession believed, and still seems to believe, that the dreaded scourge of polio was at last being vanquished. We read predictions that it will be wiped out by the year 2000.

But a body of evidence is growing linking myalgic encephalomyelitis (ME) to this terrible disease largely caused by attempts to eradicate polio. An alternative polio seems to be upon us.

The proceedings of the first international scientific conference on the Post-Polio Syndrome in the US have been collated in the Annals of the New York Academy of Science. It includes 50 papers written by 118 contributors from a wide range of specialties, including clinical neurology, neuroscience, electrophysiology, brain imaging, histology, virology, immunology, epidemiology and rehabilitation.

In particular, papers by Dr Richard Bruno, assistant professor at the New Jersey Medical School’s department of physical medicine and rehabilitation and director of Post-Polio Rehabilitation and Research Service at the Kessler Institute for Rehabilitation in New Jersey, and four other specialists compare in graphic detail ME now often called Chronic Fatigue Syndrome and Post-Polio Syndrome (Dalakas, et al, ed. The Post Polio Syndrome: Advances in the Pathogenesis and Treatment, Annals, NY Academy, Sciences, 1995: 273: 1-409). Post-Polio is developing in those who had polio 25-30 years previously. Clinically, it is indistinguishable from ME.

Other researchers demonstrate that ME is just another form of polio, which has increased with the advent of polio vaccination. As one type of gut virus has been eradicated, so other forms have had the space to proliferate.

To understand the link one needs to understand the microbiological habits of both polio and other enterovirus disease that is, gut bugs.

A historical accident has led to various names being given to viruses, all of which share physical, chemical and epidemiological characteristics of what we consider the classic polio virus, which science refers to as polio viruses 1,2 and 3 (Dowsett: Journal of Hospital Infection, 1988; 11: 103-15). In 1948 a polio-like illness in New York state prompted scientists to culture the virus. But what grew looked to them at that time like a new virus.

They called it “Coxsackie” after the small town up the Hudson River where it was found. And they called the disease “Atypical Polio” because its symptoms identified it as a kind of polio, despite the virus being apparently different.

This kind of polio, “Atypical Polio”, has since been renamed “ME” and even more recently, “Chronic Fatigue Syndrome”. But it remains a kind of polio despite the change of name, and newer technology has shown up the generic similarities of the most frequent agent that causes it.

These techniques place Coxsackie, the virus most often implicated in ME, in the polio family tree, along with so-called Echo viruses. Coxsackie has been further divided into Coxsackie type A (with 24 viruses) and Coxsackie type B (six viruses). There are 34 Echo viruses. In total, there are at least 72 enteroviruses in all, with new ones still being discovered.

All this has been unnecessarily confusing and complicated, even for doctors. These days newly discovered enteroviruses are just given a new number, not a new name, since their inter-relationship is recognized.

Had the techniques been available that we now have at our disposal, all these viruses might simply have been called “Polio 1 through 72”.

There are several angles from which to investigate the hypothesis that ME is a type of polio. One is its clinical symptoms. Dr Elizabeth Dowsett , consultant microbiologist of the Southeast Essex NHS Trust who is in the forefront of ME research, explains that true ME (as opposed to fatigue states with other etiologies) strikes one clinically as being polio-like, and it has often been diagnosed as a “non-paralytic polio”. “These patients have weakness, pain down their spines and are systemically ill,” she says.

She feels that it has been an unfortunate mistake to turn to the label “Chronic Fatigue” because true ME is a neurological condition that usually originates with a gut virus infection like Coxsackie.

Apart from clinical examination, in some cases of ME you can actually demonstrate the presence of gut virus infection in the patient. The requirement to put off diagnosing ME for six months after the patient falls ill has unwittingly militated against this. If tests are not done very rapidly after the onset of infection, it is too late to identify the virus.

A blood screening test called the IGM, which shows up recent infection, is an NHS procedure. This can be positive up to three months after infection in adults. As the enteroviruses are characterized by their relapsing nature (on average, three-week intervals), it could also be identified on relapse.

Apart from modern techniques, a research procedure called the acid elution test can remove antibody from circulating virus and can be applied to viruses multiplying in the bowel. Years ago it was difficult to diagnose polio, and it was this very test which was used.

A third way to compare ME with polio is by looking at studies of actual outbreaks which identified the viruses causing it. Here the evidence is particularly striking.

A recent paper by Richard T Johnson, at the Department of Neurology, John Hopkins University School of Medicine, in Baltimore, Maryland, published in the 1995 Annals of the New York Academy of Sciences mentioned above, sets out evidence that has been available since the 1950s. “In the spring of 1957, ” he wrote,” we investigated an epidemic of poliomyelitis in Hawaii. . . of the 39 cases of nonparalytic poliomyelitis, only four were related to type 1 poliovirus. There were 16 cases of echovirus 9, seven cases of Coxsackie, and four to five other enteroviruses.”

The very enteroviruses known to be implicated in so-called ME were here identified as causing “non-paralytic polio”. ME has often been diagnosed as “non-paralytic polio”. And even more interestingly, two of the 38 cases of paralytic disease were not caused by the polio virus at all, but by one of the Coxsackie viruses.

So we know that enteroviruses in general can cause varying forms of the disease we call polio.

Other parallels between ME and polio concern neurological damage.

In the November 1991 edition of Orthopedics, Dr Bruno says that “all the evidence available shows conclusively that every case of poliomyelitis, human or experimental, exhibits lesions of the brain. In the experimental animal this included non-paralytic and abortive cases as well as paralytic cases.” ME has been diagnosed by both italicized names. In fact, brain abnormalities can now be demonstrated in the brains of people with ME using SPECT and MRI scans.

One would expect there to be differences in the diseases caused by different viruses, but if these viruses are all of the same family and use the same receptor sites in the body, one would also expect there to be similarities. This is just what we find.

Dr Bruno says: “Despite the differences between poliomyelitis and ME, an association with the polio virus was suggested by the fact that, of the more than one dozen ME outbreaks before the introduction of the Salk vaccine, nine occurred during or immediately after outbreaks of polio, and several involved hospital staff who cared for polio patients” (Annals, NY Academy of Sciences ,1995).

There is also the case of a woman who fell ill with classical ME/CFS while nursing a lady friend with acute paralytic polio (Hyde et al: Epidemiological Aspects of ME/CFS, Nightingale Research Foundation, Ottowa, Canada, 1994).

But if ME is a type of polio, why doesn’t everyone exposed to the relevant viruses develop ME just as they did polio?

It has been forgotten that, as Dr Thomas Stuttaford of The Times explains, “. . .only a small number of those infected with the polio virus became paralyzed; about 90 per cent didn’t even realize that they had anything more threatening than a cold.” With polio and ME, the state of your immune system governs whether you will be susceptible.

By altering the population’s resistance to a particular organism, we alter the balance of infectious agents in the environment. The circulation of wild polio viruses 1-3 has declined through vaccination. However, this has left us open to the other 69 polio-related viruses, which have thrived (see box, this page).

It is therefore not surprising that since the late 1950s the incidence of ME has risen and risen, and experts predict that it will be the neurological disease of the 21st century. By suppressing the spread of three enteroviruses we have opened the door to the rest.

The argument about whether enterovirus infection persists over many years is still raging. In her 1995 review of the proceedings of the 1994 Post-Polio Conference, Dr Dowsett draws attention to new evidence of persistent enterovirus infection in the central nervous system

of Post-Polio patients.

She concluded: “Three separate groups of virologists from the USA, UK and France have found fragments of enteroviral RNA in the spinal cord, cerebrospinal fluid and blood of some patients with Post-Polio syndrome. The fragments are identified as polio virus by some and as Coxsackie virus by others,” she said.

It is thought that the emergence of late-onset Post-Polio fatigue may result from age-related changes in brain cells that survived the original polio infection (Bruno, Annals, NY Academy of Sciences 1995).

But it can be observed through case histories that just as we see Post-Polio Syndrome 30 years after initial infection, so we are seeing “Post-ME” as well. The Nightingale Research Foundation in Ottawa proposes that in fact they are one and the same condition others believe they may be variations of each other.

What has arisen is “two new diseases with different names, with different degrees of acceptance and exactly the same set of symptoms at exactly the same time. It is unrealistic to believe that we are dealing with two different disease processes and two different causes,” the researchers concluded.

A paper investigating the epidemiological aspects of ME/CFS has revealed further convincing parallels between the behaviour of this disease and polio. It describes the onset of ME as mainly being ushered in by a “minor illness” which has “recently been described as a flu-like illness. . .” The researchers continue: “. . .in reality it is identical to and has all of the features and variability of the ‘minor illness’ of missed or abortive poliomyelitis.”

In comparisons with epidemic polio going back to 1916, they note that “we see the same two typical features” in a typical year with an epidemic of ME : “a decreasing incidence from January to reach a summer low; then . . . the strong late summer increased incidence, peaking in the August to October period.” (Hyde etal: Nightingale Research Foundation,Ottowa, 1994).

ME, or Atypical Polio, is a serious and devastatingly debilitating multi-system malfunction leading to such profound weakness in some children that they are unable to speak and have to be tube-fed. But they can breathe; enteroviruses have an affinity for certain tissues and many do not attack the respiratory centre causing its paralysis, as in polio itself.

Children with polio were given intensive physiotherapy and exercised. Now, up to a half of survivors have gone on to develop Post-Polio. It has been predicted that this will eventually rise to 100 per cent.

What are we doing to our teenage ME sufferers when we force them back to school, deny home tuition and tell them to exercise as a form of therapy?

The “treatment of choice” for those with Post-Polio is “adequate rest, energy conservation, the pacing of activities, and reducing physical and emotional stress” (Bruno: Annals NY Academy of Sciences 1995).

What on earth will happen in 30 years’ time to children now getting ME in a climate where they are disbelieved and told to push themselves through the pain barrier? The condition “Post-ME”, which we are already seeing in adults, may well await them with a vengeance.

We have to ask ourselves the disturbing question: if polio victims had been able to breathe, would we ever have taken that disease seriously?

Jane Colby

!AJane Colby is author of ME: The New Plague (First and Best in Education Ltd, 34 Nene Valley Business Park, Oundle, Peterborough, PE 8 4HL)

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).

However, certain UK psychiatrists have taken it upon themselves to ‘reclassify’ ME as a mental disorder. This is not in accordance with WHO rules and regulations.

ME is only considered ‘all in the mind’ by psychiatrists. – Doris M. Jones, Ilford

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

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.

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) .